Modulation of tissue transglutaminase in tubular epithelial cells alters extracellular matrix levels: A potential mechanism of tissue scarring
Modulation of tissue transglutaminase in tubular epithelial cells alters extracellular matrix levels: A potential mechanism of tissue scarring
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DOI：
10.1016/j.matbio.2008.10.003
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发表时间：
2009-01-01
期刊：
影响因子：
6.9
通讯作者：
Johnson, Timothy S.
中科院分区：
文献类型：
--
作者：
Fisher, Marie;Jones, Richard A.;Johnson, Timothy S.
肾小管上皮细胞(TEC)对组织转谷氨酰胺酶(TG2)的上调和转运参与了肾脏瘢痕的形成。TG2通过形成高度稳定的β(γ-谷氨酰基)赖氨酸键催化蛋白质的交联。我们认为TG2可能通过促进细胞外基质(ECM)的沉积和稳定ECM抵抗蛋白水解性降解来促进肾脏瘢痕形成。为了研究这一点，我们研究了稳定表达TG2的负鼠肾TEC和TG2基因敲除小鼠肾小管上皮细胞的ECM代谢。TG2的表达增加导致细胞外TG2活性增加(p<0.05)。
The up-regulation and trafficking of tissue transglutaminase (TG2) by tubular epithelial cells (TEC) has been implicated in the development of kidney scarring. TG2 catalyses the crosslinking of proteins via the formation of highly stable epsilon(gamma-glutamyl) lysine bonds. We have proposed that TG2 may contribute to kidney scarring by accelerating extracellular matrix (ECM) deposition and by stabilising the ECM against proteolytic decay.To investigate this, we have studied ECM metabolism in Opossum kidney (OK) TEC induced to over-express TG2 by stable transfection and in tubular cells isolated from TG2 knockout mice.Increasing the expression of TG2 led to increased extracellular TG2 activity (p