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缺血再灌注损伤大鼠肾脏中睫状神经营养因子(CNTF)及其受体α的上调

Upregulation of ciliary neurotrophic factor (CNTF) and CNTF receptor alpha in rat kidney with ischemia-reperfusion injury.

作者信息

Yang Chul Woo, Lim Sun Woo, Han Ki Whan, Ahn Hee Jong, Park Jung Hee, Kim Young Hee, Kirsh Matthias, Cha Jung Ho, Park Joo Hyun, Kim Yong Soo, Kim Jin, Bang Byung Kee

机构信息

Division of Nephrology, Department of Internal Medicine, Kangnam St. Mary's Hospital, The Catholic University of Korea, Seoul, Korea.

Department of Anatomy, The College of Medicine, The Catholic University of Korea, Seoul, Korea.

出版信息

J Am Soc Nephrol. 2001 Apr;12(4):749-757. doi: 10.1681/ASN.V124749.

Abstract

Ciliary neurotrophic factor (CNTF) is presumed to play a role as a survival factor in neuronal cells, but little is known about its role in the kidney. To investigate this, the expression of CNTF and CNTF receptor alpha (CNTFR alpha) was analyzed in the ischemic rat kidney. An ischemia/reperfusion (I/R) injury was induced by clamping both renal arteries for 45 min. Animals were killed at 1, 2, 3, 5, 7, 14, and 28 d after ischemia. The expression of CNTF and CNTFR alpha was monitored by reverse transcription-PCR, in situ hybridization, immunoblotting, immunohistochemistry, and electron microscopy. In sham-operated rat kidneys, CNTF expression was weak and limited to the descending thin limb of the loop of Henle. With I/R injury, CNTF mRNA and protein expressions were strikingly increased as compared with the sham-operated rat kidney, and the immunoreactivity of CNTF was mainly observed in the regenerating proximal tubules. The expression of CNTFR alpha mRNA was also increased after I/R injury, and its location and expression patterns were similar to the expression of CNTF. These findings suggest a possible role of CNTF as a growth factor during renal tubular repair processes after I/R injury and an autocrine or paracrine function of CNTF acting against CNTFR alpha.

摘要

睫状神经营养因子(CNTF)被认为在神经元细胞中作为一种存活因子发挥作用,但对其在肾脏中的作用了解甚少。为了对此进行研究,在缺血大鼠肾脏中分析了CNTF和CNTF受体α(CNTFRα)的表达。通过夹闭双侧肾动脉45分钟诱导缺血/再灌注(I/R)损伤。在缺血后1、2、3、5、7、14和28天处死动物。通过逆转录-聚合酶链反应、原位杂交、免疫印迹、免疫组织化学和电子显微镜监测CNTF和CNTFRα的表达。在假手术大鼠肾脏中,CNTF表达较弱,且仅限于髓袢降支细段。与假手术大鼠肾脏相比,I/R损伤后CNTF mRNA和蛋白表达显著增加,且CNTF的免疫反应性主要在再生的近端小管中观察到。I/R损伤后CNTFRα mRNA表达也增加,其定位和表达模式与CNTF的表达相似。这些发现提示CNTF在I/R损伤后肾小管修复过程中可能作为一种生长因子发挥作用,且CNTF对CNTFRα具有自分泌或旁分泌功能。

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