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《鈣信號(hào)調(diào)節(jié)小鼠前體脂肪細(xì)胞分化和脂質(zhì)蓄積的機(jī)制》由會(huì)員上傳分享，免費(fèi)在線閱讀，更多相關(guān)內(nèi)容在工程資料-天天文庫。
1、生物工程學(xué)報(bào)ChinJBiotech2009,May25;25(5):739-744journals.im.ac.cnChineseJournalofBiotechnologyISSN1000-3061cjb@im.ac.cn?2009InstituteofMicrobiology,CAS&CSM,Allrightsreserved組織工程與細(xì)胞培養(yǎng)鈣信號(hào)調(diào)節(jié)小鼠前體脂肪細(xì)胞分化和脂質(zhì)蓄積的機(jī)制112王麗,孫超,康靖全1西北農(nóng)林科技大學(xué)動(dòng)物科技學(xué)院,楊凌7121002西北農(nóng)林科技大學(xué)生命科學(xué)學(xué)院,楊凌712100摘要:本試驗(yàn)用醋酸鈣、p38絲裂原激活蛋白激酶(p38MAPK)
2、抑制劑SB203580及鈣通道阻滯劑和激動(dòng)劑刺激小鼠前體脂肪細(xì)胞。通過實(shí)時(shí)定量PCR技術(shù)檢測(cè)前體脂肪細(xì)胞分化標(biāo)志基因和鈣信號(hào)相關(guān)受體基因表達(dá)水平,用油紅O染色2+2+提取法和Fura-2/AM熒光法測(cè)定胞內(nèi)脂質(zhì)蓄積情況及胞漿游離Ca濃度([Ca]i)變化,以探討鈣信號(hào)調(diào)節(jié)前體脂肪細(xì)胞分化的潛在機(jī)制。結(jié)果表明：鈣通道阻滯劑和激動(dòng)劑顯著改變了脂蛋白脂酶(LPL),過氧化物增殖激活受體γ(PPARγ)、脂肪酸合成酶(FAS)的表達(dá)水平，且影響細(xì)胞內(nèi)的脂質(zhì)蓄積。與降低外鈣攝入相比，降低內(nèi)鈣釋放能促進(jìn)前體脂肪細(xì)胞分化(P<0.01)，而提高外鈣攝入與提高內(nèi)鈣釋放相比，提高外鈣攝入顯著抑
3、制前體脂肪細(xì)胞分化(P<0.01)。2+SB203580可降低胞漿[Ca]i濃度，促進(jìn)前體細(xì)胞分化和脂質(zhì)蓄積(P<0.01)。但鈣信號(hào)并未影響維生素D受體(VDR)和細(xì)胞外鈣敏感受體(CaSR)的表達(dá)水平。提示鈣信號(hào)可能通過p38MAPK通路影響前體脂肪細(xì)胞分化和脂質(zhì)蓄積。關(guān)鍵詞:鈣信號(hào),p38MAPK,小鼠,前體脂肪細(xì)胞分化,脂質(zhì)蓄積Themechanismofcalciumsignalregulatepreadipocytedifferentiationandlipidaccumulationinmice112LiWang,ChaoSun,andJingquanKang1
4、CollegeofAnimalScience&Technology,NorthwestAgricultureandForestryUniversity,Yangling712100,China2CollegeofLifeSciences,NorthwestAgricultureandForestryUniversity,Yangling712100,ChinaAbstract:Westimulatedpreadipocyteofmicewithcalciumacetate,p38mitogen-activatedproteinkinase(p38MAPK)inhibitorS
5、B203580,theparalysorsandexcitomotorsofcalciumchannel.Thenwedetectedexpressionlevelofpreadipocytedifferentiation’s2+markergenesandcalciumsignalrelatedacceptorgenesbyreal-timePCR,anddeterminedintracellularfreeCaconcentration2+([Ca]i])withFura-2/AM,intracellularlipidaccumulationbyoilredOstaini
6、ng.Ouraimwastoinvestigatethepotentialmechanismbetweencalciumsignalandpreadipocytedifferentiation.Theresultsindicatedthattheparalysorsandexcitomotorsofcalciumchannelchangedtheexpressionleveloflipoproteinlipase(LPL),peroxisomeproliferators-activatedreceptorgamma(PPARγ),fatty2+acidsynthetase(F
7、AS),andthelipidaccumulation,markedly.ComparedwithexocellularCa’sdecrease,inhibitedintracellular2+2+Ca’sliberationcanpromotedpreadipocytedifferentiation(P<0.01),andcomparedwithintracellularCa’sincrease,promoted2+2+exocellularCa’singestinhibitedpreadipocyt
