rabbit anti fn1 Search Results


fibronectin  (Boster Bio)
91
Boster Bio fibronectin
Figure 1. Authentication of primary cultured rat trabecular meshwork (TM) cells. (A) Isolation and proliferation of primary TM cells observed under light microscope. a. Tissue scraps cut from corneoscleral rims. Co: cornea; Ir: iris. Blue triangles indicate the location where TM is supposed to reside. b. Primary TM cells started to crawl out of tissue scraps (indi cated by *) and adhere (indicated by black triangles). c. The attached cells gradually formed “clusters” and became contact-inhibited. d-f. Passage 3 TM cells presented typical spindle-like “fibroblast” phenotype and became cobblestone-like once confluent. Scale bars = 100 μm. (B) Immunofluorescence staining of cultured TM cells with <t>anti-fibronectin,</t> anti-laminin, anti-neuron-specific enolase (NSE), anti-factor- Ⅷ-related antigen (FⅧRAg) antibodies. Scale bar = 100 μm. (C–E) Cells were treated with 200 nM dexamethasone (Dex) for 7 days. Immunohistochem istry staining showed that over fifty percent of TM cells were myocilin-positive (the whole cell was yellow-stained) and was statistically different to that of vehicle control. Western blotting with anti- myocilin antibody showed a doublet at 55 kDa for the Dex-treated group. MYOC: myocilin. Scale bar = 300 μm. (F) Cells were treated with 100 nM Dex or ethanol control for 7 days and dyed with phalloidin. Cross-linked actin networks (CLANs) were observed and indicated by white triangles. Scale bars = 100 μm.
Fibronectin, supplied by Boster Bio, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/fibronectin/product/Boster Bio
Average 91 stars, based on 1 article reviews
fibronectin - by Bioz Stars, 2026-02
91/100 stars
  Buy from Supplier
fn1  (Cusabio)
92
Cusabio fn1
The compound-target-signaling networks generated using Cytoscape_v3.8.0. The active compounds cyclopamine, quercetin, kaempferol and mairin could target 12 IDD disease genes including HMGB1, PTEN, IGFBP6, FGFR3, COL3A1, MMP2, SMAD2, HSPG2, GPC1, <t>FN1,</t> CUL4B, CSGALNACT1 (Among 13 target genes, INTS8 did not have pathway enrichment). The compound-targeted disease genes were enriched in 23 pathways.
Fn1, supplied by Cusabio, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/fn1/product/Cusabio
Average 92 stars, based on 1 article reviews
fn1 - by Bioz Stars, 2026-02
92/100 stars
  Buy from Supplier
anti-fn1/fibronectin  (Merck & Co)
90
Merck & Co anti-fn1/fibronectin
Effect of tnfaip2 deletion on diabetes-induced glomerular structural abnormalities, markers of fibrosis, and inflammation. Renal cortex samples from diabetic (DM) and non-diabetic (ND) both WT (ND-WT, DM-WT) and tnfaip2 KO (ND-KO, DM-KO) mice were studied 12 weeks after diabetes onset. (A) Representative periodic acid Schiff (PAS) staining images (magnification 400X, scale bar: 50 µm) and (B) quantification of glomerulosclerosis are shown ( n = 6 mice per group; ***p < 0.001 DM-WT vs. ND-WT; DM-KO vs. DM-WT). (C) Electron microscopy images showing a more prominent mesangial expansion in the glomeruli from DM-KO mice compared to DM-WT mice (magnification 3200X). (D) Immunofluorescence images of glomerular <t>FN1</t> <t>(fibronectin</t> 1) are shown (magnification 400X, scale bar: 50 µm). (E) Quantification of the percent area of glomerular FN1-positive staining ( n = 6 mice per group; ***p < 0.001 DM-WT vs. ND-WT; DM-KO vs. DM-WT). (F) Tgfb1 mRNA levels were measured by real-time PCR in total renal cortex and corrected for the expression of the housekeeping gene Hprt ( n = 5 mice per group; *p < 0.05 DM-WT vs. ND-WT; DM-KO vs. DM-WT). (G) Glomerular macrophage accrual was evaluated by counting the number of LGALS3/MAC2-positive cells per glomerulus ( n = 6 mice per group; ***p < 0.001 DM-WT vs. ND-WT; DM-KO vs. DM-WT). mRNA levels of Ly6c2 (H), Ccl2 (I), Ccr2 (J), and Tnf (K) were measured in the renal cortex by real time-PCR and the results corrected for the expression of the housekeeping gene Hprt ( n = 5 mice per group; *p < 0.05 DM-WT vs. ND-WT; **p < 0.01 DM-KO vs. DM-WT). (L) Schematic illustration of the protocol used for generating diabetic (DM) tnfaip2 KO chimeric mice. Recipient tnfaip2 KO mice were lethally irradiated, and then reconstituted with bone marrow (BM) from either WT (DM-KO-c WT ) or KO (DM-KO-c KO ) mice. (M) PCR genotyping of peripheral blood cells from chimeric animals. M: marker; NC: no template control. (N) ALB (albumin) excretion rate (AER) was measured after 12 weeks of diabetes in transplanted animals. (*p < 0.05 DM-WT-c WT vs. ND-WT-c WT ; DM-KO-c WT and DM-KO-c KO vs. DM-WT-c WT. (O) Representative images of PAS staining of renal cortex sections from transplanted animals (magnification 400X, scale bar: 50 µm).
Anti Fn1/Fibronectin, supplied by Merck & Co, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti-fn1/fibronectin/product/Merck & Co
Average 90 stars, based on 1 article reviews
anti-fn1/fibronectin - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier
fn1 rabbit polyclonal anti-fibronectin-1  (Becton Dickinson)
90
Becton Dickinson fn1 rabbit polyclonal anti-fibronectin-1
Effect of tnfaip2 deletion on diabetes-induced glomerular structural abnormalities, markers of fibrosis, and inflammation. Renal cortex samples from diabetic (DM) and non-diabetic (ND) both WT (ND-WT, DM-WT) and tnfaip2 KO (ND-KO, DM-KO) mice were studied 12 weeks after diabetes onset. (A) Representative periodic acid Schiff (PAS) staining images (magnification 400X, scale bar: 50 µm) and (B) quantification of glomerulosclerosis are shown ( n = 6 mice per group; ***p < 0.001 DM-WT vs. ND-WT; DM-KO vs. DM-WT). (C) Electron microscopy images showing a more prominent mesangial expansion in the glomeruli from DM-KO mice compared to DM-WT mice (magnification 3200X). (D) Immunofluorescence images of glomerular <t>FN1</t> <t>(fibronectin</t> 1) are shown (magnification 400X, scale bar: 50 µm). (E) Quantification of the percent area of glomerular FN1-positive staining ( n = 6 mice per group; ***p < 0.001 DM-WT vs. ND-WT; DM-KO vs. DM-WT). (F) Tgfb1 mRNA levels were measured by real-time PCR in total renal cortex and corrected for the expression of the housekeeping gene Hprt ( n = 5 mice per group; *p < 0.05 DM-WT vs. ND-WT; DM-KO vs. DM-WT). (G) Glomerular macrophage accrual was evaluated by counting the number of LGALS3/MAC2-positive cells per glomerulus ( n = 6 mice per group; ***p < 0.001 DM-WT vs. ND-WT; DM-KO vs. DM-WT). mRNA levels of Ly6c2 (H), Ccl2 (I), Ccr2 (J), and Tnf (K) were measured in the renal cortex by real time-PCR and the results corrected for the expression of the housekeeping gene Hprt ( n = 5 mice per group; *p < 0.05 DM-WT vs. ND-WT; **p < 0.01 DM-KO vs. DM-WT). (L) Schematic illustration of the protocol used for generating diabetic (DM) tnfaip2 KO chimeric mice. Recipient tnfaip2 KO mice were lethally irradiated, and then reconstituted with bone marrow (BM) from either WT (DM-KO-c WT ) or KO (DM-KO-c KO ) mice. (M) PCR genotyping of peripheral blood cells from chimeric animals. M: marker; NC: no template control. (N) ALB (albumin) excretion rate (AER) was measured after 12 weeks of diabetes in transplanted animals. (*p < 0.05 DM-WT-c WT vs. ND-WT-c WT ; DM-KO-c WT and DM-KO-c KO vs. DM-WT-c WT. (O) Representative images of PAS staining of renal cortex sections from transplanted animals (magnification 400X, scale bar: 50 µm).
Fn1 Rabbit Polyclonal Anti Fibronectin 1, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/fn1 rabbit polyclonal anti-fibronectin-1/product/Becton Dickinson
Average 90 stars, based on 1 article reviews
fn1 rabbit polyclonal anti-fibronectin-1 - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier

Image Search Results


Figure 1. Authentication of primary cultured rat trabecular meshwork (TM) cells. (A) Isolation and proliferation of primary TM cells observed under light microscope. a. Tissue scraps cut from corneoscleral rims. Co: cornea; Ir: iris. Blue triangles indicate the location where TM is supposed to reside. b. Primary TM cells started to crawl out of tissue scraps (indi cated by *) and adhere (indicated by black triangles). c. The attached cells gradually formed “clusters” and became contact-inhibited. d-f. Passage 3 TM cells presented typical spindle-like “fibroblast” phenotype and became cobblestone-like once confluent. Scale bars = 100 μm. (B) Immunofluorescence staining of cultured TM cells with anti-fibronectin, anti-laminin, anti-neuron-specific enolase (NSE), anti-factor- Ⅷ-related antigen (FⅧRAg) antibodies. Scale bar = 100 μm. (C–E) Cells were treated with 200 nM dexamethasone (Dex) for 7 days. Immunohistochem istry staining showed that over fifty percent of TM cells were myocilin-positive (the whole cell was yellow-stained) and was statistically different to that of vehicle control. Western blotting with anti- myocilin antibody showed a doublet at 55 kDa for the Dex-treated group. MYOC: myocilin. Scale bar = 300 μm. (F) Cells were treated with 100 nM Dex or ethanol control for 7 days and dyed with phalloidin. Cross-linked actin networks (CLANs) were observed and indicated by white triangles. Scale bars = 100 μm.

Journal: Experimental eye research

Article Title: Sympathetic activation leads to Schlemm's canal expansion via increasing vasoactive intestinal polypeptide secretion from trabecular meshwork.

doi: 10.1016/j.exer.2022.109235

Figure Lengend Snippet: Figure 1. Authentication of primary cultured rat trabecular meshwork (TM) cells. (A) Isolation and proliferation of primary TM cells observed under light microscope. a. Tissue scraps cut from corneoscleral rims. Co: cornea; Ir: iris. Blue triangles indicate the location where TM is supposed to reside. b. Primary TM cells started to crawl out of tissue scraps (indi cated by *) and adhere (indicated by black triangles). c. The attached cells gradually formed “clusters” and became contact-inhibited. d-f. Passage 3 TM cells presented typical spindle-like “fibroblast” phenotype and became cobblestone-like once confluent. Scale bars = 100 μm. (B) Immunofluorescence staining of cultured TM cells with anti-fibronectin, anti-laminin, anti-neuron-specific enolase (NSE), anti-factor- Ⅷ-related antigen (FⅧRAg) antibodies. Scale bar = 100 μm. (C–E) Cells were treated with 200 nM dexamethasone (Dex) for 7 days. Immunohistochem istry staining showed that over fifty percent of TM cells were myocilin-positive (the whole cell was yellow-stained) and was statistically different to that of vehicle control. Western blotting with anti- myocilin antibody showed a doublet at 55 kDa for the Dex-treated group. MYOC: myocilin. Scale bar = 300 μm. (F) Cells were treated with 100 nM Dex or ethanol control for 7 days and dyed with phalloidin. Cross-linked actin networks (CLANs) were observed and indicated by white triangles. Scale bars = 100 μm.

Article Snippet: Expression of fibronectin (M00564-3, BOSTER, China, 1:50), laminin (A03522, BOSTER, China, 1:50), neuron-specific enolase D. Xu et al.

Techniques: Cell Culture, Isolation, Light Microscopy, Immunofluorescence, Staining, Control, Western Blot

The compound-target-signaling networks generated using Cytoscape_v3.8.0. The active compounds cyclopamine, quercetin, kaempferol and mairin could target 12 IDD disease genes including HMGB1, PTEN, IGFBP6, FGFR3, COL3A1, MMP2, SMAD2, HSPG2, GPC1, FN1, CUL4B, CSGALNACT1 (Among 13 target genes, INTS8 did not have pathway enrichment). The compound-targeted disease genes were enriched in 23 pathways.

Journal: Journal of Orthopaedic Translation

Article Title: Pharmacological network analysis of the functions and mechanism of kaempferol from Du Zhong in intervertebral disc degeneration (IDD)

doi: 10.1016/j.jot.2023.01.002

Figure Lengend Snippet: The compound-target-signaling networks generated using Cytoscape_v3.8.0. The active compounds cyclopamine, quercetin, kaempferol and mairin could target 12 IDD disease genes including HMGB1, PTEN, IGFBP6, FGFR3, COL3A1, MMP2, SMAD2, HSPG2, GPC1, FN1, CUL4B, CSGALNACT1 (Among 13 target genes, INTS8 did not have pathway enrichment). The compound-targeted disease genes were enriched in 23 pathways.

Article Snippet: The following primary antibodies were used in this study: p16 (CSB-PA003618, CUSABIO, Wuhan, China), p21 (ab109520, Abcam, Cambridge, UK), Rb (ab224426, Abcam), hTERT (DF7129, Affinity Biotech), Nrf2 (CSB-RA225569A0HU,Cusabio), HO-1 (10701-1-AP, Proteintech), NQO-1 (11451-1-AP, Proteintech), SOD1 (10269-1-AP, Proteintech), SOD2 (ab227091, Abcam), Cleaved-caspase 3 (ab2302, Abcam), Caspase 3 (ab13847, Abcam), Bax (50599-2-Ig, Proteintech), Bcl-2 (12789-1-AP, Proteintech), aggrecan (13880-1-AP, Proteintech), collagen II (CSB-PA005739ESR2HU, Cusabio), SOX9 (ab185966, Abcam), FN1 (AF5335, Affinity Biotech), MMP2 (CSB-PA003258, Cusabio), MMP3 (17873-1-AP, Proteintech), MMP13 (CSB-PA07029A0Rb, Cusabio), ADAMTS-4 (DF6986, Affinity Biotech), ADAMTS-5 (DF13268, Affinity Biotech), p-p38 (AF4001, Affinity Biotech), p38 (14064-1-AP, Proteintech), p-JNK (AF3318, Affinity Biotech), JNK (AF6319, Affinity Biotech), p-ERK1/2 (sc-81492, Santa Cruz, Dallas, DX, USA), ERK1/2 (16443-1-AP, Proteintech).

Techniques: Generated

Compound-target-signaling networks.

Journal: Journal of Orthopaedic Translation

Article Title: Pharmacological network analysis of the functions and mechanism of kaempferol from Du Zhong in intervertebral disc degeneration (IDD)

doi: 10.1016/j.jot.2023.01.002

Figure Lengend Snippet: Compound-target-signaling networks.

Article Snippet: The following primary antibodies were used in this study: p16 (CSB-PA003618, CUSABIO, Wuhan, China), p21 (ab109520, Abcam, Cambridge, UK), Rb (ab224426, Abcam), hTERT (DF7129, Affinity Biotech), Nrf2 (CSB-RA225569A0HU,Cusabio), HO-1 (10701-1-AP, Proteintech), NQO-1 (11451-1-AP, Proteintech), SOD1 (10269-1-AP, Proteintech), SOD2 (ab227091, Abcam), Cleaved-caspase 3 (ab2302, Abcam), Caspase 3 (ab13847, Abcam), Bax (50599-2-Ig, Proteintech), Bcl-2 (12789-1-AP, Proteintech), aggrecan (13880-1-AP, Proteintech), collagen II (CSB-PA005739ESR2HU, Cusabio), SOX9 (ab185966, Abcam), FN1 (AF5335, Affinity Biotech), MMP2 (CSB-PA003258, Cusabio), MMP3 (17873-1-AP, Proteintech), MMP13 (CSB-PA07029A0Rb, Cusabio), ADAMTS-4 (DF6986, Affinity Biotech), ADAMTS-5 (DF13268, Affinity Biotech), p-p38 (AF4001, Affinity Biotech), p38 (14064-1-AP, Proteintech), p-JNK (AF3318, Affinity Biotech), JNK (AF6319, Affinity Biotech), p-ERK1/2 (sc-81492, Santa Cruz, Dallas, DX, USA), ERK1/2 (16443-1-AP, Proteintech).

Techniques: Activity Assay, Migration

Effects of Kaempferol IL-1β-induced ECM deposition NPCs were exposed to IL-1β stimulation (10 ​ng/ml, 24 ​h), treated with 10 ​μM kaempferol, and examined for the mRNA and protein levels of aggrecan, collagen II, SOX9, FN1 (A–B), MMP3, MMP13, ADAMTS-4, and ADAMTS-5 (C–D) using qRT-PCR and Immunoblotting, respectively. . One-way ANOVA followed by Tukey's post hoc test. N ​= ​3, ∗∗p ​< ​0.01, compared to PBS group; #p ​< ​0.05, ##p ​< ​0.01, compared with IL-1β group.

Journal: Journal of Orthopaedic Translation

Article Title: Pharmacological network analysis of the functions and mechanism of kaempferol from Du Zhong in intervertebral disc degeneration (IDD)

doi: 10.1016/j.jot.2023.01.002

Figure Lengend Snippet: Effects of Kaempferol IL-1β-induced ECM deposition NPCs were exposed to IL-1β stimulation (10 ​ng/ml, 24 ​h), treated with 10 ​μM kaempferol, and examined for the mRNA and protein levels of aggrecan, collagen II, SOX9, FN1 (A–B), MMP3, MMP13, ADAMTS-4, and ADAMTS-5 (C–D) using qRT-PCR and Immunoblotting, respectively. . One-way ANOVA followed by Tukey's post hoc test. N ​= ​3, ∗∗p ​< ​0.01, compared to PBS group; #p ​< ​0.05, ##p ​< ​0.01, compared with IL-1β group.

Article Snippet: The following primary antibodies were used in this study: p16 (CSB-PA003618, CUSABIO, Wuhan, China), p21 (ab109520, Abcam, Cambridge, UK), Rb (ab224426, Abcam), hTERT (DF7129, Affinity Biotech), Nrf2 (CSB-RA225569A0HU,Cusabio), HO-1 (10701-1-AP, Proteintech), NQO-1 (11451-1-AP, Proteintech), SOD1 (10269-1-AP, Proteintech), SOD2 (ab227091, Abcam), Cleaved-caspase 3 (ab2302, Abcam), Caspase 3 (ab13847, Abcam), Bax (50599-2-Ig, Proteintech), Bcl-2 (12789-1-AP, Proteintech), aggrecan (13880-1-AP, Proteintech), collagen II (CSB-PA005739ESR2HU, Cusabio), SOX9 (ab185966, Abcam), FN1 (AF5335, Affinity Biotech), MMP2 (CSB-PA003258, Cusabio), MMP3 (17873-1-AP, Proteintech), MMP13 (CSB-PA07029A0Rb, Cusabio), ADAMTS-4 (DF6986, Affinity Biotech), ADAMTS-5 (DF13268, Affinity Biotech), p-p38 (AF4001, Affinity Biotech), p38 (14064-1-AP, Proteintech), p-JNK (AF3318, Affinity Biotech), JNK (AF6319, Affinity Biotech), p-ERK1/2 (sc-81492, Santa Cruz, Dallas, DX, USA), ERK1/2 (16443-1-AP, Proteintech).

Techniques: Quantitative RT-PCR, Western Blot

Table S1 The primers for qRT-PCR

Journal: Journal of Orthopaedic Translation

Article Title: Pharmacological network analysis of the functions and mechanism of kaempferol from Du Zhong in intervertebral disc degeneration (IDD)

doi: 10.1016/j.jot.2023.01.002

Figure Lengend Snippet: Table S1 The primers for qRT-PCR

Article Snippet: The following primary antibodies were used in this study: p16 (CSB-PA003618, CUSABIO, Wuhan, China), p21 (ab109520, Abcam, Cambridge, UK), Rb (ab224426, Abcam), hTERT (DF7129, Affinity Biotech), Nrf2 (CSB-RA225569A0HU,Cusabio), HO-1 (10701-1-AP, Proteintech), NQO-1 (11451-1-AP, Proteintech), SOD1 (10269-1-AP, Proteintech), SOD2 (ab227091, Abcam), Cleaved-caspase 3 (ab2302, Abcam), Caspase 3 (ab13847, Abcam), Bax (50599-2-Ig, Proteintech), Bcl-2 (12789-1-AP, Proteintech), aggrecan (13880-1-AP, Proteintech), collagen II (CSB-PA005739ESR2HU, Cusabio), SOX9 (ab185966, Abcam), FN1 (AF5335, Affinity Biotech), MMP2 (CSB-PA003258, Cusabio), MMP3 (17873-1-AP, Proteintech), MMP13 (CSB-PA07029A0Rb, Cusabio), ADAMTS-4 (DF6986, Affinity Biotech), ADAMTS-5 (DF13268, Affinity Biotech), p-p38 (AF4001, Affinity Biotech), p38 (14064-1-AP, Proteintech), p-JNK (AF3318, Affinity Biotech), JNK (AF6319, Affinity Biotech), p-ERK1/2 (sc-81492, Santa Cruz, Dallas, DX, USA), ERK1/2 (16443-1-AP, Proteintech).

Techniques:

Effect of tnfaip2 deletion on diabetes-induced glomerular structural abnormalities, markers of fibrosis, and inflammation. Renal cortex samples from diabetic (DM) and non-diabetic (ND) both WT (ND-WT, DM-WT) and tnfaip2 KO (ND-KO, DM-KO) mice were studied 12 weeks after diabetes onset. (A) Representative periodic acid Schiff (PAS) staining images (magnification 400X, scale bar: 50 µm) and (B) quantification of glomerulosclerosis are shown ( n = 6 mice per group; ***p < 0.001 DM-WT vs. ND-WT; DM-KO vs. DM-WT). (C) Electron microscopy images showing a more prominent mesangial expansion in the glomeruli from DM-KO mice compared to DM-WT mice (magnification 3200X). (D) Immunofluorescence images of glomerular FN1 (fibronectin 1) are shown (magnification 400X, scale bar: 50 µm). (E) Quantification of the percent area of glomerular FN1-positive staining ( n = 6 mice per group; ***p < 0.001 DM-WT vs. ND-WT; DM-KO vs. DM-WT). (F) Tgfb1 mRNA levels were measured by real-time PCR in total renal cortex and corrected for the expression of the housekeeping gene Hprt ( n = 5 mice per group; *p < 0.05 DM-WT vs. ND-WT; DM-KO vs. DM-WT). (G) Glomerular macrophage accrual was evaluated by counting the number of LGALS3/MAC2-positive cells per glomerulus ( n = 6 mice per group; ***p < 0.001 DM-WT vs. ND-WT; DM-KO vs. DM-WT). mRNA levels of Ly6c2 (H), Ccl2 (I), Ccr2 (J), and Tnf (K) were measured in the renal cortex by real time-PCR and the results corrected for the expression of the housekeeping gene Hprt ( n = 5 mice per group; *p < 0.05 DM-WT vs. ND-WT; **p < 0.01 DM-KO vs. DM-WT). (L) Schematic illustration of the protocol used for generating diabetic (DM) tnfaip2 KO chimeric mice. Recipient tnfaip2 KO mice were lethally irradiated, and then reconstituted with bone marrow (BM) from either WT (DM-KO-c WT ) or KO (DM-KO-c KO ) mice. (M) PCR genotyping of peripheral blood cells from chimeric animals. M: marker; NC: no template control. (N) ALB (albumin) excretion rate (AER) was measured after 12 weeks of diabetes in transplanted animals. (*p < 0.05 DM-WT-c WT vs. ND-WT-c WT ; DM-KO-c WT and DM-KO-c KO vs. DM-WT-c WT. (O) Representative images of PAS staining of renal cortex sections from transplanted animals (magnification 400X, scale bar: 50 µm).

Journal: Autophagy

Article Title: Protective effect of the tunneling nanotube-TNFAIP2/M-sec system on podocyte autophagy in diabetic nephropathy

doi: 10.1080/15548627.2022.2080382

Figure Lengend Snippet: Effect of tnfaip2 deletion on diabetes-induced glomerular structural abnormalities, markers of fibrosis, and inflammation. Renal cortex samples from diabetic (DM) and non-diabetic (ND) both WT (ND-WT, DM-WT) and tnfaip2 KO (ND-KO, DM-KO) mice were studied 12 weeks after diabetes onset. (A) Representative periodic acid Schiff (PAS) staining images (magnification 400X, scale bar: 50 µm) and (B) quantification of glomerulosclerosis are shown ( n = 6 mice per group; ***p < 0.001 DM-WT vs. ND-WT; DM-KO vs. DM-WT). (C) Electron microscopy images showing a more prominent mesangial expansion in the glomeruli from DM-KO mice compared to DM-WT mice (magnification 3200X). (D) Immunofluorescence images of glomerular FN1 (fibronectin 1) are shown (magnification 400X, scale bar: 50 µm). (E) Quantification of the percent area of glomerular FN1-positive staining ( n = 6 mice per group; ***p < 0.001 DM-WT vs. ND-WT; DM-KO vs. DM-WT). (F) Tgfb1 mRNA levels were measured by real-time PCR in total renal cortex and corrected for the expression of the housekeeping gene Hprt ( n = 5 mice per group; *p < 0.05 DM-WT vs. ND-WT; DM-KO vs. DM-WT). (G) Glomerular macrophage accrual was evaluated by counting the number of LGALS3/MAC2-positive cells per glomerulus ( n = 6 mice per group; ***p < 0.001 DM-WT vs. ND-WT; DM-KO vs. DM-WT). mRNA levels of Ly6c2 (H), Ccl2 (I), Ccr2 (J), and Tnf (K) were measured in the renal cortex by real time-PCR and the results corrected for the expression of the housekeeping gene Hprt ( n = 5 mice per group; *p < 0.05 DM-WT vs. ND-WT; **p < 0.01 DM-KO vs. DM-WT). (L) Schematic illustration of the protocol used for generating diabetic (DM) tnfaip2 KO chimeric mice. Recipient tnfaip2 KO mice were lethally irradiated, and then reconstituted with bone marrow (BM) from either WT (DM-KO-c WT ) or KO (DM-KO-c KO ) mice. (M) PCR genotyping of peripheral blood cells from chimeric animals. M: marker; NC: no template control. (N) ALB (albumin) excretion rate (AER) was measured after 12 weeks of diabetes in transplanted animals. (*p < 0.05 DM-WT-c WT vs. ND-WT-c WT ; DM-KO-c WT and DM-KO-c KO vs. DM-WT-c WT. (O) Representative images of PAS staining of renal cortex sections from transplanted animals (magnification 400X, scale bar: 50 µm).

Article Snippet: Slides were fixed in acetone for 5 min and blocked in 3% BSA, then incubated overnight at 4°C with guinea pig anti-NPHS1/Nephrin (Progen, GP-N2; 1:100), rabbit anti-NPHS2/Podocin, or rabbit anti-FN1/Fibronectin (Merck Life Science, F3648; 1:200) primary antibodies.

Techniques: Staining, Electron Microscopy, Immunofluorescence, Real-time Polymerase Chain Reaction, Expressing, Irradiation, Marker