anti asic1a (Alomone Labs)
Structured Review

Anti Asic1a, supplied by Alomone Labs, 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/product/aqp-001-ar/pmc06484315-71-16-18?v=Alomone+Labs
Average 90 stars, based on 1 article reviews
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1) Product Images from "Acid‐sensing ion channel 1a is involved in ischaemia/reperfusion induced kidney injury by increasing renal epithelia cell apoptosis"
Article Title: Acid‐sensing ion channel 1a is involved in ischaemia/reperfusion induced kidney injury by increasing renal epithelia cell apoptosis
Journal: Journal of Cellular and Molecular Medicine
doi: 10.1111/jcmm.14238
Figure Legend Snippet: Immunohistochemical analysis of ASIC1a expression in renal tissue. Immunostaining for ASIC1a, AQP1, THP and SYN in renal tissue. ASIC1a was colocalized with AQP and SYN, but not THP. ASIC1a, acid sensing ion channel 1a; AQP1, aquaporin 1, proximal tubular cells marker; THP, Tamm‐Horsfall protein, thick ascending limb and distal tubular cells marker; SYN, Synaptopodin, podocyte marker; DAPI, 4,6‐diamidino‐2‐phenylindole, nuclear
Techniques Used: Immunohistochemical staining, Expressing, Immunostaining, Marker
Figure Legend Snippet: Inhibiting ASIC1a by PcTx1 attenuate I/R induced kidney injury. Different doses of PcTx1 (0.2, 2, 4, 10 nmol L −1 kg −1 body weight) or vehicle were injected by tail vein, 30 min before I/R operation. Twenty‐four hours after reperfusion, the expression of ASIC1a in the kidney of sham and I/R operating mouse was measured by Western blotting and PCR; functional and histological changes were assessed by serum creatinine, Urea and PAS staining; apoptosis of renal tubular epithelia cells was assessed by TUNEL staining. A, I/R increase protein and RNA level of ASIC1a in the kidney, however, administration of PcTx1 had no effect on expression of ASIC1a. B‐C, injection of PcTx1 reduced serum creatinine and urea in a dose dependent manner; D, Typical visual field of PAS staining and pathological score calculated from PAS staining. PcTx1 (4 nmol L −1 kg −1 body weight) significantly attenuated I/R induced renal injury. * P < 0.05, ** P < 0.01, *** P < 0.001, compared with sham; # P < 0.05, ### P < 0.001, compared with vehicle+I/R, n = 6
Techniques Used: Injection, Expressing, Western Blot, Functional Assay, Staining, TUNEL Assay
Figure Legend Snippet: Inhibiting ASIC1a by PcTx1 attenuate I/R induced apoptosis of renal tubule, in vivo. Typical image of TUNEL staining in renal coronal section from sham, vehicle+I/R and PcTx1+ I/R animal. *** P < 0.001, compared with sham; # P < 0.05, ### P < 0.001, compared with vehicle+I/R, n = 6
Techniques Used: In Vivo, TUNEL Assay, Staining
Figure Legend Snippet: Inhibiting ASIC1a by PcTx1 reduced H/R induced apoptosis of HK‐2 cells. A, H/R increase protein level of ASIC1a in the HK‐2 cells. * P < 0.05, n = 6. B, HK‐2 cells were pre‐treated with different doses of PcTx1 (5, 25, 100, and 500 ng/mL) or vehicle before H/R treatment. Apoptosis of HK‐2 cells was measured by Annexin‐V/PI staining and evaluated by flow cytometry. C, the group data from B. PcTx1 attenuated H/R induced apoptosis especially early apoptosis dose dependently. *** P < 0.001, compared with Normoxia; # P < 0.05, ## P < 0.01, compared with vehicle+H/R, n = 6. E, Cell variability was measured by MTT assay. Treatment of PcTx1 for 6 h had no effect on variability of HK‐2 cells
Techniques Used: Staining, Flow Cytometry, MTT Assay
Figure Legend Snippet: Inhibiting ASIC1a by PcTx1 reduced H/R induced intracellular calcium overload and loss of mitochondrial membrane potential. HK‐2 cells were administrated with different doses of PcTx1 as Figure . A, Intracellular calcium concentration were measured by fluo4 and evaluated by flow cytometry. PcTx1 attenuated H/R induced intracellular calcium overload dose dependently. B, Intracellular calcium concentration was measured by fluo4 immunofluorescence staining. As expected, PcTx1 attenuated H/R induced intracellular calcium overload. C, mitochondrial membrane potential were monitored by JC‐1 dye and evaluated by flow cytometry. *** P < 0.001, compared with Normoxia; # P < 0.05, ## P < 0.01, compared with vehicle+H/R, n = 6
Techniques Used: Concentration Assay, Flow Cytometry, Immunofluorescence, Staining
Figure Legend Snippet: Inhibiting ASIC1a by PcTx1 reduced expression of cleaved‐caspase3 in renal tubule. A: PcTx1 (4 nmol L −1 kg −1 body weight) or vehicle were injected by tail vein, 30 min before I/R operation. Twenty‐four hours after reperfusion, apoptosis of renal tubular epithelia cells was assessed by immunohistochemical reaction of cleaved‐caspase3. Typical image of cleaved‐caspase3 immunohistochemical staining in renal coronal section from sham, vehicle + I/R and PcTx1+ I/R animal; B, detailed information of immunohistochemical reaction of cleaved‐caspase3 under high‐power lens; ** P < 0.01, compared with sham; ## P < 0.001, compared with vehicle + I/R, n = 6. C, HK‐2 cells were pre‐treated with PcTx1 (100 ng/mL) before H/R treatment, cleaved‐caspase3 was measured by Western blotting; ** P < 0.01, compared with Normoxia; ## P < 0.01, compared with vehicle+H/R, n = 6
Techniques Used: Expressing, Injection, Immunohistochemical staining, Staining, Western Blot
Figure Legend Snippet: Schema of I/R induced the local microenvironment acidification and the activation of ASIC1a on renal injury and the involved underlying mechanism. Ischaemia caused accumulation of extracellular protons (H + ). ASIC1a are activated by extracellular H + and induce influx of Ca 2+ , which induced loss of mitochondrial membrane potential. The damage of mitochondrial increased cleaved‐caspase3, which resulted in apoptosis of renal tubular epithelia cells. Administration of the specific inhibitor of ASIC1a, PcTx1 ameliorated ischaemic renal injury by inhibiting ASIC1a, which implied a potential therapeutic choice for AKI
Techniques Used: Activation Assay