Human PRMT5 expression is enhanced during in vitro tubule formation and after in vivo ischemic injury in renal epithelial cells

被引:11
作者
Braun, MC
Kelly, CN
Prada, AE
Mishra, J
Chand, D
Devarajan, P
Zahedi, K
机构
[1] Childrens Hosp Res Fdn, Div Nephrol & Hypertens, Cincinnati, OH 45229 USA
[2] Inst Mol Med, Div Pediat Nephrol & Hypertens, Houston, TX USA
[3] Univ Cincinnati, Coll Med, Dept Pediat, Cincinnati, OH USA
关键词
protein arginine methyl transferase 5; tubulogenesis; ischemia with reperfusion injury;
D O I
10.1159/000077397
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Background: The interactions between cells and the extracellular matrix (ECM) are important in the regulation of cell growth and differentiation. Cells cultured in ECM differentiate and develop tubular structures. The kidney has the ability to partially recover function after an ischemic insult through repairing its tubular epithelium. The factors that contribute to tubule formation in vitro may mediate tubule regeneration in the recovery stage of acute tubular necrosis. Methods: RNA purified from cells grown on plastic, on Matrigel and in Matrigel matrix were subjected to differential display analysis to identify the transcripts that are differentially expressed during in vitro tubulogenesis. Results: Protein arginine methyltransferase 5 (PRMT5) expression increased in renal epithelial cells undergoing tubule formation. PRMT5 expression is developmentally regulated and ubiquitously expressed in a variety of adult tissues. We also demonstrated that expression of PRMT5 is enhanced in the renal tubular epithelium of animals subjected to ischemic reperfusion injury (IRI). Conclusion: The role of PRMT5 in the regulation of mitosis, its induction in renal epithelial cells undergoing tubule formation in vitro and its expression in the tubules of the kidneys subjected to IRI suggest that it functions in the regulation of cell growth and differentiation during tubule formation and regeneration. Copyright (C) 2004 S. Karger AG, Basel.
引用
收藏
页码:250 / 257
页数:8
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