Objective:To investigate the effects of calcium-activated chloride(ClCa)channels on proliferation of pulmonary artery smooth muscle cells(PASMCs)in rats under chronic hypoxic condition.Methods:The cultured PASMCs were...Objective:To investigate the effects of calcium-activated chloride(ClCa)channels on proliferation of pulmonary artery smooth muscle cells(PASMCs)in rats under chronic hypoxic condition.Methods:The cultured PASMCs were placed under normoxic and chronic hypoxic conditions:The cells were observed by light and electron microscope;The cell cycles were observed by flow-cytometry;Immunocytochemistry staining was used to detect the expressions of PCNA,c-fos and c-jun of PASMCs;Cytoplasmic free Ca2+ con-cweenrter actoionntr a([cCtiale2+ ]pi)h einn oPtAypSeM uCndse wr anso rimnvoexsitcig caotnedd ibtiyo nfslu.oOrbessceervnat tqiouna nbtyit atrtaionnsm uissisnigo nfl euloercotsropne cmtriocprohsoctoompee:t Ienr.kRyteospulaltssm:T ohfe c PonAtSraMctCiles phenotype cells,myofilament bundles were abundant and the content of cell organs such as Golgi's bodies were rare.The PASMCs were synthetic phenotype under chronic hypoxic condition.There were increased free ribosomes,dilated rough endoplasmic reticulums,highly developed Golgi complexes,decreased or disappeared thick filaments and dense body in kytoplasm of synthetic phenotype cells.Acofntedri tNioFnA;Tahned NIAFAA-9a4n,d t hIAe sAit-u9a4t iwonesr ew sehroew renv teor sseidg nTifhiec annutmlyb deerc orfe aSs+eG th2Mem P fAroSmM(C2s8.w6±ere1 s.0ig)n%if ticoa(n1t6ly.0 in±cr1e.a6s)e%d iann dch trhoen nicu hmybpeorx oicf Gof0 Gpr1o PliAfeSraMtiCngs scieglnl infuiccalnetulsy ainnctirgeeanse wd afsro smig n(7if1ic.4a±ntl1y.9in)%cr etaos(e8d3;.T9±he1 N.6F)A% a(Pnd < I A0.A01-9).4 I nw cehrer osnhiocw hny ptoo xsiicg nciofnicdaintitolyn sd,etchree eaxsep riet sfsroiomn(81±6)% to(27±7)%(P < 0.01).The expression of c-fos and c-jun were significantly increased in chronic hypoxic conditions;The NFA and IAA-94 were shown to significantly decrease them from 0.15±0.02,0.32±0.05 to 0.05±0.01,0.12±0.05,respectively(toP(<1 01.70.17)±;U15n.d4e)rn mchorlo/Lni(cP h<y 0p.o0x1i)c.Ccoonndcitliuosniso,n[C:Hay2+p]io wxiaas i ninitciraeteadse tdh;e T chhea nNgFe Aof aPnAdS IMAAC-s9 f4ro dmec croenastreadc tiitl efr toom sy(n2t8h1e.t8ic± ph1e6n.5o)tnypmeo aln/Ld increased proliferation of PASMCs.NFA and IAA-94 depressed cell proliferation by blocking ClCa channels in hypoxic condition.These may play an important role in proliferation of PASMCs under chronic hypoxic conditions.展开更多
The aim of this study was to investigate the role of pirh2(p53-induced RING-H2)protein in the proliferation,apoptosis and cell cycle control of the lung cancer cell line A549.Pirh2 expression was detected by immunoflu...The aim of this study was to investigate the role of pirh2(p53-induced RING-H2)protein in the proliferation,apoptosis and cell cycle control of the lung cancer cell line A549.Pirh2 expression was detected by immunofluores-cence,Western blot analysis and real-time polymerase chain reaction(PCR).Cell proliferation was assessed by cell counting kit-8(CCK-8).Cell cycle control and apoptosis were analyzed by flow cytometry.The results showed that pirh2 was expressed in the cytoplasm of A549 cells.The inhi-bition of pirh2 expression by siRNA(psiRNA-pirh2)resulted in reduced cell proliferation and increased apoptosis.In addition,the number of G0/G1 phase cells was increased but G2/M cells were not affected significantly.Taken together,the inhibition of pirh2 expression in the lung adenocarcinoma cell line A549 resulted in reduced tumor cell growth via the inhibition of cell proliferation,the activation of apoptosis and the interruption of cell cycle transition.展开更多
文摘Objective:To investigate the effects of calcium-activated chloride(ClCa)channels on proliferation of pulmonary artery smooth muscle cells(PASMCs)in rats under chronic hypoxic condition.Methods:The cultured PASMCs were placed under normoxic and chronic hypoxic conditions:The cells were observed by light and electron microscope;The cell cycles were observed by flow-cytometry;Immunocytochemistry staining was used to detect the expressions of PCNA,c-fos and c-jun of PASMCs;Cytoplasmic free Ca2+ con-cweenrter actoionntr a([cCtiale2+ ]pi)h einn oPtAypSeM uCndse wr anso rimnvoexsitcig caotnedd ibtiyo nfslu.oOrbessceervnat tqiouna nbtyit atrtaionnsm uissisnigo nfl euloercotsropne cmtriocprohsoctoompee:t Ienr.kRyteospulaltssm:T ohfe c PonAtSraMctCiles phenotype cells,myofilament bundles were abundant and the content of cell organs such as Golgi's bodies were rare.The PASMCs were synthetic phenotype under chronic hypoxic condition.There were increased free ribosomes,dilated rough endoplasmic reticulums,highly developed Golgi complexes,decreased or disappeared thick filaments and dense body in kytoplasm of synthetic phenotype cells.Acofntedri tNioFnA;Tahned NIAFAA-9a4n,d t hIAe sAit-u9a4t iwonesr ew sehroew renv teor sseidg nTifhiec annutmlyb deerc orfe aSs+eG th2Mem P fAroSmM(C2s8.w6±ere1 s.0ig)n%if ticoa(n1t6ly.0 in±cr1e.a6s)e%d iann dch trhoen nicu hmybpeorx oicf Gof0 Gpr1o PliAfeSraMtiCngs scieglnl infuiccalnetulsy ainnctirgeeanse wd afsro smig n(7if1ic.4a±ntl1y.9in)%cr etaos(e8d3;.T9±he1 N.6F)A% a(Pnd < I A0.A01-9).4 I nw cehrer osnhiocw hny ptoo xsiicg nciofnicdaintitolyn sd,etchree eaxsep riet sfsroiomn(81±6)% to(27±7)%(P < 0.01).The expression of c-fos and c-jun were significantly increased in chronic hypoxic conditions;The NFA and IAA-94 were shown to significantly decrease them from 0.15±0.02,0.32±0.05 to 0.05±0.01,0.12±0.05,respectively(toP(<1 01.70.17)±;U15n.d4e)rn mchorlo/Lni(cP h<y 0p.o0x1i)c.Ccoonndcitliuosniso,n[C:Hay2+p]io wxiaas i ninitciraeteadse tdh;e T chhea nNgFe Aof aPnAdS IMAAC-s9 f4ro dmec croenastreadc tiitl efr toom sy(n2t8h1e.t8ic± ph1e6n.5o)tnypmeo aln/Ld increased proliferation of PASMCs.NFA and IAA-94 depressed cell proliferation by blocking ClCa channels in hypoxic condition.These may play an important role in proliferation of PASMCs under chronic hypoxic conditions.
文摘The aim of this study was to investigate the role of pirh2(p53-induced RING-H2)protein in the proliferation,apoptosis and cell cycle control of the lung cancer cell line A549.Pirh2 expression was detected by immunofluores-cence,Western blot analysis and real-time polymerase chain reaction(PCR).Cell proliferation was assessed by cell counting kit-8(CCK-8).Cell cycle control and apoptosis were analyzed by flow cytometry.The results showed that pirh2 was expressed in the cytoplasm of A549 cells.The inhi-bition of pirh2 expression by siRNA(psiRNA-pirh2)resulted in reduced cell proliferation and increased apoptosis.In addition,the number of G0/G1 phase cells was increased but G2/M cells were not affected significantly.Taken together,the inhibition of pirh2 expression in the lung adenocarcinoma cell line A549 resulted in reduced tumor cell growth via the inhibition of cell proliferation,the activation of apoptosis and the interruption of cell cycle transition.
