AIM： To explore the possibility of using the Noninvasive Micro-test Technique （NMT） to investigate the role of Transient Receptor Potential Canonical 1 （TRPC1） in regulating Ca^2＋ influxes in HL-7702 cells, a no...AIM： To explore the possibility of using the Noninvasive Micro-test Technique （NMT） to investigate the role of Transient Receptor Potential Canonical 1 （TRPC1） in regulating Ca^2＋ influxes in HL-7702 cells, a normal human liver cell line.METHODS： Net Ca^2＋ fluxes were measured with NMT, a technology that can obtain dynamic information of specific/selective ionic/molecular activities on material surfaces, non-invasively. The expression levels of TRPCl were increased by liposomal transfection, whose effectiveness was evaluated by Western-blotting and single cell reverse transcription-polymerase chain reaction.RESULTS： Ca^2＋ influxes could be elicited by adding 1 mmol/L CaCl2 to the test solution of HL-7702 cells. They were enhanced by addition of 20 μmol/L noradrenalin and inhibited by 100 μmol/L LaCl3 （a non-selective Ca^2＋ channel blocker）; 5 μmol/L nifedipine did not induce any change. Overexpression of TRPCl caused increased Ca^2＋ influx. Five micromoles per liter nifedipine did not inhibit this elevation, whereas 100 μmol/L LaCI3 did.CONCLUSION： In HL-7702 cells, there is a type of TRPCl-dependent Ca^2＋ channel, which could be detected v/a NMT and inhibited by La^3＋.展开更多
Objective:To investigate the effects of TGF-β1 on the expression of TRPC6 in glomerular mesangial cells(GMC).Methods:GMC were cultured in vitro with indicated concentration of TGF-β1 10 ng/ml for 24 h.The expression...Objective:To investigate the effects of TGF-β1 on the expression of TRPC6 in glomerular mesangial cells(GMC).Methods:GMC were cultured in vitro with indicated concentration of TGF-β1 10 ng/ml for 24 h.The expression of TRPC6 protein was examined by immunofluorescent staining and Western blotting.Results:TRPC6 was expressed mainly in the membrane of GMC,also some expressed in the plasma.In the TGF-β1 group,the expression of TRPC6 significantly decreased.Conclusion:Glomerular mesangial cells express TRPC6,and TGF-β1 decreases the expression of TRPC6, which might be one of the mechanisms of TGF-β1 in DN.展开更多
基金Supported by The National Natural Science Foundation of China,No.30270532 and No.30670774Tsinghua-Yue-Yuen Medical Science Foundation,No.20240000531 and No.20240000547
文摘AIM： To explore the possibility of using the Noninvasive Micro-test Technique （NMT） to investigate the role of Transient Receptor Potential Canonical 1 （TRPC1） in regulating Ca^2＋ influxes in HL-7702 cells, a normal human liver cell line.METHODS： Net Ca^2＋ fluxes were measured with NMT, a technology that can obtain dynamic information of specific/selective ionic/molecular activities on material surfaces, non-invasively. The expression levels of TRPCl were increased by liposomal transfection, whose effectiveness was evaluated by Western-blotting and single cell reverse transcription-polymerase chain reaction.RESULTS： Ca^2＋ influxes could be elicited by adding 1 mmol/L CaCl2 to the test solution of HL-7702 cells. They were enhanced by addition of 20 μmol/L noradrenalin and inhibited by 100 μmol/L LaCl3 （a non-selective Ca^2＋ channel blocker）; 5 μmol/L nifedipine did not induce any change. Overexpression of TRPCl caused increased Ca^2＋ influx. Five micromoles per liter nifedipine did not inhibit this elevation, whereas 100 μmol/L LaCI3 did.CONCLUSION： In HL-7702 cells, there is a type of TRPCl-dependent Ca^2＋ channel, which could be detected v/a NMT and inhibited by La^3＋.
文摘Objective:To investigate the effects of TGF-β1 on the expression of TRPC6 in glomerular mesangial cells(GMC).Methods:GMC were cultured in vitro with indicated concentration of TGF-β1 10 ng/ml for 24 h.The expression of TRPC6 protein was examined by immunofluorescent staining and Western blotting.Results:TRPC6 was expressed mainly in the membrane of GMC,also some expressed in the plasma.In the TGF-β1 group,the expression of TRPC6 significantly decreased.Conclusion:Glomerular mesangial cells express TRPC6,and TGF-β1 decreases the expression of TRPC6, which might be one of the mechanisms of TGF-β1 in DN.
