anti nav1 8 scn10a antibody  (Alomone Labs)


Bioz Verified Symbol Alomone Labs is a verified supplier
Bioz Manufacturer Symbol Alomone Labs manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94

    Structured Review

    Alomone Labs anti nav1 8 scn10a antibody
    PGE2 upregulates Na V 1.8 through PKA signaling. ( a ) RT-QPCR analysis <t>of</t> <t>Nav1.8</t> in cultured lumbar DRG neurons treated with PGE2 (1 μM) for 2–12 hr. n = 6 per group. ( b ) Representative of western blots of PKA-c, CREB and p-CREB in cultured lumbar DRG neurons treated with PGE2 (1 μM) for 40–160 min. ( c ) Representative of western blots of <t>the</t> <t>Nav1.8</t> in cultured lumbar DRG neurons treated with PGE2 (1 μM), forskolin (10 μM), or 666–15 (1 μM) for 6 hr. Representative traces of action potentials (d, upper) and Nav1.8 currents (d, lower) and statistical analysis of maximal Nav1.8 current density ( f ) of cultured lumbar DRG neurons after sham or ACLT surgery at 1 m. n = 6 per group. ( e, f ) Co-immunostaining of NeuN and Nav1.8 ( g ) and statistical analysis of merged cell numbers ( h ) in ipsilateral L4 DRGs after sham or ACLT surgery at 1 m. n = 6 per group.( i–k ) ChIP experiment showing putative primers ( i ), PCR ( j ) and gel running results ( k ) of Na V 1.8 promoter, the experiments were repeated three times. n.s, non significant, *p
    Anti Nav1 8 Scn10a Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti nav1 8 scn10a antibody/product/Alomone Labs
    Average 94 stars, based on 11 article reviews
    Price from $9.99 to $1999.99
    anti nav1 8 scn10a antibody - by Bioz Stars, 2022-10
    94/100 stars

    Images

    1) Product Images from "Aberrant subchondral osteoblastic metabolism modifies NaV1.8 for osteoarthritis"

    Article Title: Aberrant subchondral osteoblastic metabolism modifies NaV1.8 for osteoarthritis

    Journal: eLife

    doi: 10.7554/eLife.57656

    PGE2 upregulates Na V 1.8 through PKA signaling. ( a ) RT-QPCR analysis of Nav1.8 in cultured lumbar DRG neurons treated with PGE2 (1 μM) for 2–12 hr. n = 6 per group. ( b ) Representative of western blots of PKA-c, CREB and p-CREB in cultured lumbar DRG neurons treated with PGE2 (1 μM) for 40–160 min. ( c ) Representative of western blots of the Nav1.8 in cultured lumbar DRG neurons treated with PGE2 (1 μM), forskolin (10 μM), or 666–15 (1 μM) for 6 hr. Representative traces of action potentials (d, upper) and Nav1.8 currents (d, lower) and statistical analysis of maximal Nav1.8 current density ( f ) of cultured lumbar DRG neurons after sham or ACLT surgery at 1 m. n = 6 per group. ( e, f ) Co-immunostaining of NeuN and Nav1.8 ( g ) and statistical analysis of merged cell numbers ( h ) in ipsilateral L4 DRGs after sham or ACLT surgery at 1 m. n = 6 per group.( i–k ) ChIP experiment showing putative primers ( i ), PCR ( j ) and gel running results ( k ) of Na V 1.8 promoter, the experiments were repeated three times. n.s, non significant, *p
    Figure Legend Snippet: PGE2 upregulates Na V 1.8 through PKA signaling. ( a ) RT-QPCR analysis of Nav1.8 in cultured lumbar DRG neurons treated with PGE2 (1 μM) for 2–12 hr. n = 6 per group. ( b ) Representative of western blots of PKA-c, CREB and p-CREB in cultured lumbar DRG neurons treated with PGE2 (1 μM) for 40–160 min. ( c ) Representative of western blots of the Nav1.8 in cultured lumbar DRG neurons treated with PGE2 (1 μM), forskolin (10 μM), or 666–15 (1 μM) for 6 hr. Representative traces of action potentials (d, upper) and Nav1.8 currents (d, lower) and statistical analysis of maximal Nav1.8 current density ( f ) of cultured lumbar DRG neurons after sham or ACLT surgery at 1 m. n = 6 per group. ( e, f ) Co-immunostaining of NeuN and Nav1.8 ( g ) and statistical analysis of merged cell numbers ( h ) in ipsilateral L4 DRGs after sham or ACLT surgery at 1 m. n = 6 per group.( i–k ) ChIP experiment showing putative primers ( i ), PCR ( j ) and gel running results ( k ) of Na V 1.8 promoter, the experiments were repeated three times. n.s, non significant, *p

    Techniques Used: Quantitative RT-PCR, Cell Culture, Western Blot, Immunostaining, Chromatin Immunoprecipitation, Polymerase Chain Reaction

    Subchondral bone remodeling in Cox2:OCN cKO and EP4:Avil cKO mice after ACLT. ( a, b ) Representative photos of knee joint Safranin Orange and fast green staining ( a ) and statistical analysis ( b ) in Bglap-Cre::Cox2 fl/fl or Cox2 fl/f mice 4 weeks after sham or ACLT surgery at 1 m. Scale bars, 500 μm. ( c, d ) Statistical analysis of BV/TV ( c ) and Tb. Pf ( d ) in Bglap-Cre::Cox2 fl/f mice 4 weeks after sham or ACLT surgery at 1 m. n = 6 per group. ( e, f ) Representative photos of knee joint Safranin Orange and fast green staining ( e ) and statistical analysis ( f ) in Avil-Cre::Ptger4 fl/fl or Ptger4 fl/fl mice 4 weeks after sham or ACLT surgery at 1 m. Scale bars, 500 μm. ( g, h ) Statistical analysis of BV/TV ( g ) and Tb. Pf ( h ) in Ptger4 Avi -/- mice 4 weeks after sham or ACLT surgery at 1 m. n = 6 per group. ( i ) western blot of EPs knockdown on the effect of Nav1.8 upregulation after PGE2 stimulation in DRG. *p
    Figure Legend Snippet: Subchondral bone remodeling in Cox2:OCN cKO and EP4:Avil cKO mice after ACLT. ( a, b ) Representative photos of knee joint Safranin Orange and fast green staining ( a ) and statistical analysis ( b ) in Bglap-Cre::Cox2 fl/fl or Cox2 fl/f mice 4 weeks after sham or ACLT surgery at 1 m. Scale bars, 500 μm. ( c, d ) Statistical analysis of BV/TV ( c ) and Tb. Pf ( d ) in Bglap-Cre::Cox2 fl/f mice 4 weeks after sham or ACLT surgery at 1 m. n = 6 per group. ( e, f ) Representative photos of knee joint Safranin Orange and fast green staining ( e ) and statistical analysis ( f ) in Avil-Cre::Ptger4 fl/fl or Ptger4 fl/fl mice 4 weeks after sham or ACLT surgery at 1 m. Scale bars, 500 μm. ( g, h ) Statistical analysis of BV/TV ( g ) and Tb. Pf ( h ) in Ptger4 Avi -/- mice 4 weeks after sham or ACLT surgery at 1 m. n = 6 per group. ( i ) western blot of EPs knockdown on the effect of Nav1.8 upregulation after PGE2 stimulation in DRG. *p

    Techniques Used: Mouse Assay, Staining, Western Blot

    Mechanical allodynia is reduced in Scn10a-Cre :: Rosa26 iDTRfl/fl ACLT mice. ( a–d ) Representative photos of knee joint Safranin Orange and fast green staining ( a ), Na v 1.8 (green) and DAPI (blue) immunofluorescence in subchondral bone ( b ) and NeuN (red, Na v 1.8 (green) and DAPI (blue) co-immunostaining of ipsilateral L4 DRGs ( c ) and APs ( d ) after sham or ACLT surgery at 1 m. Scale bars, 500 μm ( a ), 20 μm ( b ) and 100 μm ( c ), n = 6 per group. ( e–j ) Statistical analysis of OARSI score ( e ), Nav1.8 immunofluorescence signal in subchondral bone ( f ), number of NeuN, Na v 1.8 co-immunostained neurons in ipsilateral L4 DRG ( g ), number of AP ( h ), catwalk gait analysis ( i ) and left hindpaw PWT ( j ) after sham or ACLT surgery. n = 6 per group, *p
    Figure Legend Snippet: Mechanical allodynia is reduced in Scn10a-Cre :: Rosa26 iDTRfl/fl ACLT mice. ( a–d ) Representative photos of knee joint Safranin Orange and fast green staining ( a ), Na v 1.8 (green) and DAPI (blue) immunofluorescence in subchondral bone ( b ) and NeuN (red, Na v 1.8 (green) and DAPI (blue) co-immunostaining of ipsilateral L4 DRGs ( c ) and APs ( d ) after sham or ACLT surgery at 1 m. Scale bars, 500 μm ( a ), 20 μm ( b ) and 100 μm ( c ), n = 6 per group. ( e–j ) Statistical analysis of OARSI score ( e ), Nav1.8 immunofluorescence signal in subchondral bone ( f ), number of NeuN, Na v 1.8 co-immunostained neurons in ipsilateral L4 DRG ( g ), number of AP ( h ), catwalk gait analysis ( i ) and left hindpaw PWT ( j ) after sham or ACLT surgery. n = 6 per group, *p

    Techniques Used: Mouse Assay, Staining, Immunofluorescence, Immunostaining

    Decreased Na V 1.8 expression and ameliorated mechanical allodynia in Avil-Cre :: Ptger4 fl/fl ACLT mice. ( a, b ) Na V 1.8 immunostaining in subchondral bone ( a ), Activated neurons in ipsilateral L4 DRG using in vivo Pirt-GCaMP3 imaging ( b ) after sham or ACLT surgery at 1 m. Scale bars, 20 μm ( a ), 100 μm ( b ). ( c ) Representative traces of action potentials (upper) and Nav1.8 currents (lower) of ipsilateral L3-5 DRG neurons after sham or ACLT surgery at 1 m. ( d–i ) Statistical analysis of Nav1.8 immunofluorescence signal in subchondral bone ( d ), number of activated neurons in ipsilateral L4 DRG using in vivo Pirt-GCaMP3 imaging ( e ), AP traces ( f ), max Nav1.8 current density ( g ), catwalk gait analysis ( h ) and left hindpaw PWT ( i ) after sham or ACLT surgery. n = 6 per group, *p
    Figure Legend Snippet: Decreased Na V 1.8 expression and ameliorated mechanical allodynia in Avil-Cre :: Ptger4 fl/fl ACLT mice. ( a, b ) Na V 1.8 immunostaining in subchondral bone ( a ), Activated neurons in ipsilateral L4 DRG using in vivo Pirt-GCaMP3 imaging ( b ) after sham or ACLT surgery at 1 m. Scale bars, 20 μm ( a ), 100 μm ( b ). ( c ) Representative traces of action potentials (upper) and Nav1.8 currents (lower) of ipsilateral L3-5 DRG neurons after sham or ACLT surgery at 1 m. ( d–i ) Statistical analysis of Nav1.8 immunofluorescence signal in subchondral bone ( d ), number of activated neurons in ipsilateral L4 DRG using in vivo Pirt-GCaMP3 imaging ( e ), AP traces ( f ), max Nav1.8 current density ( g ), catwalk gait analysis ( h ) and left hindpaw PWT ( i ) after sham or ACLT surgery. n = 6 per group, *p

    Techniques Used: Expressing, Mouse Assay, Immunostaining, In Vivo, Imaging, Immunofluorescence

    2) Product Images from "Neuronal Nav1.8 Channels as a Novel Therapeutic Target of Acute Atrial Fibrillation Prevention"

    Article Title: Neuronal Nav1.8 Channels as a Novel Therapeutic Target of Acute Atrial Fibrillation Prevention

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    doi: 10.1161/JAHA.116.004050

    Immunochemical study of Nav1.8, Nav1.5, PGP 9.5, anti‐choline acetyltransferase (Ch AT ), and anti‐tyrosine hydroxylase (TH) in partial dissected intracardiac ganglia. Protein expression of Nav1.8 (A and B), Nav1.5 (C and D), PGP 9.5 (E and F), Ch AT (G and H), and TH (I and J) present in intracardiac ganglia. Images on the left side show fluorescein isothiocyanate green fluorescence. Images on the right side show nonstained components of the ganglia. Calibration bars in (A through D) are 20 μm and in (E through J) are 50 μm.
    Figure Legend Snippet: Immunochemical study of Nav1.8, Nav1.5, PGP 9.5, anti‐choline acetyltransferase (Ch AT ), and anti‐tyrosine hydroxylase (TH) in partial dissected intracardiac ganglia. Protein expression of Nav1.8 (A and B), Nav1.5 (C and D), PGP 9.5 (E and F), Ch AT (G and H), and TH (I and J) present in intracardiac ganglia. Images on the left side show fluorescein isothiocyanate green fluorescence. Images on the right side show nonstained components of the ganglia. Calibration bars in (A through D) are 20 μm and in (E through J) are 50 μm.

    Techniques Used: Expressing, Fluorescence

    3) Product Images from "Pharmacological Targeting of the Mammalian Clock Reveals a Novel Analgesic for Osteoarthritis-Induced Pain"

    Article Title: Pharmacological Targeting of the Mammalian Clock Reveals a Novel Analgesic for Osteoarthritis-Induced Pain

    Journal: Gene

    doi: 10.1016/j.gene.2018.02.048

    Loss of the clock gene Bmal1 in Nav1.8+ sensory neurons leads to reduced OA (osteoarthritis) pain. (Fig. 4A) Mechanical hyperalgesia was measured using von Frey filament test. The paw withdrawal threshold (PWT) of the bmal1f/f Nav1.8CreERT(−) group (n = 5) were low starting at 2 weeks after OA induction, and were lower than bmal1f/f Nav1.8CreERT(+) group (n = 5) at all time points. (Fig. 4B) Heat hyperalgesia was measured using hot-plate test. The paw thermal threshold (PTT) in the bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) group was not significantly changed. However, expression of Rev-Erb-α in the dorsal root ganglia (DRG) following OA surgery was higher and TRPV1 was lower in in bmal1f/f Nav1.8CreERT(+) vs. bmal1f/f Nav1.8CreERT(−) mice. Double immunofluorescence staining of Rev-Erb-α (red; Fig. 4C and Fig. 4F) and TRPV1 (green; Fig. 4D Fig. 4G) in DRGs of bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups mice. Co-localization of the two stains appears yellow (Fig. Fig. 4E Fig. 4H). A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of Rev-Erb-α and TRPV1 expression in DRG (Fig. 4I-4J). Values are mean±SEM.
    Figure Legend Snippet: Loss of the clock gene Bmal1 in Nav1.8+ sensory neurons leads to reduced OA (osteoarthritis) pain. (Fig. 4A) Mechanical hyperalgesia was measured using von Frey filament test. The paw withdrawal threshold (PWT) of the bmal1f/f Nav1.8CreERT(−) group (n = 5) were low starting at 2 weeks after OA induction, and were lower than bmal1f/f Nav1.8CreERT(+) group (n = 5) at all time points. (Fig. 4B) Heat hyperalgesia was measured using hot-plate test. The paw thermal threshold (PTT) in the bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) group was not significantly changed. However, expression of Rev-Erb-α in the dorsal root ganglia (DRG) following OA surgery was higher and TRPV1 was lower in in bmal1f/f Nav1.8CreERT(+) vs. bmal1f/f Nav1.8CreERT(−) mice. Double immunofluorescence staining of Rev-Erb-α (red; Fig. 4C and Fig. 4F) and TRPV1 (green; Fig. 4D Fig. 4G) in DRGs of bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups mice. Co-localization of the two stains appears yellow (Fig. Fig. 4E Fig. 4H). A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of Rev-Erb-α and TRPV1 expression in DRG (Fig. 4I-4J). Values are mean±SEM.

    Techniques Used: Hot Plate Test, Expressing, Mouse Assay, Double Immunofluorescence Staining

    Loss of the clock gene bmal1 in Nav1.8+ sensory neurons leads to reduced BMAL1 protein in DRG. Expression of BMAL1 protein targets in the dorsal root ganglia (DRG) following OA surgery in bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups. Double immunofluorescence staining of BMAL1 (green; 3A 3D) and NeuN (red; 3B 3E) in DRG of bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups mice. Co-localization of the two stains appears yellow (Fig. 3C 3F). A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of BMAL1 expression in DRGs shows lower expression in the bmal1f/f Nav1.8CreERT(+) group (Fig. 3G). Values are mean±SEM.
    Figure Legend Snippet: Loss of the clock gene bmal1 in Nav1.8+ sensory neurons leads to reduced BMAL1 protein in DRG. Expression of BMAL1 protein targets in the dorsal root ganglia (DRG) following OA surgery in bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups. Double immunofluorescence staining of BMAL1 (green; 3A 3D) and NeuN (red; 3B 3E) in DRG of bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups mice. Co-localization of the two stains appears yellow (Fig. 3C 3F). A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of BMAL1 expression in DRGs shows lower expression in the bmal1f/f Nav1.8CreERT(+) group (Fig. 3G). Values are mean±SEM.

    Techniques Used: Expressing, Double Immunofluorescence Staining, Mouse Assay

    Loss of the clock gene Bmal1 in Nav1.8+ sensory neurons leads to reduced pain-related protein in DRG. Expression of pain-related targets in the dorsal root ganglia (DRG) following OA surgery in bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups. Double immunofluorescence staining of substance P (red; 5A-5B), NGF (red; 5C-5D), CGRP (red; 5E-5F), TrkA (red; 5G-5H) and Nav1.7 (red; 5I-5J) and NeuN (green) in DRG of bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups mice. Co-localization of the two stains appear yellow. A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of substance P, NGF, CGRP, TrkA and Nav1.7 expression in DRGs shows lower expression in the bmal1f/f Nav1.8CreERT(+) group (Fig. 5K-4O). Values are mean±SEM.
    Figure Legend Snippet: Loss of the clock gene Bmal1 in Nav1.8+ sensory neurons leads to reduced pain-related protein in DRG. Expression of pain-related targets in the dorsal root ganglia (DRG) following OA surgery in bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups. Double immunofluorescence staining of substance P (red; 5A-5B), NGF (red; 5C-5D), CGRP (red; 5E-5F), TrkA (red; 5G-5H) and Nav1.7 (red; 5I-5J) and NeuN (green) in DRG of bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups mice. Co-localization of the two stains appear yellow. A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of substance P, NGF, CGRP, TrkA and Nav1.7 expression in DRGs shows lower expression in the bmal1f/f Nav1.8CreERT(+) group (Fig. 5K-4O). Values are mean±SEM.

    Techniques Used: Expressing, Double Immunofluorescence Staining, Mouse Assay

    Analgesic activity of the i.a. REV-ERB agonist SR9009 in a model of OA (osteoarthritis) induced pain. Expression of pain-related targets in the dorsal root ganglia (DRG) following groups of mice including naïve, PMM and SR9009 treated mice. Double immunofluorescence staining of TrkA (red; 7A-7C), NGF (red; 7D-7F), Nav1.7 (red; 7G-7I), Nav1.8 (red; 7J-7L) and TRPV1 (red; 7M-7O) and NeuN (green) in DRGs of Naïve, PMM and SR9009 treated groups mice. Co-localization of the two stains appears yellow. A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of TrkA, NGF, Nav1.7, Nav1.8 and TRPV1expression in DRGs (Fig. 7P-7T) showed that they were increased in OA mice, but that was reduced with i.a. SR9009. Values are mean±SEM.
    Figure Legend Snippet: Analgesic activity of the i.a. REV-ERB agonist SR9009 in a model of OA (osteoarthritis) induced pain. Expression of pain-related targets in the dorsal root ganglia (DRG) following groups of mice including naïve, PMM and SR9009 treated mice. Double immunofluorescence staining of TrkA (red; 7A-7C), NGF (red; 7D-7F), Nav1.7 (red; 7G-7I), Nav1.8 (red; 7J-7L) and TRPV1 (red; 7M-7O) and NeuN (green) in DRGs of Naïve, PMM and SR9009 treated groups mice. Co-localization of the two stains appears yellow. A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of TrkA, NGF, Nav1.7, Nav1.8 and TRPV1expression in DRGs (Fig. 7P-7T) showed that they were increased in OA mice, but that was reduced with i.a. SR9009. Values are mean±SEM.

    Techniques Used: Activity Assay, Expressing, Mouse Assay, Double Immunofluorescence Staining

    4) Product Images from "α-lipoic acid suppresses neuronal excitability and attenuates colonic hypersensitivity to colorectal distention in diabetic rats"

    Article Title: α-lipoic acid suppresses neuronal excitability and attenuates colonic hypersensitivity to colorectal distention in diabetic rats

    Journal: Journal of Pain Research

    doi: 10.2147/JPR.S135017

    ALA downregulated NaV1.7 and NaV1.8 expression. Notes: (A) Western blots for NaV1.7 of T13-L2 DRGs from NS- and ALA-treatment rats. Bar graph showed mean density relative to GAPHD for NaV1.7. ALA treatment greatly reduced expressions of NaV1.7 (n=4 for each group, ** p
    Figure Legend Snippet: ALA downregulated NaV1.7 and NaV1.8 expression. Notes: (A) Western blots for NaV1.7 of T13-L2 DRGs from NS- and ALA-treatment rats. Bar graph showed mean density relative to GAPHD for NaV1.7. ALA treatment greatly reduced expressions of NaV1.7 (n=4 for each group, ** p

    Techniques Used: Expressing, Western Blot

    5) Product Images from "Lidocaine reduces pain behaviors by inhibiting the expression of Nav1.7 and Nav1.8 and diminishing sympathetic sprouting in SNI rats"

    Article Title: Lidocaine reduces pain behaviors by inhibiting the expression of Nav1.7 and Nav1.8 and diminishing sympathetic sprouting in SNI rats

    Journal: Molecular Pain

    doi: 10.1177/17448069221124925

    Lidocaine inhibited expression of Nav1.8 and declined basket-like structure around Nav1.8 positive neurons. (a–c) lidocaine inhibited increase of Nav1.8 protein and mRNA. (d) Lidocaine reduced Spared nerve injury-induced abnormal structure. Size = 50 μm, basket-like structure (yellow arrow), sympathetic sprouting (red), Nav1.8 positive (green). Compared with sham group, * p
    Figure Legend Snippet: Lidocaine inhibited expression of Nav1.8 and declined basket-like structure around Nav1.8 positive neurons. (a–c) lidocaine inhibited increase of Nav1.8 protein and mRNA. (d) Lidocaine reduced Spared nerve injury-induced abnormal structure. Size = 50 μm, basket-like structure (yellow arrow), sympathetic sprouting (red), Nav1.8 positive (green). Compared with sham group, * p

    Techniques Used: Expressing

    Lidocaine inhibited Nav1.7 expression and reducing basket-like structure. (a–b) Lidocaine did not completely reverse Spared nerve injury-induced increase in Nav1.7 protein expression. (c) Lidocaine reduced the increase in Nav1.7 mRNA. (d) Lidocaine inhibits basket structure. Scale = 50 μm, basket-like structure (yellow arrow), sympathetic sprouting (red), Nav1.7 positive (green). Compared with Sham group, *** p
    Figure Legend Snippet: Lidocaine inhibited Nav1.7 expression and reducing basket-like structure. (a–b) Lidocaine did not completely reverse Spared nerve injury-induced increase in Nav1.7 protein expression. (c) Lidocaine reduced the increase in Nav1.7 mRNA. (d) Lidocaine inhibits basket structure. Scale = 50 μm, basket-like structure (yellow arrow), sympathetic sprouting (red), Nav1.7 positive (green). Compared with Sham group, *** p

    Techniques Used: Expressing

    Spared nerve injury promotes the expression of Nav1.7 and induces abnormal basket-like structure. (a) Immunofluorescence showed that the expression of Nav1.7 in DRG increased significantly on the 7th and 21st after SNI. (b) Double immunofluorescence of basket structure in DRG after SNI, which surrounded Nav1.7 positive neurons by TH. Scale = 50 μm. Basket-like structure (yellow arrow), sympathetic sprouting (red) Nav1.7positive (green) (c–d) Western blotting: SNI promoted the expression of Nav1.7 in DRG. (e) Q-PCR results. Compared with Sham group, * p
    Figure Legend Snippet: Spared nerve injury promotes the expression of Nav1.7 and induces abnormal basket-like structure. (a) Immunofluorescence showed that the expression of Nav1.7 in DRG increased significantly on the 7th and 21st after SNI. (b) Double immunofluorescence of basket structure in DRG after SNI, which surrounded Nav1.7 positive neurons by TH. Scale = 50 μm. Basket-like structure (yellow arrow), sympathetic sprouting (red) Nav1.7positive (green) (c–d) Western blotting: SNI promoted the expression of Nav1.7 in DRG. (e) Q-PCR results. Compared with Sham group, * p

    Techniques Used: Expressing, Immunofluorescence, Western Blot, Polymerase Chain Reaction

    Spared nerve injury stimulates the expression of Nav1.8 and induces an abnormal basket-like structure in DRG. (a) Immunofluorescence showed that SNI induced Nav1.8 protein increased significantly. (b) Double immunofluorescence of the basket-like structure of Nav1.8 and TH in DRG after SNI. Scale = 50 μm. Basket-like structure (yellow arrow), sympathetic sprouting (red), Nav1.8 positive (green). (c–e) Western blotting and q-PCR: SNI promoted the expression of Nav1.8 in DRG. Compared with Sham, * p
    Figure Legend Snippet: Spared nerve injury stimulates the expression of Nav1.8 and induces an abnormal basket-like structure in DRG. (a) Immunofluorescence showed that SNI induced Nav1.8 protein increased significantly. (b) Double immunofluorescence of the basket-like structure of Nav1.8 and TH in DRG after SNI. Scale = 50 μm. Basket-like structure (yellow arrow), sympathetic sprouting (red), Nav1.8 positive (green). (c–e) Western blotting and q-PCR: SNI promoted the expression of Nav1.8 in DRG. Compared with Sham, * p

    Techniques Used: Expressing, Immunofluorescence, Western Blot, Polymerase Chain Reaction

    6) Product Images from "Nav1.8 in keratinocytes contributes to ROS-mediated inflammation in inflammatory skin diseases"

    Article Title: Nav1.8 in keratinocytes contributes to ROS-mediated inflammation in inflammatory skin diseases

    Journal: Redox Biology

    doi: 10.1016/j.redox.2022.102427

    Nav1.8 induced ROS accumulation in keratinocyte by interacting with SOD2 directly. A, Nav.18 expression in NC and Nav1.8 knockdown keratinocyte treated with TNFα. B, IL-1β and IL-6 expression in NC and Nav1.8 knockdown keratinocyte treated with TNFα. C, P38, p-P38, P65, p-P65 expression in control and Nav1.8 knockdown keratinocyte treated with TNFα. D, IL-1β and IL-6 expression in control and A-803467-treated keratinocyte stimulated with TNFα. E, The ROS levels of keratinocyte treated with TNFα and Nav1.8 siRNA or A803467. F, The DHE straining of skin lesion from NC and Nav1.8 knockdown mice treated with IMQ or control or PBS or LL37. G, GO enrichment analysis of potential interaction proteins of Nav1.8 C-terminal. H, The ROS levels of and mRNA levels of IL-1β and IL-6 in Nav1.8-C overexpressed keratinocyte treated with mitoTEMPO. I, Co-IP revealed the interaction between Nav1.8-C and SOD2 in keratinocytes. J, The endogenous Co-IP revealed the interaction between Nav1.8 and SOD2 in DRG (Dorsal root ganglion). Data represents the mean ± SEM. and *p
    Figure Legend Snippet: Nav1.8 induced ROS accumulation in keratinocyte by interacting with SOD2 directly. A, Nav.18 expression in NC and Nav1.8 knockdown keratinocyte treated with TNFα. B, IL-1β and IL-6 expression in NC and Nav1.8 knockdown keratinocyte treated with TNFα. C, P38, p-P38, P65, p-P65 expression in control and Nav1.8 knockdown keratinocyte treated with TNFα. D, IL-1β and IL-6 expression in control and A-803467-treated keratinocyte stimulated with TNFα. E, The ROS levels of keratinocyte treated with TNFα and Nav1.8 siRNA or A803467. F, The DHE straining of skin lesion from NC and Nav1.8 knockdown mice treated with IMQ or control or PBS or LL37. G, GO enrichment analysis of potential interaction proteins of Nav1.8 C-terminal. H, The ROS levels of and mRNA levels of IL-1β and IL-6 in Nav1.8-C overexpressed keratinocyte treated with mitoTEMPO. I, Co-IP revealed the interaction between Nav1.8-C and SOD2 in keratinocytes. J, The endogenous Co-IP revealed the interaction between Nav1.8 and SOD2 in DRG (Dorsal root ganglion). Data represents the mean ± SEM. and *p

    Techniques Used: Expressing, Mouse Assay, Co-Immunoprecipitation Assay

    Nav1.8 affects the translocation and acetylation levels of SOD2. A, SOD2 expression in NC and Nav1.8 knockdown keratinocytes treated with TNFα. B, SOD2 activity of NC and Nav1.8 knockdown keratinocyte treated with TNFα, or SOD2 activity of Nav1.8C-overexpressed keratinocyte cells, or SOD2 activity of A803467 treated keratinocyte cells. C, Western blots revealed the effects of Nav1.8-siRNA, Nav1.8-C, or TNFα on the levels of SOD2 in the cytosolic and mitochondrial fractions. D, The immunofluorescence revealed the mitochondrial SOD2 localization. E, Western blots revealed the effects of Nav1.8-siRNA, Nav1.8-C, or TNFα on the levels of SOD2 K68 acetylation.
    Figure Legend Snippet: Nav1.8 affects the translocation and acetylation levels of SOD2. A, SOD2 expression in NC and Nav1.8 knockdown keratinocytes treated with TNFα. B, SOD2 activity of NC and Nav1.8 knockdown keratinocyte treated with TNFα, or SOD2 activity of Nav1.8C-overexpressed keratinocyte cells, or SOD2 activity of A803467 treated keratinocyte cells. C, Western blots revealed the effects of Nav1.8-siRNA, Nav1.8-C, or TNFα on the levels of SOD2 in the cytosolic and mitochondrial fractions. D, The immunofluorescence revealed the mitochondrial SOD2 localization. E, Western blots revealed the effects of Nav1.8-siRNA, Nav1.8-C, or TNFα on the levels of SOD2 K68 acetylation.

    Techniques Used: Translocation Assay, Expressing, Activity Assay, Western Blot, Immunofluorescence

    Nav1.8 expression in rosacea and psoriasis. A, Immunohistochemistry (IHC) of Nav1.8 on skin tissues from HS (healthy individuals) and rosacea patients. Data represents the mean ± SEM. *P
    Figure Legend Snippet: Nav1.8 expression in rosacea and psoriasis. A, Immunohistochemistry (IHC) of Nav1.8 on skin tissues from HS (healthy individuals) and rosacea patients. Data represents the mean ± SEM. *P

    Techniques Used: Expressing, Immunohistochemistry

    Nav1.8 knockdown block rosacea-like development. A, Schematic diagram of intradermal injection of Nav1.8 for continuous 3 days before intradermal injection of LL37 in mice. B, The mRNA levels of Nav1.8 by siRNA in LL37-induced mice. C, The back skins of NC (negative control siRNA) and Nav1.8 knockdown (Nav1.8 siRNA) mice injected with LL37 or PBS. D, The reduced redness score, area of erythema and skin thickness of skin tissues in PBS/LL37-induced mice. Data represents the mean ± SEM. **p
    Figure Legend Snippet: Nav1.8 knockdown block rosacea-like development. A, Schematic diagram of intradermal injection of Nav1.8 for continuous 3 days before intradermal injection of LL37 in mice. B, The mRNA levels of Nav1.8 by siRNA in LL37-induced mice. C, The back skins of NC (negative control siRNA) and Nav1.8 knockdown (Nav1.8 siRNA) mice injected with LL37 or PBS. D, The reduced redness score, area of erythema and skin thickness of skin tissues in PBS/LL37-induced mice. Data represents the mean ± SEM. **p

    Techniques Used: Blocking Assay, Injection, Mouse Assay, Negative Control

    Nav1.8 promoted the progression inflammatory skin disease by regulating cytokines expression in keratinocytes. A, The upregulated genes in NC_LL37 group compared to NC_PBS group. B, The downregulated genes in NC_LL37 group compared to NC_PBS group. C, The GO and KEGG enrichment analysis of the 2390 genes upregulated in NC_LL37 group which were attenuated by Nav1.8 siRNA. D, The T cell activation, Th1/Th17 differentiation, macrophage and neutrophils activation-related genes expression in NC_LL37 group compared to NC_PBS group and in Si_LL37 group compared to NC_LL37 group. E, PPI network analysis revealed the hub genes of these immune-cell related genes. F, The IL1β and IL6 expression in the keratinocytes of rosacea and psoriasis from HRA000809 and GSE166388 datasets. Data represents the mean ± SEM. *p
    Figure Legend Snippet: Nav1.8 promoted the progression inflammatory skin disease by regulating cytokines expression in keratinocytes. A, The upregulated genes in NC_LL37 group compared to NC_PBS group. B, The downregulated genes in NC_LL37 group compared to NC_PBS group. C, The GO and KEGG enrichment analysis of the 2390 genes upregulated in NC_LL37 group which were attenuated by Nav1.8 siRNA. D, The T cell activation, Th1/Th17 differentiation, macrophage and neutrophils activation-related genes expression in NC_LL37 group compared to NC_PBS group and in Si_LL37 group compared to NC_LL37 group. E, PPI network analysis revealed the hub genes of these immune-cell related genes. F, The IL1β and IL6 expression in the keratinocytes of rosacea and psoriasis from HRA000809 and GSE166388 datasets. Data represents the mean ± SEM. *p

    Techniques Used: Expressing, Activation Assay

    Knockdown Nav1.8 attenuated psoriasis-like development in mice. A, Schematic diagram of NC/Nav1.8 siRNA-injected mice treated with IMQ or control. B, The mRNA levels of Nav1.8 silenced by siRNA in the skin tissues from IMQ-induced inflammation mice. Data represents the mean ± SEM. and *p
    Figure Legend Snippet: Knockdown Nav1.8 attenuated psoriasis-like development in mice. A, Schematic diagram of NC/Nav1.8 siRNA-injected mice treated with IMQ or control. B, The mRNA levels of Nav1.8 silenced by siRNA in the skin tissues from IMQ-induced inflammation mice. Data represents the mean ± SEM. and *p

    Techniques Used: Mouse Assay, Injection

    7) Product Images from "Lidocaine reduces pain behaviors by inhibiting the expression of Nav1.7 and Nav1.8 and diminishing sympathetic sprouting in SNI rats"

    Article Title: Lidocaine reduces pain behaviors by inhibiting the expression of Nav1.7 and Nav1.8 and diminishing sympathetic sprouting in SNI rats

    Journal: Molecular Pain

    doi: 10.1177/17448069221124925

    Lidocaine inhibited expression of Nav1.8 and declined basket-like structure around Nav1.8 positive neurons. (a–c) lidocaine inhibited increase of Nav1.8 protein and mRNA. (d) Lidocaine reduced Spared nerve injury-induced abnormal structure. Size = 50 μm, basket-like structure (yellow arrow), sympathetic sprouting (red), Nav1.8 positive (green). Compared with sham group, * p
    Figure Legend Snippet: Lidocaine inhibited expression of Nav1.8 and declined basket-like structure around Nav1.8 positive neurons. (a–c) lidocaine inhibited increase of Nav1.8 protein and mRNA. (d) Lidocaine reduced Spared nerve injury-induced abnormal structure. Size = 50 μm, basket-like structure (yellow arrow), sympathetic sprouting (red), Nav1.8 positive (green). Compared with sham group, * p

    Techniques Used: Expressing

    Lidocaine inhibited Nav1.7 expression and reducing basket-like structure. (a–b) Lidocaine did not completely reverse Spared nerve injury-induced increase in Nav1.7 protein expression. (c) Lidocaine reduced the increase in Nav1.7 mRNA. (d) Lidocaine inhibits basket structure. Scale = 50 μm, basket-like structure (yellow arrow), sympathetic sprouting (red), Nav1.7 positive (green). Compared with Sham group, *** p
    Figure Legend Snippet: Lidocaine inhibited Nav1.7 expression and reducing basket-like structure. (a–b) Lidocaine did not completely reverse Spared nerve injury-induced increase in Nav1.7 protein expression. (c) Lidocaine reduced the increase in Nav1.7 mRNA. (d) Lidocaine inhibits basket structure. Scale = 50 μm, basket-like structure (yellow arrow), sympathetic sprouting (red), Nav1.7 positive (green). Compared with Sham group, *** p

    Techniques Used: Expressing

    Spared nerve injury promotes the expression of Nav1.7 and induces abnormal basket-like structure. (a) Immunofluorescence showed that the expression of Nav1.7 in DRG increased significantly on the 7th and 21st after SNI. (b) Double immunofluorescence of basket structure in DRG after SNI, which surrounded Nav1.7 positive neurons by TH. Scale = 50 μm. Basket-like structure (yellow arrow), sympathetic sprouting (red) Nav1.7positive (green) (c–d) Western blotting: SNI promoted the expression of Nav1.7 in DRG. (e) Q-PCR results. Compared with Sham group, * p
    Figure Legend Snippet: Spared nerve injury promotes the expression of Nav1.7 and induces abnormal basket-like structure. (a) Immunofluorescence showed that the expression of Nav1.7 in DRG increased significantly on the 7th and 21st after SNI. (b) Double immunofluorescence of basket structure in DRG after SNI, which surrounded Nav1.7 positive neurons by TH. Scale = 50 μm. Basket-like structure (yellow arrow), sympathetic sprouting (red) Nav1.7positive (green) (c–d) Western blotting: SNI promoted the expression of Nav1.7 in DRG. (e) Q-PCR results. Compared with Sham group, * p

    Techniques Used: Expressing, Immunofluorescence, Western Blot, Polymerase Chain Reaction

    Spared nerve injury stimulates the expression of Nav1.8 and induces an abnormal basket-like structure in DRG. (a) Immunofluorescence showed that SNI induced Nav1.8 protein increased significantly. (b) Double immunofluorescence of the basket-like structure of Nav1.8 and TH in DRG after SNI. Scale = 50 μm. Basket-like structure (yellow arrow), sympathetic sprouting (red), Nav1.8 positive (green). (c–e) Western blotting and q-PCR: SNI promoted the expression of Nav1.8 in DRG. Compared with Sham, * p
    Figure Legend Snippet: Spared nerve injury stimulates the expression of Nav1.8 and induces an abnormal basket-like structure in DRG. (a) Immunofluorescence showed that SNI induced Nav1.8 protein increased significantly. (b) Double immunofluorescence of the basket-like structure of Nav1.8 and TH in DRG after SNI. Scale = 50 μm. Basket-like structure (yellow arrow), sympathetic sprouting (red), Nav1.8 positive (green). (c–e) Western blotting and q-PCR: SNI promoted the expression of Nav1.8 in DRG. Compared with Sham, * p

    Techniques Used: Expressing, Immunofluorescence, Western Blot, Polymerase Chain Reaction

    8) Product Images from "Nav1.8 in keratinocytes contributes to ROS-mediated inflammation in inflammatory skin diseases"

    Article Title: Nav1.8 in keratinocytes contributes to ROS-mediated inflammation in inflammatory skin diseases

    Journal: Redox Biology

    doi: 10.1016/j.redox.2022.102427

    Nav1.8 induced ROS accumulation in keratinocyte by interacting with SOD2 directly. A, Nav.18 expression in NC and Nav1.8 knockdown keratinocyte treated with TNFα. B, IL-1β and IL-6 expression in NC and Nav1.8 knockdown keratinocyte treated with TNFα. C, P38, p-P38, P65, p-P65 expression in control and Nav1.8 knockdown keratinocyte treated with TNFα. D, IL-1β and IL-6 expression in control and A-803467-treated keratinocyte stimulated with TNFα. E, The ROS levels of keratinocyte treated with TNFα and Nav1.8 siRNA or A803467. F, The DHE straining of skin lesion from NC and Nav1.8 knockdown mice treated with IMQ or control or PBS or LL37. G, GO enrichment analysis of potential interaction proteins of Nav1.8 C-terminal. H, The ROS levels of and mRNA levels of IL-1β and IL-6 in Nav1.8-C overexpressed keratinocyte treated with mitoTEMPO. I, Co-IP revealed the interaction between Nav1.8-C and SOD2 in keratinocytes. J, The endogenous Co-IP revealed the interaction between Nav1.8 and SOD2 in DRG (Dorsal root ganglion). Data represents the mean ± SEM. and *p
    Figure Legend Snippet: Nav1.8 induced ROS accumulation in keratinocyte by interacting with SOD2 directly. A, Nav.18 expression in NC and Nav1.8 knockdown keratinocyte treated with TNFα. B, IL-1β and IL-6 expression in NC and Nav1.8 knockdown keratinocyte treated with TNFα. C, P38, p-P38, P65, p-P65 expression in control and Nav1.8 knockdown keratinocyte treated with TNFα. D, IL-1β and IL-6 expression in control and A-803467-treated keratinocyte stimulated with TNFα. E, The ROS levels of keratinocyte treated with TNFα and Nav1.8 siRNA or A803467. F, The DHE straining of skin lesion from NC and Nav1.8 knockdown mice treated with IMQ or control or PBS or LL37. G, GO enrichment analysis of potential interaction proteins of Nav1.8 C-terminal. H, The ROS levels of and mRNA levels of IL-1β and IL-6 in Nav1.8-C overexpressed keratinocyte treated with mitoTEMPO. I, Co-IP revealed the interaction between Nav1.8-C and SOD2 in keratinocytes. J, The endogenous Co-IP revealed the interaction between Nav1.8 and SOD2 in DRG (Dorsal root ganglion). Data represents the mean ± SEM. and *p

    Techniques Used: Expressing, Mouse Assay, Co-Immunoprecipitation Assay

    Nav1.8 affects the translocation and acetylation levels of SOD2. A, SOD2 expression in NC and Nav1.8 knockdown keratinocytes treated with TNFα. B, SOD2 activity of NC and Nav1.8 knockdown keratinocyte treated with TNFα, or SOD2 activity of Nav1.8C-overexpressed keratinocyte cells, or SOD2 activity of A803467 treated keratinocyte cells. C, Western blots revealed the effects of Nav1.8-siRNA, Nav1.8-C, or TNFα on the levels of SOD2 in the cytosolic and mitochondrial fractions. D, The immunofluorescence revealed the mitochondrial SOD2 localization. E, Western blots revealed the effects of Nav1.8-siRNA, Nav1.8-C, or TNFα on the levels of SOD2 K68 acetylation.
    Figure Legend Snippet: Nav1.8 affects the translocation and acetylation levels of SOD2. A, SOD2 expression in NC and Nav1.8 knockdown keratinocytes treated with TNFα. B, SOD2 activity of NC and Nav1.8 knockdown keratinocyte treated with TNFα, or SOD2 activity of Nav1.8C-overexpressed keratinocyte cells, or SOD2 activity of A803467 treated keratinocyte cells. C, Western blots revealed the effects of Nav1.8-siRNA, Nav1.8-C, or TNFα on the levels of SOD2 in the cytosolic and mitochondrial fractions. D, The immunofluorescence revealed the mitochondrial SOD2 localization. E, Western blots revealed the effects of Nav1.8-siRNA, Nav1.8-C, or TNFα on the levels of SOD2 K68 acetylation.

    Techniques Used: Translocation Assay, Expressing, Activity Assay, Western Blot, Immunofluorescence

    Nav1.8 expression in rosacea and psoriasis. A, Immunohistochemistry (IHC) of Nav1.8 on skin tissues from HS (healthy individuals) and rosacea patients. Data represents the mean ± SEM. *P
    Figure Legend Snippet: Nav1.8 expression in rosacea and psoriasis. A, Immunohistochemistry (IHC) of Nav1.8 on skin tissues from HS (healthy individuals) and rosacea patients. Data represents the mean ± SEM. *P

    Techniques Used: Expressing, Immunohistochemistry

    Nav1.8 knockdown block rosacea-like development. A, Schematic diagram of intradermal injection of Nav1.8 for continuous 3 days before intradermal injection of LL37 in mice. B, The mRNA levels of Nav1.8 by siRNA in LL37-induced mice. C, The back skins of NC (negative control siRNA) and Nav1.8 knockdown (Nav1.8 siRNA) mice injected with LL37 or PBS. D, The reduced redness score, area of erythema and skin thickness of skin tissues in PBS/LL37-induced mice. Data represents the mean ± SEM. **p
    Figure Legend Snippet: Nav1.8 knockdown block rosacea-like development. A, Schematic diagram of intradermal injection of Nav1.8 for continuous 3 days before intradermal injection of LL37 in mice. B, The mRNA levels of Nav1.8 by siRNA in LL37-induced mice. C, The back skins of NC (negative control siRNA) and Nav1.8 knockdown (Nav1.8 siRNA) mice injected with LL37 or PBS. D, The reduced redness score, area of erythema and skin thickness of skin tissues in PBS/LL37-induced mice. Data represents the mean ± SEM. **p

    Techniques Used: Blocking Assay, Injection, Mouse Assay, Negative Control

    Nav1.8 promoted the progression inflammatory skin disease by regulating cytokines expression in keratinocytes. A, The upregulated genes in NC_LL37 group compared to NC_PBS group. B, The downregulated genes in NC_LL37 group compared to NC_PBS group. C, The GO and KEGG enrichment analysis of the 2390 genes upregulated in NC_LL37 group which were attenuated by Nav1.8 siRNA. D, The T cell activation, Th1/Th17 differentiation, macrophage and neutrophils activation-related genes expression in NC_LL37 group compared to NC_PBS group and in Si_LL37 group compared to NC_LL37 group. E, PPI network analysis revealed the hub genes of these immune-cell related genes. F, The IL1β and IL6 expression in the keratinocytes of rosacea and psoriasis from HRA000809 and GSE166388 datasets. Data represents the mean ± SEM. *p
    Figure Legend Snippet: Nav1.8 promoted the progression inflammatory skin disease by regulating cytokines expression in keratinocytes. A, The upregulated genes in NC_LL37 group compared to NC_PBS group. B, The downregulated genes in NC_LL37 group compared to NC_PBS group. C, The GO and KEGG enrichment analysis of the 2390 genes upregulated in NC_LL37 group which were attenuated by Nav1.8 siRNA. D, The T cell activation, Th1/Th17 differentiation, macrophage and neutrophils activation-related genes expression in NC_LL37 group compared to NC_PBS group and in Si_LL37 group compared to NC_LL37 group. E, PPI network analysis revealed the hub genes of these immune-cell related genes. F, The IL1β and IL6 expression in the keratinocytes of rosacea and psoriasis from HRA000809 and GSE166388 datasets. Data represents the mean ± SEM. *p

    Techniques Used: Expressing, Activation Assay

    Knockdown Nav1.8 attenuated psoriasis-like development in mice. A, Schematic diagram of NC/Nav1.8 siRNA-injected mice treated with IMQ or control. B, The mRNA levels of Nav1.8 silenced by siRNA in the skin tissues from IMQ-induced inflammation mice. Data represents the mean ± SEM. and *p
    Figure Legend Snippet: Knockdown Nav1.8 attenuated psoriasis-like development in mice. A, Schematic diagram of NC/Nav1.8 siRNA-injected mice treated with IMQ or control. B, The mRNA levels of Nav1.8 silenced by siRNA in the skin tissues from IMQ-induced inflammation mice. Data represents the mean ± SEM. and *p

    Techniques Used: Mouse Assay, Injection

    9) Product Images from "Growth Differentiation Factor-15 Produces Analgesia by Inhibiting Tetrodotoxin-Resistant Nav1.8 Sodium Channel Activity in Rat Primary Sensory Neurons"

    Article Title: Growth Differentiation Factor-15 Produces Analgesia by Inhibiting Tetrodotoxin-Resistant Nav1.8 Sodium Channel Activity in Rat Primary Sensory Neurons

    Journal: Neuroscience Bulletin

    doi: 10.1007/s12264-021-00709-5

    GDF-15 reduces Nav1.8 currents via ALK2 and intracellular signaling of PKA and ERK in small-diameter DRG neurons. A–C. The ALK2-specific inhibitor DMH-1 blocks GDF-15-induced inhibition of Nav1.8 currents. DMH-1 per se does not affect Nav1.8 currents (** P
    Figure Legend Snippet: GDF-15 reduces Nav1.8 currents via ALK2 and intracellular signaling of PKA and ERK in small-diameter DRG neurons. A–C. The ALK2-specific inhibitor DMH-1 blocks GDF-15-induced inhibition of Nav1.8 currents. DMH-1 per se does not affect Nav1.8 currents (** P

    Techniques Used: Inhibition

    Schematic showing how GDF-15 modulates peripheral nociceptive information. GDF-15 inhibits Nav1.8 on nociceptors by membrane ALK2 and downstream intracellular signals, such as PKA and ERK, leading to a reduction in the excitability of DRG neurons and pain relief.
    Figure Legend Snippet: Schematic showing how GDF-15 modulates peripheral nociceptive information. GDF-15 inhibits Nav1.8 on nociceptors by membrane ALK2 and downstream intracellular signals, such as PKA and ERK, leading to a reduction in the excitability of DRG neurons and pain relief.

    Techniques Used:

    GDF-15 inhibits Nav1.8 currents in small-diameter DRG neurons. A. Isolation of TTX-resistant Nav1.8 currents in the presence of 500 nmol/L TTX. Cells were depolarized to a variety of potentials (–50 mV to +40 mV) from a holding potential of –60 mV, to elicit Nav1.8 currents. B. I–V curve of Nav1.8 currents. C and D. Nav1.8 currents are reduced following incubation with GDF-15 for 10, 20, and 30 min (* P
    Figure Legend Snippet: GDF-15 inhibits Nav1.8 currents in small-diameter DRG neurons. A. Isolation of TTX-resistant Nav1.8 currents in the presence of 500 nmol/L TTX. Cells were depolarized to a variety of potentials (–50 mV to +40 mV) from a holding potential of –60 mV, to elicit Nav1.8 currents. B. I–V curve of Nav1.8 currents. C and D. Nav1.8 currents are reduced following incubation with GDF-15 for 10, 20, and 30 min (* P

    Techniques Used: Isolation, Incubation

    ALK2 expression in DRG neurons. A–D. Double immunofluorescence reveals the expression of ALK2 in peripherin- ( A ), substance P- (SP, B ), calcitonin gene-related peptide- (CGRP, C ), and isolectin B4- (IB4, D ) positive neurons in the DRG (scale bars, 50 μm). E. Immunocytochemistry double staining of ALK2 and Nav1.8 in isolated DRG neurons (scale bar, 30 μm).
    Figure Legend Snippet: ALK2 expression in DRG neurons. A–D. Double immunofluorescence reveals the expression of ALK2 in peripherin- ( A ), substance P- (SP, B ), calcitonin gene-related peptide- (CGRP, C ), and isolectin B4- (IB4, D ) positive neurons in the DRG (scale bars, 50 μm). E. Immunocytochemistry double staining of ALK2 and Nav1.8 in isolated DRG neurons (scale bar, 30 μm).

    Techniques Used: Expressing, Immunofluorescence, Immunocytochemistry, Double Staining, Isolation

    Effects of GDF-15 on the kinetic properties of Nav1.8 channels. A. GDF-15 (1.2 nmol/L) does not shift the voltage-dependent activation curve of Nav1.8 channels. B. GDF-15 left-shifts the steady-state inactivation curve of Nav1.8 channels in a hyperpolarizing direction. C–F. GDF-15 (1.2 nmol/L) exaggerates the frequency-dependent reduction of Nav1.8 currents with increasing stimulation frequency from 1 to 10 Hz (* P
    Figure Legend Snippet: Effects of GDF-15 on the kinetic properties of Nav1.8 channels. A. GDF-15 (1.2 nmol/L) does not shift the voltage-dependent activation curve of Nav1.8 channels. B. GDF-15 left-shifts the steady-state inactivation curve of Nav1.8 channels in a hyperpolarizing direction. C–F. GDF-15 (1.2 nmol/L) exaggerates the frequency-dependent reduction of Nav1.8 currents with increasing stimulation frequency from 1 to 10 Hz (* P

    Techniques Used: Activation Assay

    10) Product Images from "Scorpion Neurotoxin Syb-prII-1 Exerts Analgesic Effect through Nav1.8 Channel and MAPKs Pathway"

    Article Title: Scorpion Neurotoxin Syb-prII-1 Exerts Analgesic Effect through Nav1.8 Channel and MAPKs Pathway

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms23137065

    Effects of Syb-prII-1 on steady-state inactivation curves of Nav1.8 and Nav1.9. ( A ) Nav1.8 inactivation current was generated in 10 mV progressive steps between −120 mV and 0 mV from a holding potential of −100 mV. ( B ) Nav1.8 steady-state inactivation curve. IoN-CCI surgery shifted the steady-state inactivation curve in a hyperpolarizing direction; 4.0 mg/kg Syb-prⅡ-1 shifted the steady-state inactivation curve in a depolarization direction ( n = 9). ( C ) The protocol to elicit Nav1.9 inactivation currents starting from a holding potential of −100 mV, applying conditioning pulses ranging from −110 mV to −35 mV in increments of 5 mV, and applying a test pulse at −50 mV. ( D ) Nav1.9 steady-state inactivation curve IoN-CCI surgery shifted the steady-state inactivation curve in a hyperpolarizing direction; 4.0 mg/kg Syb-prⅡ-1 shifted the steady-state inactivation curve in a depolarization direction ( n = 6).
    Figure Legend Snippet: Effects of Syb-prII-1 on steady-state inactivation curves of Nav1.8 and Nav1.9. ( A ) Nav1.8 inactivation current was generated in 10 mV progressive steps between −120 mV and 0 mV from a holding potential of −100 mV. ( B ) Nav1.8 steady-state inactivation curve. IoN-CCI surgery shifted the steady-state inactivation curve in a hyperpolarizing direction; 4.0 mg/kg Syb-prⅡ-1 shifted the steady-state inactivation curve in a depolarization direction ( n = 9). ( C ) The protocol to elicit Nav1.9 inactivation currents starting from a holding potential of −100 mV, applying conditioning pulses ranging from −110 mV to −35 mV in increments of 5 mV, and applying a test pulse at −50 mV. ( D ) Nav1.9 steady-state inactivation curve IoN-CCI surgery shifted the steady-state inactivation curve in a hyperpolarizing direction; 4.0 mg/kg Syb-prⅡ-1 shifted the steady-state inactivation curve in a depolarization direction ( n = 6).

    Techniques Used: Generated

    Changes in peak currents of Nav1.8 and Nav1.9 after IoN-CCI model and Syb-prII-1 injection. ( A ) The Nav1.8 current was evoked by a depolarizing voltage step from −50 mV to +50 mV in 10 mV increments from a holding potential of −100 mV ( n = 9). ( B ) Effect of Syb-prII-1 on Nav1.8 current density in TG neurons ( n = 9). ( C ) The Nav1.9 current was evoked by a single voltage step at −35 mV from a holding potential of −100 mV ( n = 9). ( D ) Effect of Syb-prII-1 on Nav1.9 current density in TG neurons. Data were shown as mean ± SEM. ### p
    Figure Legend Snippet: Changes in peak currents of Nav1.8 and Nav1.9 after IoN-CCI model and Syb-prII-1 injection. ( A ) The Nav1.8 current was evoked by a depolarizing voltage step from −50 mV to +50 mV in 10 mV increments from a holding potential of −100 mV ( n = 9). ( B ) Effect of Syb-prII-1 on Nav1.8 current density in TG neurons ( n = 9). ( C ) The Nav1.9 current was evoked by a single voltage step at −35 mV from a holding potential of −100 mV ( n = 9). ( D ) Effect of Syb-prII-1 on Nav1.9 current density in TG neurons. Data were shown as mean ± SEM. ### p

    Techniques Used: Injection

    Changes in Nav1.8 and Nav1.9 current I-V curves and steady-state activation curves in TG neurons after IoN-CCI treatment and Syb-prⅡ-1 injection. ( A ) A series of Nav1.8 currents recorded in the presence of 1000 nM TTX. Cells were depolarized to a variety of potentials (−50 mV to +50 mV) from a holding potential of −100 mV to elicit Nav1.8 currents ( n = 9). ( B ) I-V curves of Nav1.8 currents. ( C ) A series of Nav1.9 currents recorded in the presence of 1000 nM TTX. Cells were depolarized to a variety of potentials (−80 mV to −35 mV) from a holding potential of −100 mV to elicit Nav1.9 currents ( n = 9). ( D ) I-V curves of Nav1.9 currents. ( E ) Changes in the steady-state activation curves of Nav1.8 in TG neurons. IoN-CCI surgery shifted the steady-state activation curve in a depolarization direction; 4.0 mg/kg Syb-prⅡ-1 shifted the steady-state activation curve in a hyperpolarizing direction ( n = 9). ( F ) Changes in the steady-state activation curves of Nav1.9 in TG neurons IoN-CCI surgery shifted the steady-state activation curve in a depolarization direction; 4.0 mg/kg Syb-prⅡ-1 shifted the steady-state activation curve in a hyperpolarizing direction ( n = 9).
    Figure Legend Snippet: Changes in Nav1.8 and Nav1.9 current I-V curves and steady-state activation curves in TG neurons after IoN-CCI treatment and Syb-prⅡ-1 injection. ( A ) A series of Nav1.8 currents recorded in the presence of 1000 nM TTX. Cells were depolarized to a variety of potentials (−50 mV to +50 mV) from a holding potential of −100 mV to elicit Nav1.8 currents ( n = 9). ( B ) I-V curves of Nav1.8 currents. ( C ) A series of Nav1.9 currents recorded in the presence of 1000 nM TTX. Cells were depolarized to a variety of potentials (−80 mV to −35 mV) from a holding potential of −100 mV to elicit Nav1.9 currents ( n = 9). ( D ) I-V curves of Nav1.9 currents. ( E ) Changes in the steady-state activation curves of Nav1.8 in TG neurons. IoN-CCI surgery shifted the steady-state activation curve in a depolarization direction; 4.0 mg/kg Syb-prⅡ-1 shifted the steady-state activation curve in a hyperpolarizing direction ( n = 9). ( F ) Changes in the steady-state activation curves of Nav1.9 in TG neurons IoN-CCI surgery shifted the steady-state activation curve in a depolarization direction; 4.0 mg/kg Syb-prⅡ-1 shifted the steady-state activation curve in a hyperpolarizing direction ( n = 9).

    Techniques Used: Activation Assay, Injection

    Expression of Nav1.8 and Nav1.9 in TG neurons. ( A ) TG neurons were labeled with anti-NF200 and anti-Nav1.8/anti-Nav1.9 antibodies. The panel in the columns marked “Merged” is the merged image of the panel in the two left columns. ( B ) Effects of Syb-prII-1 on the expression of Nav1.8 in different groups of trigeminal ganglia. There was a significant decrease in the expression level of Nav1.8 after Syb-prⅡ-1(4.0 mg/kg) treatment. ( C ) Effects of Syb-prII-1 on the expression of Nav1.9 in different groups of trigeminal ganglia. There was no significant decrease in the expression level of Nav1.9 after Syb-prⅡ-1 treatment. All data were presented as mean ± SEM. n = 3. * p
    Figure Legend Snippet: Expression of Nav1.8 and Nav1.9 in TG neurons. ( A ) TG neurons were labeled with anti-NF200 and anti-Nav1.8/anti-Nav1.9 antibodies. The panel in the columns marked “Merged” is the merged image of the panel in the two left columns. ( B ) Effects of Syb-prII-1 on the expression of Nav1.8 in different groups of trigeminal ganglia. There was a significant decrease in the expression level of Nav1.8 after Syb-prⅡ-1(4.0 mg/kg) treatment. ( C ) Effects of Syb-prII-1 on the expression of Nav1.9 in different groups of trigeminal ganglia. There was no significant decrease in the expression level of Nav1.9 after Syb-prⅡ-1 treatment. All data were presented as mean ± SEM. n = 3. * p

    Techniques Used: Expressing, Labeling

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94
    Alomone Labs anti nav1 8 scn10a antibody
    PGE2 upregulates Na V 1.8 through PKA signaling. ( a ) RT-QPCR analysis <t>of</t> <t>Nav1.8</t> in cultured lumbar DRG neurons treated with PGE2 (1 μM) for 2–12 hr. n = 6 per group. ( b ) Representative of western blots of PKA-c, CREB and p-CREB in cultured lumbar DRG neurons treated with PGE2 (1 μM) for 40–160 min. ( c ) Representative of western blots of <t>the</t> <t>Nav1.8</t> in cultured lumbar DRG neurons treated with PGE2 (1 μM), forskolin (10 μM), or 666–15 (1 μM) for 6 hr. Representative traces of action potentials (d, upper) and Nav1.8 currents (d, lower) and statistical analysis of maximal Nav1.8 current density ( f ) of cultured lumbar DRG neurons after sham or ACLT surgery at 1 m. n = 6 per group. ( e, f ) Co-immunostaining of NeuN and Nav1.8 ( g ) and statistical analysis of merged cell numbers ( h ) in ipsilateral L4 DRGs after sham or ACLT surgery at 1 m. n = 6 per group.( i–k ) ChIP experiment showing putative primers ( i ), PCR ( j ) and gel running results ( k ) of Na V 1.8 promoter, the experiments were repeated three times. n.s, non significant, *p
    Anti Nav1 8 Scn10a Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti nav1 8 scn10a antibody/product/Alomone Labs
    Average 94 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    anti nav1 8 scn10a antibody - by Bioz Stars, 2022-10
    94/100 stars
      Buy from Supplier

    Image Search Results


    PGE2 upregulates Na V 1.8 through PKA signaling. ( a ) RT-QPCR analysis of Nav1.8 in cultured lumbar DRG neurons treated with PGE2 (1 μM) for 2–12 hr. n = 6 per group. ( b ) Representative of western blots of PKA-c, CREB and p-CREB in cultured lumbar DRG neurons treated with PGE2 (1 μM) for 40–160 min. ( c ) Representative of western blots of the Nav1.8 in cultured lumbar DRG neurons treated with PGE2 (1 μM), forskolin (10 μM), or 666–15 (1 μM) for 6 hr. Representative traces of action potentials (d, upper) and Nav1.8 currents (d, lower) and statistical analysis of maximal Nav1.8 current density ( f ) of cultured lumbar DRG neurons after sham or ACLT surgery at 1 m. n = 6 per group. ( e, f ) Co-immunostaining of NeuN and Nav1.8 ( g ) and statistical analysis of merged cell numbers ( h ) in ipsilateral L4 DRGs after sham or ACLT surgery at 1 m. n = 6 per group.( i–k ) ChIP experiment showing putative primers ( i ), PCR ( j ) and gel running results ( k ) of Na V 1.8 promoter, the experiments were repeated three times. n.s, non significant, *p

    Journal: eLife

    Article Title: Aberrant subchondral osteoblastic metabolism modifies NaV1.8 for osteoarthritis

    doi: 10.7554/eLife.57656

    Figure Lengend Snippet: PGE2 upregulates Na V 1.8 through PKA signaling. ( a ) RT-QPCR analysis of Nav1.8 in cultured lumbar DRG neurons treated with PGE2 (1 μM) for 2–12 hr. n = 6 per group. ( b ) Representative of western blots of PKA-c, CREB and p-CREB in cultured lumbar DRG neurons treated with PGE2 (1 μM) for 40–160 min. ( c ) Representative of western blots of the Nav1.8 in cultured lumbar DRG neurons treated with PGE2 (1 μM), forskolin (10 μM), or 666–15 (1 μM) for 6 hr. Representative traces of action potentials (d, upper) and Nav1.8 currents (d, lower) and statistical analysis of maximal Nav1.8 current density ( f ) of cultured lumbar DRG neurons after sham or ACLT surgery at 1 m. n = 6 per group. ( e, f ) Co-immunostaining of NeuN and Nav1.8 ( g ) and statistical analysis of merged cell numbers ( h ) in ipsilateral L4 DRGs after sham or ACLT surgery at 1 m. n = 6 per group.( i–k ) ChIP experiment showing putative primers ( i ), PCR ( j ) and gel running results ( k ) of Na V 1.8 promoter, the experiments were repeated three times. n.s, non significant, *p

    Article Snippet: The primary antibodies used are as follow rabbit anti-NaV 1.8 (1:500, ASC-016, Alomone), rabbit anti-CREB (1:2000, #9179, Cell Signaling Technology), rabbit anti-pCREB (1:1000, 9198, Cell Signaling Technology), rabbit anti-PKA c- c-α (1:1000, 4782, Cell Signaling Technology) and rabbit anti-GAPDH (1:1000, 5174, Cell Signaling Technology).

    Techniques: Quantitative RT-PCR, Cell Culture, Western Blot, Immunostaining, Chromatin Immunoprecipitation, Polymerase Chain Reaction

    Subchondral bone remodeling in Cox2:OCN cKO and EP4:Avil cKO mice after ACLT. ( a, b ) Representative photos of knee joint Safranin Orange and fast green staining ( a ) and statistical analysis ( b ) in Bglap-Cre::Cox2 fl/fl or Cox2 fl/f mice 4 weeks after sham or ACLT surgery at 1 m. Scale bars, 500 μm. ( c, d ) Statistical analysis of BV/TV ( c ) and Tb. Pf ( d ) in Bglap-Cre::Cox2 fl/f mice 4 weeks after sham or ACLT surgery at 1 m. n = 6 per group. ( e, f ) Representative photos of knee joint Safranin Orange and fast green staining ( e ) and statistical analysis ( f ) in Avil-Cre::Ptger4 fl/fl or Ptger4 fl/fl mice 4 weeks after sham or ACLT surgery at 1 m. Scale bars, 500 μm. ( g, h ) Statistical analysis of BV/TV ( g ) and Tb. Pf ( h ) in Ptger4 Avi -/- mice 4 weeks after sham or ACLT surgery at 1 m. n = 6 per group. ( i ) western blot of EPs knockdown on the effect of Nav1.8 upregulation after PGE2 stimulation in DRG. *p

    Journal: eLife

    Article Title: Aberrant subchondral osteoblastic metabolism modifies NaV1.8 for osteoarthritis

    doi: 10.7554/eLife.57656

    Figure Lengend Snippet: Subchondral bone remodeling in Cox2:OCN cKO and EP4:Avil cKO mice after ACLT. ( a, b ) Representative photos of knee joint Safranin Orange and fast green staining ( a ) and statistical analysis ( b ) in Bglap-Cre::Cox2 fl/fl or Cox2 fl/f mice 4 weeks after sham or ACLT surgery at 1 m. Scale bars, 500 μm. ( c, d ) Statistical analysis of BV/TV ( c ) and Tb. Pf ( d ) in Bglap-Cre::Cox2 fl/f mice 4 weeks after sham or ACLT surgery at 1 m. n = 6 per group. ( e, f ) Representative photos of knee joint Safranin Orange and fast green staining ( e ) and statistical analysis ( f ) in Avil-Cre::Ptger4 fl/fl or Ptger4 fl/fl mice 4 weeks after sham or ACLT surgery at 1 m. Scale bars, 500 μm. ( g, h ) Statistical analysis of BV/TV ( g ) and Tb. Pf ( h ) in Ptger4 Avi -/- mice 4 weeks after sham or ACLT surgery at 1 m. n = 6 per group. ( i ) western blot of EPs knockdown on the effect of Nav1.8 upregulation after PGE2 stimulation in DRG. *p

    Article Snippet: The primary antibodies used are as follow rabbit anti-NaV 1.8 (1:500, ASC-016, Alomone), rabbit anti-CREB (1:2000, #9179, Cell Signaling Technology), rabbit anti-pCREB (1:1000, 9198, Cell Signaling Technology), rabbit anti-PKA c- c-α (1:1000, 4782, Cell Signaling Technology) and rabbit anti-GAPDH (1:1000, 5174, Cell Signaling Technology).

    Techniques: Mouse Assay, Staining, Western Blot

    Mechanical allodynia is reduced in Scn10a-Cre :: Rosa26 iDTRfl/fl ACLT mice. ( a–d ) Representative photos of knee joint Safranin Orange and fast green staining ( a ), Na v 1.8 (green) and DAPI (blue) immunofluorescence in subchondral bone ( b ) and NeuN (red, Na v 1.8 (green) and DAPI (blue) co-immunostaining of ipsilateral L4 DRGs ( c ) and APs ( d ) after sham or ACLT surgery at 1 m. Scale bars, 500 μm ( a ), 20 μm ( b ) and 100 μm ( c ), n = 6 per group. ( e–j ) Statistical analysis of OARSI score ( e ), Nav1.8 immunofluorescence signal in subchondral bone ( f ), number of NeuN, Na v 1.8 co-immunostained neurons in ipsilateral L4 DRG ( g ), number of AP ( h ), catwalk gait analysis ( i ) and left hindpaw PWT ( j ) after sham or ACLT surgery. n = 6 per group, *p

    Journal: eLife

    Article Title: Aberrant subchondral osteoblastic metabolism modifies NaV1.8 for osteoarthritis

    doi: 10.7554/eLife.57656

    Figure Lengend Snippet: Mechanical allodynia is reduced in Scn10a-Cre :: Rosa26 iDTRfl/fl ACLT mice. ( a–d ) Representative photos of knee joint Safranin Orange and fast green staining ( a ), Na v 1.8 (green) and DAPI (blue) immunofluorescence in subchondral bone ( b ) and NeuN (red, Na v 1.8 (green) and DAPI (blue) co-immunostaining of ipsilateral L4 DRGs ( c ) and APs ( d ) after sham or ACLT surgery at 1 m. Scale bars, 500 μm ( a ), 20 μm ( b ) and 100 μm ( c ), n = 6 per group. ( e–j ) Statistical analysis of OARSI score ( e ), Nav1.8 immunofluorescence signal in subchondral bone ( f ), number of NeuN, Na v 1.8 co-immunostained neurons in ipsilateral L4 DRG ( g ), number of AP ( h ), catwalk gait analysis ( i ) and left hindpaw PWT ( j ) after sham or ACLT surgery. n = 6 per group, *p

    Article Snippet: The primary antibodies used are as follow rabbit anti-NaV 1.8 (1:500, ASC-016, Alomone), rabbit anti-CREB (1:2000, #9179, Cell Signaling Technology), rabbit anti-pCREB (1:1000, 9198, Cell Signaling Technology), rabbit anti-PKA c- c-α (1:1000, 4782, Cell Signaling Technology) and rabbit anti-GAPDH (1:1000, 5174, Cell Signaling Technology).

    Techniques: Mouse Assay, Staining, Immunofluorescence, Immunostaining

    Decreased Na V 1.8 expression and ameliorated mechanical allodynia in Avil-Cre :: Ptger4 fl/fl ACLT mice. ( a, b ) Na V 1.8 immunostaining in subchondral bone ( a ), Activated neurons in ipsilateral L4 DRG using in vivo Pirt-GCaMP3 imaging ( b ) after sham or ACLT surgery at 1 m. Scale bars, 20 μm ( a ), 100 μm ( b ). ( c ) Representative traces of action potentials (upper) and Nav1.8 currents (lower) of ipsilateral L3-5 DRG neurons after sham or ACLT surgery at 1 m. ( d–i ) Statistical analysis of Nav1.8 immunofluorescence signal in subchondral bone ( d ), number of activated neurons in ipsilateral L4 DRG using in vivo Pirt-GCaMP3 imaging ( e ), AP traces ( f ), max Nav1.8 current density ( g ), catwalk gait analysis ( h ) and left hindpaw PWT ( i ) after sham or ACLT surgery. n = 6 per group, *p

    Journal: eLife

    Article Title: Aberrant subchondral osteoblastic metabolism modifies NaV1.8 for osteoarthritis

    doi: 10.7554/eLife.57656

    Figure Lengend Snippet: Decreased Na V 1.8 expression and ameliorated mechanical allodynia in Avil-Cre :: Ptger4 fl/fl ACLT mice. ( a, b ) Na V 1.8 immunostaining in subchondral bone ( a ), Activated neurons in ipsilateral L4 DRG using in vivo Pirt-GCaMP3 imaging ( b ) after sham or ACLT surgery at 1 m. Scale bars, 20 μm ( a ), 100 μm ( b ). ( c ) Representative traces of action potentials (upper) and Nav1.8 currents (lower) of ipsilateral L3-5 DRG neurons after sham or ACLT surgery at 1 m. ( d–i ) Statistical analysis of Nav1.8 immunofluorescence signal in subchondral bone ( d ), number of activated neurons in ipsilateral L4 DRG using in vivo Pirt-GCaMP3 imaging ( e ), AP traces ( f ), max Nav1.8 current density ( g ), catwalk gait analysis ( h ) and left hindpaw PWT ( i ) after sham or ACLT surgery. n = 6 per group, *p

    Article Snippet: The primary antibodies used are as follow rabbit anti-NaV 1.8 (1:500, ASC-016, Alomone), rabbit anti-CREB (1:2000, #9179, Cell Signaling Technology), rabbit anti-pCREB (1:1000, 9198, Cell Signaling Technology), rabbit anti-PKA c- c-α (1:1000, 4782, Cell Signaling Technology) and rabbit anti-GAPDH (1:1000, 5174, Cell Signaling Technology).

    Techniques: Expressing, Mouse Assay, Immunostaining, In Vivo, Imaging, Immunofluorescence

    Immunochemical study of Nav1.8, Nav1.5, PGP 9.5, anti‐choline acetyltransferase (Ch AT ), and anti‐tyrosine hydroxylase (TH) in partial dissected intracardiac ganglia. Protein expression of Nav1.8 (A and B), Nav1.5 (C and D), PGP 9.5 (E and F), Ch AT (G and H), and TH (I and J) present in intracardiac ganglia. Images on the left side show fluorescein isothiocyanate green fluorescence. Images on the right side show nonstained components of the ganglia. Calibration bars in (A through D) are 20 μm and in (E through J) are 50 μm.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Neuronal Nav1.8 Channels as a Novel Therapeutic Target of Acute Atrial Fibrillation Prevention

    doi: 10.1161/JAHA.116.004050

    Figure Lengend Snippet: Immunochemical study of Nav1.8, Nav1.5, PGP 9.5, anti‐choline acetyltransferase (Ch AT ), and anti‐tyrosine hydroxylase (TH) in partial dissected intracardiac ganglia. Protein expression of Nav1.8 (A and B), Nav1.5 (C and D), PGP 9.5 (E and F), Ch AT (G and H), and TH (I and J) present in intracardiac ganglia. Images on the left side show fluorescein isothiocyanate green fluorescence. Images on the right side show nonstained components of the ganglia. Calibration bars in (A through D) are 20 μm and in (E through J) are 50 μm.

    Article Snippet: Tissue sections were incubated at 4°C overnight with primary antibody specific for rabbit polyclonal anti‐Nav1.8 (Alomone Labs, Jerusalem, Israel), rabbit polyclonal anti‐Nav1.5 (Alomone Labs, Jerusalem, Israel), goat polyclonal anti‐PGP9.5 (Abcam, Cambridge, MA), goat polyclonal anti‐choline acetyltransferase (ChAT, CHEMICON International, Temecula, Canada), and mouse monoclonal anti‐tyrosine hydroxylase (TH, Alpha Diagnostic International, San Antonio, TX).

    Techniques: Expressing, Fluorescence

    Loss of the clock gene Bmal1 in Nav1.8+ sensory neurons leads to reduced OA (osteoarthritis) pain. (Fig. 4A) Mechanical hyperalgesia was measured using von Frey filament test. The paw withdrawal threshold (PWT) of the bmal1f/f Nav1.8CreERT(−) group (n = 5) were low starting at 2 weeks after OA induction, and were lower than bmal1f/f Nav1.8CreERT(+) group (n = 5) at all time points. (Fig. 4B) Heat hyperalgesia was measured using hot-plate test. The paw thermal threshold (PTT) in the bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) group was not significantly changed. However, expression of Rev-Erb-α in the dorsal root ganglia (DRG) following OA surgery was higher and TRPV1 was lower in in bmal1f/f Nav1.8CreERT(+) vs. bmal1f/f Nav1.8CreERT(−) mice. Double immunofluorescence staining of Rev-Erb-α (red; Fig. 4C and Fig. 4F) and TRPV1 (green; Fig. 4D Fig. 4G) in DRGs of bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups mice. Co-localization of the two stains appears yellow (Fig. Fig. 4E Fig. 4H). A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of Rev-Erb-α and TRPV1 expression in DRG (Fig. 4I-4J). Values are mean±SEM.

    Journal: Gene

    Article Title: Pharmacological Targeting of the Mammalian Clock Reveals a Novel Analgesic for Osteoarthritis-Induced Pain

    doi: 10.1016/j.gene.2018.02.048

    Figure Lengend Snippet: Loss of the clock gene Bmal1 in Nav1.8+ sensory neurons leads to reduced OA (osteoarthritis) pain. (Fig. 4A) Mechanical hyperalgesia was measured using von Frey filament test. The paw withdrawal threshold (PWT) of the bmal1f/f Nav1.8CreERT(−) group (n = 5) were low starting at 2 weeks after OA induction, and were lower than bmal1f/f Nav1.8CreERT(+) group (n = 5) at all time points. (Fig. 4B) Heat hyperalgesia was measured using hot-plate test. The paw thermal threshold (PTT) in the bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) group was not significantly changed. However, expression of Rev-Erb-α in the dorsal root ganglia (DRG) following OA surgery was higher and TRPV1 was lower in in bmal1f/f Nav1.8CreERT(+) vs. bmal1f/f Nav1.8CreERT(−) mice. Double immunofluorescence staining of Rev-Erb-α (red; Fig. 4C and Fig. 4F) and TRPV1 (green; Fig. 4D Fig. 4G) in DRGs of bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups mice. Co-localization of the two stains appears yellow (Fig. Fig. 4E Fig. 4H). A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of Rev-Erb-α and TRPV1 expression in DRG (Fig. 4I-4J). Values are mean±SEM.

    Article Snippet: After that, the DRG sections were incubated overnight with anti-rabbit TrkA antibody (1:200, Ab76291; Abcam), anti-rabbit NGF antibody (1:200; Sc-548; Santa Cruz Biotechnology), anti-rabbit Substance-P antibody (1:200; AB1566; Millipore Sigma), anti-rabbit CGRP antibody (1:500; ; Abcam), anti-rabbit Nav1.7 antibody (1:200; ASC-008; Alamone labs), anti-rabbit Nav1.8 antibody (1:200; ASC-016; Alamone labs), anti-guinea pig TRPV1 antibody (1:200; AB5566; Millipore), anti-mouse NeuN antibody (1:500; MAB377; Millipore), anti-rabbit Bmal1 antibody (1:100; NB1002288; Novus) and anti-mouse Rev-erb-α antibody (1:50,Sc-100910; Santa Cruz Biotechnology).

    Techniques: Hot Plate Test, Expressing, Mouse Assay, Double Immunofluorescence Staining

    Loss of the clock gene bmal1 in Nav1.8+ sensory neurons leads to reduced BMAL1 protein in DRG. Expression of BMAL1 protein targets in the dorsal root ganglia (DRG) following OA surgery in bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups. Double immunofluorescence staining of BMAL1 (green; 3A 3D) and NeuN (red; 3B 3E) in DRG of bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups mice. Co-localization of the two stains appears yellow (Fig. 3C 3F). A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of BMAL1 expression in DRGs shows lower expression in the bmal1f/f Nav1.8CreERT(+) group (Fig. 3G). Values are mean±SEM.

    Journal: Gene

    Article Title: Pharmacological Targeting of the Mammalian Clock Reveals a Novel Analgesic for Osteoarthritis-Induced Pain

    doi: 10.1016/j.gene.2018.02.048

    Figure Lengend Snippet: Loss of the clock gene bmal1 in Nav1.8+ sensory neurons leads to reduced BMAL1 protein in DRG. Expression of BMAL1 protein targets in the dorsal root ganglia (DRG) following OA surgery in bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups. Double immunofluorescence staining of BMAL1 (green; 3A 3D) and NeuN (red; 3B 3E) in DRG of bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups mice. Co-localization of the two stains appears yellow (Fig. 3C 3F). A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of BMAL1 expression in DRGs shows lower expression in the bmal1f/f Nav1.8CreERT(+) group (Fig. 3G). Values are mean±SEM.

    Article Snippet: After that, the DRG sections were incubated overnight with anti-rabbit TrkA antibody (1:200, Ab76291; Abcam), anti-rabbit NGF antibody (1:200; Sc-548; Santa Cruz Biotechnology), anti-rabbit Substance-P antibody (1:200; AB1566; Millipore Sigma), anti-rabbit CGRP antibody (1:500; ; Abcam), anti-rabbit Nav1.7 antibody (1:200; ASC-008; Alamone labs), anti-rabbit Nav1.8 antibody (1:200; ASC-016; Alamone labs), anti-guinea pig TRPV1 antibody (1:200; AB5566; Millipore), anti-mouse NeuN antibody (1:500; MAB377; Millipore), anti-rabbit Bmal1 antibody (1:100; NB1002288; Novus) and anti-mouse Rev-erb-α antibody (1:50,Sc-100910; Santa Cruz Biotechnology).

    Techniques: Expressing, Double Immunofluorescence Staining, Mouse Assay

    Loss of the clock gene Bmal1 in Nav1.8+ sensory neurons leads to reduced pain-related protein in DRG. Expression of pain-related targets in the dorsal root ganglia (DRG) following OA surgery in bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups. Double immunofluorescence staining of substance P (red; 5A-5B), NGF (red; 5C-5D), CGRP (red; 5E-5F), TrkA (red; 5G-5H) and Nav1.7 (red; 5I-5J) and NeuN (green) in DRG of bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups mice. Co-localization of the two stains appear yellow. A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of substance P, NGF, CGRP, TrkA and Nav1.7 expression in DRGs shows lower expression in the bmal1f/f Nav1.8CreERT(+) group (Fig. 5K-4O). Values are mean±SEM.

    Journal: Gene

    Article Title: Pharmacological Targeting of the Mammalian Clock Reveals a Novel Analgesic for Osteoarthritis-Induced Pain

    doi: 10.1016/j.gene.2018.02.048

    Figure Lengend Snippet: Loss of the clock gene Bmal1 in Nav1.8+ sensory neurons leads to reduced pain-related protein in DRG. Expression of pain-related targets in the dorsal root ganglia (DRG) following OA surgery in bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups. Double immunofluorescence staining of substance P (red; 5A-5B), NGF (red; 5C-5D), CGRP (red; 5E-5F), TrkA (red; 5G-5H) and Nav1.7 (red; 5I-5J) and NeuN (green) in DRG of bmal1f/f Nav1.8CreERT(−) bmal1f/f Nav1.8CreERT(+) groups mice. Co-localization of the two stains appear yellow. A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of substance P, NGF, CGRP, TrkA and Nav1.7 expression in DRGs shows lower expression in the bmal1f/f Nav1.8CreERT(+) group (Fig. 5K-4O). Values are mean±SEM.

    Article Snippet: After that, the DRG sections were incubated overnight with anti-rabbit TrkA antibody (1:200, Ab76291; Abcam), anti-rabbit NGF antibody (1:200; Sc-548; Santa Cruz Biotechnology), anti-rabbit Substance-P antibody (1:200; AB1566; Millipore Sigma), anti-rabbit CGRP antibody (1:500; ; Abcam), anti-rabbit Nav1.7 antibody (1:200; ASC-008; Alamone labs), anti-rabbit Nav1.8 antibody (1:200; ASC-016; Alamone labs), anti-guinea pig TRPV1 antibody (1:200; AB5566; Millipore), anti-mouse NeuN antibody (1:500; MAB377; Millipore), anti-rabbit Bmal1 antibody (1:100; NB1002288; Novus) and anti-mouse Rev-erb-α antibody (1:50,Sc-100910; Santa Cruz Biotechnology).

    Techniques: Expressing, Double Immunofluorescence Staining, Mouse Assay

    Analgesic activity of the i.a. REV-ERB agonist SR9009 in a model of OA (osteoarthritis) induced pain. Expression of pain-related targets in the dorsal root ganglia (DRG) following groups of mice including naïve, PMM and SR9009 treated mice. Double immunofluorescence staining of TrkA (red; 7A-7C), NGF (red; 7D-7F), Nav1.7 (red; 7G-7I), Nav1.8 (red; 7J-7L) and TRPV1 (red; 7M-7O) and NeuN (green) in DRGs of Naïve, PMM and SR9009 treated groups mice. Co-localization of the two stains appears yellow. A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of TrkA, NGF, Nav1.7, Nav1.8 and TRPV1expression in DRGs (Fig. 7P-7T) showed that they were increased in OA mice, but that was reduced with i.a. SR9009. Values are mean±SEM.

    Journal: Gene

    Article Title: Pharmacological Targeting of the Mammalian Clock Reveals a Novel Analgesic for Osteoarthritis-Induced Pain

    doi: 10.1016/j.gene.2018.02.048

    Figure Lengend Snippet: Analgesic activity of the i.a. REV-ERB agonist SR9009 in a model of OA (osteoarthritis) induced pain. Expression of pain-related targets in the dorsal root ganglia (DRG) following groups of mice including naïve, PMM and SR9009 treated mice. Double immunofluorescence staining of TrkA (red; 7A-7C), NGF (red; 7D-7F), Nav1.7 (red; 7G-7I), Nav1.8 (red; 7J-7L) and TRPV1 (red; 7M-7O) and NeuN (green) in DRGs of Naïve, PMM and SR9009 treated groups mice. Co-localization of the two stains appears yellow. A scale bar was 20μm and is shown in white in color for all images. Quantitative analyses of TrkA, NGF, Nav1.7, Nav1.8 and TRPV1expression in DRGs (Fig. 7P-7T) showed that they were increased in OA mice, but that was reduced with i.a. SR9009. Values are mean±SEM.

    Article Snippet: After that, the DRG sections were incubated overnight with anti-rabbit TrkA antibody (1:200, Ab76291; Abcam), anti-rabbit NGF antibody (1:200; Sc-548; Santa Cruz Biotechnology), anti-rabbit Substance-P antibody (1:200; AB1566; Millipore Sigma), anti-rabbit CGRP antibody (1:500; ; Abcam), anti-rabbit Nav1.7 antibody (1:200; ASC-008; Alamone labs), anti-rabbit Nav1.8 antibody (1:200; ASC-016; Alamone labs), anti-guinea pig TRPV1 antibody (1:200; AB5566; Millipore), anti-mouse NeuN antibody (1:500; MAB377; Millipore), anti-rabbit Bmal1 antibody (1:100; NB1002288; Novus) and anti-mouse Rev-erb-α antibody (1:50,Sc-100910; Santa Cruz Biotechnology).

    Techniques: Activity Assay, Expressing, Mouse Assay, Double Immunofluorescence Staining

    ALA downregulated NaV1.7 and NaV1.8 expression. Notes: (A) Western blots for NaV1.7 of T13-L2 DRGs from NS- and ALA-treatment rats. Bar graph showed mean density relative to GAPHD for NaV1.7. ALA treatment greatly reduced expressions of NaV1.7 (n=4 for each group, ** p

    Journal: Journal of Pain Research

    Article Title: α-lipoic acid suppresses neuronal excitability and attenuates colonic hypersensitivity to colorectal distention in diabetic rats

    doi: 10.2147/JPR.S135017

    Figure Lengend Snippet: ALA downregulated NaV1.7 and NaV1.8 expression. Notes: (A) Western blots for NaV1.7 of T13-L2 DRGs from NS- and ALA-treatment rats. Bar graph showed mean density relative to GAPHD for NaV1.7. ALA treatment greatly reduced expressions of NaV1.7 (n=4 for each group, ** p

    Article Snippet: The primary antibodies used to probe the target proteins included rabbit anti-NaV1.7 or anti-NaV1.8 (1:200, Alomone Labs, Jerusalem, Israel), rabbit anti-GAPDH (1:1000, Biotechnology Co., CHN), and mouse anti-actin (1:1000; Chemicon, Temecula, CA, USA).

    Techniques: Expressing, Western Blot