摘要
目的 :探讨心肌细胞内Ca2 +超负荷以及Ca2 +调控蛋白在舒张性心力衰竭 (DHF)发生中的作用。方法 :采用RT -PCR和Westernblot技术测定实验兔Ca2 +调控蛋白mRNA和蛋白质表达的变化。结果 :⑴DHF兔心肌细胞内Ca2 +含量显著高于假手术组 (P <0 0 1) ;⑵DHF兔SRCa2 +-ATPase活性明显低于假手术组 (P <0 0 1) ;⑶DHF兔SRCa2 +-ATPase和细胞膜L型Ca2 +通道的mRNA水平明显低于假手术组 (P <0 0 5 ) ,而磷酸受纳蛋白、兰尼碱受体和肌集钙蛋白的mRNA转录无明显差异 (P >0 0 5 ) ;⑷DHF兔SRCa2 +-ATPase的蛋白质表达明显低于假手术组 (P <0 0 5 ) ;磷酸受纳蛋白的相对含量与假手术组无明显差异 (P >0 0 5 )。结论 :SRCa2 +-ATPase的mRNA和蛋白质表达减低以及细胞膜L型Ca2 +通道mRNA转录减低是导致心肌细胞内Ca2
AIM: To elucidate molecular mechanisms underlying calcium handling protein in diastolic heart failure (DHF) from mRNA level and protein expression, including calcium adenosine triphosphatase (Ca 2+ -ATPase), phospholamban, ryanodine receptor, calsequestrin and L-type calcium channel. METHODS: The mRNA of these calcium handling genes were detected by RT-PCR, and the protein levels were analyzed by Western blot analysis. RESULTS: Compared with sham-operated rabbits, the steady-state levels of mRNA encoding the SR Ca 2+ -ATPase and cardiac L-type calcium channel were decreased significantly in rabbits with DHF, and protein level of SR Ca 2+ - ATPase was greatly reduced, whereas the mRNA and protein levels of other calcium handling protein were unchanged. CONCLUSION: L-type calcium channel and the sarcoplasmic reticular Ca 2+ -ATPase were down regulated in DHF. These changes may be a contributory factor for DHF.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第2期124-127,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助 (NO .3 9970 2 94 )
