摘要
目的 探讨肿瘤坏死因子 α(TNF α)对肾小球前小动脉平滑肌细胞 (RASMC)Ⅰ型三磷酸肌醇 (IP3 )受体蛋白表达的影响。方法 通过对RASMC的分离、培养和鉴定 ,应用蛋白和核酸杂交技术分别检测TNF α作用后RASMC中Ⅰ型IP3 受体蛋白和Ⅰ型IP3 受体mRNA的表达情况 ,同时测定Ⅰ型IP3 受体mRNA的半衰期。结果 TNF α能增强RASMC内Ⅰ型IP3 受体蛋白的表达 ,且两者呈剂量依赖关系 ;TNF α能促进Ⅰ型IP3 受体mRNA的表达 ,同时使受体蛋白合成增加 ;而TNF α对Ⅰ型IP3受体mRNA的影响不是抑制mRNA的降解 ,而是使其表达增加。结论 TNF α可能作用于Ⅰ型IP3 受体mRNA的基因启动子 ,使其合成增加 ,由此导致Ⅰ型IP3 受体蛋白表达增加 ,诱导RASMC内储备的Ca2 + 释放至细胞浆 ,引起肾小球前小动脉平滑肌细胞收缩 ,使肾血流量减少 ,肾小球滤过率下降 。
Objective To study the effect of tumor necrosis factor-α(TNF-α) on type Ⅰ inositol 1,4,5-triphosphate receptor (IP 3 R) expression in rat glomerular afferent arterioles smooth muscle cells (RASMC). Methods Isolation and culture of RASMC and detection of type Ⅰ IP 3 R protein and type I IP 3 R mRNA in RASMC after TNF-α treatment were carried out with Western blot and Northern blot assay. Results TNF-α enhanced the expression of type Ⅰ IP 3 R protein and type Ⅰ IP 3 R mRNA in RASMC; TNF-α did not influence the half life of type I IP 3R mRNA in RASMC treated with TNF-α. Conclusion TNF-α plays a role in the development of renal dysfunction. The mechanisms may be that TNF-α takes part in the change of signal transduction in RASMC. TNF-α may act on the promoter of type Ⅰ IP 3 R mRNA in RASMC and results in the expression of type Ⅰ IP 3 R protein that stimulates release of intracellular Ca 2+ in RASMC and induces contraction of RASMC. The renal blood flow diminution leads to the development of renal dysfunction.
出处
《中华内科杂志》
CAS
CSCD
北大核心
2002年第2期86-89,共4页
Chinese Journal of Internal Medicine
基金
国家自然科学基金资助 ( 39870 337)
