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首页> 外文期刊>American Journal of Physiology >Transforming growth factor-beta in acute renal failure: receptor expression, effects on proliferation, cellularity, and vascularization after recovery from injury.
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Transforming growth factor-beta in acute renal failure: receptor expression, effects on proliferation, cellularity, and vascularization after recovery from injury.

机译：急性肾衰竭中转化生长因子-β：损伤恢复后受体表达，对增殖，细胞性和血管形成的影响。

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摘要

Transforming growth factor (TGF)-beta1 and a number of TGF-beta-responsive genes are transiently enhanced following induction of ischemic acute renal failure (ARF) in the rat. The mRNA and protein expression of TGF-beta receptors were analyzed in postischemic rat kidneys by ribonuclease protection, in situ hybridization, and immunohistochemistry. TGF-betaRI and -RII were enhanced within 3 days of ischemia-reperfusion (I/R) injury and remained elevated for up 7 days post-I/R; TGF-beta receptor expression was localized primarily in regenerating tubules within the outer medulla. A neutralizing TGF-beta antibody exacerbated cellular proliferation observed on day 3 postischemia but had no effect on day 1 or 2. TGF-beta antibody treatment had no measurable effect on loss of renal function or the restoration of renal function during the recovery response for up to 35 days postsurgery. However, ischemic injury resulted in modest renal hypertrophy that is due, in part, to in an increase in the number of interstitial cells in the postischemic kidney. Immunohistochemistry showed that several of these cells stained positively for the fibroblast-specific marker, S100A4 positive. Anti-TGF-beta treatment substantially attenuated the renal hypertrophy, interstitial cellularity, and S100A4-positive cells present at 35 days post-I/R. Finally, TGF-beta immunoneutralization attenuated the loss of renal vascular density following recovery from I/R injury. These data suggest that the TGF-beta/TbetaR system is enhanced in the postischemic kidney. However, the current study failed to identify a prominent role for this system in the repair of proximal tubules following ARF. In contrast, the activation of this system may play an important role in the long-term structure of the postischemic kidney by influencing microvascular structure and interstitial cellularity.
机译：在大鼠中诱发缺血性急性肾衰竭（ARF）后，转化生长因子（TGF）-beta1和许多TGF-beta-响应基因被瞬时增强。通过核糖核酸酶保护，原位杂交和免疫组织化学分析缺血后大鼠肾脏中TGF-β受体的mRNA和蛋白表达。 TGF-betaRI和-RII在缺血/再灌注（I / R）损伤后3天内增强，并在I / R后7天内保持升高; TGF-β受体的表达主要位于髓质外的肾小管中。在缺血后第3天观察到中和的TGF-β抗体会加剧细胞增殖，但在第1天或第2天没有作用。TGF-β抗体治疗对肾功能丧失或恢复期间的肾功能恢复没有可测量的作用。到术后35天。然而，缺血性损伤导致适度的肾脏肥大，这部分是由于缺血后肾脏中的间质细胞数量增加所致。免疫组织化学显示，这些细胞中有几个细胞的成纤维细胞特异性标记S100A4呈阳性。抗TGF-β治疗可显着减轻I / R后35天出现的肾脏肥大，间质细胞增多和S100A4阳性细胞。最后，TGF-β免疫中和可减轻I / R损伤后肾血管密度的损失。这些数据表明，TGF-β/ TbetaR系统在缺血后肾脏中得到增强。但是，目前的研究未能确定该系统在ARF术后近端小管修复中的重要作用。相比之下，该系统的激活可能通过影响微血管结构和间质细胞结构在缺血后肾脏的长期结构中发挥重要作用。

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