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结缔组织生长因子通过上调肾间质成纤维细胞组织型转谷氨酰胺酶及III型胶原促进肾间质纤维化
Increase of tissue transglutaminase and collagen type III induced by connect tissue growth factor in renal interstitial fibroblast contributes to renal interstitial fibrosis
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DOI:
作者:
刘森炎,钱一欣,卞蓉蓉,郁胜强
LIU Senyan, QIAN Yixin, BIAN Rongrong, YU Shengqiang
作者单位:
第二军医大学附属上海长征医院肾内科
Kidney Institute of CPLA. Division of Nephrology, Changzheng Hospital of Second Military Medical University
关键词:
慢性肾脏病;结缔组织生长因子;组织型转谷氨酰胺酶;III型胶原
chronic kidney disease; connective tissue growth factor; tissue transglutaminase; collagen type III
摘要:
目的 拟观察结缔组织生长因子(CTGF)对肾间质成纤维细胞上组织型转谷氨酰胺酶(tTG)和III型胶原的影响,探讨相关的调控机制。 方法 选择大鼠肾间质成纤维细胞(NRK-49F)为研究对象。(1)给予CTGF刺激(不同剂量或不同时间),检测tTG的蛋白及mRNA水平;(2)检测CTGF对MAPKs和PI3K/Akt信号通路的激活作用;(3)检测不同的信号通路阻断对CTGF调节tTG和III型胶原作用的影响。 结果(1)CTGF显著上调 tTG蛋白和mRNA水平,上调III型胶原蛋白水平(P<0.05);(2)CTGF能刺激ERK1/2和PI3K/Akt信号通路活化,而不能刺激P38和JNK活化;(3)阻断PI3K/Akt信号通路抑制CTGF刺激的tTG和III型胶原蛋白水平增加,阻断ERK1/2信号通路没有类似作用。 结论 CTGF可以通过PI3K/Akt途径上调肾间质成纤维细胞中tTG和III型胶原水平,在肾间质纤维化中起重要作用。
Objective Renal tubulointerstitial fibrosis is a common pathway of chronic kidney disease to end-stage renal disease. Our study is to investigate the effect of connective tissue growth factor (CTGF) on tissue transglutaminase(tTG) and collagen type III in renal interstitial fibroblast and underlying mechanism. Method Renal interstitial fibroblast was treated with CTGF, then Collagen type III and tTG levels were determined by Western blot and RT-PCR. MAPKs and PI3K/Akt signal pathway were also measured. After blockade of ERK1/2 or PI3K/Akt signal pathway prior to CTGF treatment, tTG and collagen type III levels were determined. Results CTGF is a inducer of expression of tTG protein in dose-dependent and time-dependent manner (P<0.05). CTGF also upregulated the levels of collagen type III. CTGF induced activation in both of ERK1/2 and PI3K/Akt. And blockade of phosphorylation of PI3K/Akt by LY294002 could abolish CTGF-stimulated increase of tTG and collagen type III, whereas inhibition of activation of ERK1/2 by PD98059 had no similar effect. Conclusion Our data demonstrated that CTGF could induced the increase of tTG and collagen type III in NRK-49F cells through PI3K/Akt activated pathway, which both contribute to the pathgenesis of renal interstitial fibrosis.
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