Objective:To explore effect of high glucose on expression of osteoprotegerin(OPG) and receptor activator of NF- κB ligand(RANKL) in rat aortic vascular smooth muscle cells.Methods:SD rats were intraperitoneally injec...Objective:To explore effect of high glucose on expression of osteoprotegerin(OPG) and receptor activator of NF- κB ligand(RANKL) in rat aortic vascular smooth muscle cells.Methods:SD rats were intraperitoneally injected with streptozotocin,OPG and RANKL expression in rat thoracic aortas were detected by immunohistochemical staining.In cultured vascular smooth muscle cells(VSMCs)(A7r5),qRT-PCR and Western blot analysis were used to examine the mRNA and protein levels of OPG and RANKL.Results:Our results demonstrated that OPG expression was increased in hyperglycemic rat aortic VSMCs.while RANKL expression was decreased.Besides,in vitro experiments high glucose induced OPG expression,but depressed RANKL expression by dose- and time-dependent manner in cultured A7r5.Conclusions:Our findings suggested that high glucose could promote the expression of OPG,and inhibit the expression of RANKL in VSMCs,which may be partly be the molecular mechanism of diabetic vascular calcification.展开更多
Objective:To understand the role of ANP mRNA transcription regulation in gpl30-mediated cardiomyocyte hypertrophy,and the involved mitogen-aetivated protein kinase kinase(MEK)-extracellular signal-regulated kinase(ERK...Objective:To understand the role of ANP mRNA transcription regulation in gpl30-mediated cardiomyocyte hypertrophy,and the involved mitogen-aetivated protein kinase kinase(MEK)-extracellular signal-regulated kinase(ERK,also called p42/p44 MAPK)signaling pathway.Methods:isolated neonatal ventricular myocytes were treated with different concentrations of CT-1(10^(-9),10^(-8)and 10^(-7)mol/L).MTT was used to analyze the viability and RT-PCR was used to detect ANP mRNA levels in eardiomyocyte.To inhibit p42/p44 MAPK activity in hypertrophic cardiomyoeytes,the cells were pretreated with a specific MEKI inhibitor.Results:CT-1significantly induced ANP mRNA expression and the viability of canliomyocytes in a doseand time-dependent manner.Furthermore,blocking p42/p44 MAPK activity by the special MEk1 inhibitor uprcgulatcd the ANP mKNA.Conclusions:p42/p44 MAPK have an important role in suppressing ANP mRNA transcription and cell activity in gpl30-mediated hypertrophic ventricular myocytes.展开更多
基金supported by the grant from National Natural Science Foundation of China(81160020,81460042,81460070)Key Project of Chinese Ministry of Education 212137+2 种基金the gtants HJHZ2013.06 and SF201417 of Hainan ProvinceKey Program of Science and Tcchnology of Hainan Province(ZDXM20100045)partly by Programs for Changjiang Scholars and Innovative Research Team in University(IRT1119)
文摘Objective:To explore effect of high glucose on expression of osteoprotegerin(OPG) and receptor activator of NF- κB ligand(RANKL) in rat aortic vascular smooth muscle cells.Methods:SD rats were intraperitoneally injected with streptozotocin,OPG and RANKL expression in rat thoracic aortas were detected by immunohistochemical staining.In cultured vascular smooth muscle cells(VSMCs)(A7r5),qRT-PCR and Western blot analysis were used to examine the mRNA and protein levels of OPG and RANKL.Results:Our results demonstrated that OPG expression was increased in hyperglycemic rat aortic VSMCs.while RANKL expression was decreased.Besides,in vitro experiments high glucose induced OPG expression,but depressed RANKL expression by dose- and time-dependent manner in cultured A7r5.Conclusions:Our findings suggested that high glucose could promote the expression of OPG,and inhibit the expression of RANKL in VSMCs,which may be partly be the molecular mechanism of diabetic vascular calcification.
基金supported by a grant from the National Natural Science Foundation of China(30260032.81000073 and 81160020)Key Program of Science and Technology of Hainan Province(061011 and ZDXM20100045)+2 种基金Education Department of Hainan Province(Hj2007113)Natural Science Foundation of Hainan Province(310043 and 811197)Key Project of Chinese Ministry of Education(212137) and HJHZ2013-06
文摘Objective:To understand the role of ANP mRNA transcription regulation in gpl30-mediated cardiomyocyte hypertrophy,and the involved mitogen-aetivated protein kinase kinase(MEK)-extracellular signal-regulated kinase(ERK,also called p42/p44 MAPK)signaling pathway.Methods:isolated neonatal ventricular myocytes were treated with different concentrations of CT-1(10^(-9),10^(-8)and 10^(-7)mol/L).MTT was used to analyze the viability and RT-PCR was used to detect ANP mRNA levels in eardiomyocyte.To inhibit p42/p44 MAPK activity in hypertrophic cardiomyoeytes,the cells were pretreated with a specific MEKI inhibitor.Results:CT-1significantly induced ANP mRNA expression and the viability of canliomyocytes in a doseand time-dependent manner.Furthermore,blocking p42/p44 MAPK activity by the special MEk1 inhibitor uprcgulatcd the ANP mKNA.Conclusions:p42/p44 MAPK have an important role in suppressing ANP mRNA transcription and cell activity in gpl30-mediated hypertrophic ventricular myocytes.
