134
Views
3
CrossRef citations to date
0
Altmetric
Research Article

Potential signal pathway between all-trans retinoic acid and LMX1B in hypoxia-induced renal tubular epithelial cell injury

, , , &
Pages 53-56 | Received 20 Dec 2014, Accepted 17 Jan 2015, Published online: 22 Jun 2015
 

Abstract

All-trans retinoic acid (ATRA), an active metabolite of vitamin A, exerts various effects on physiological processes such as cell growth, differentiation, apoptosis and inflammation. LMX1B, a developmental LIM-homeodomain transcription factor, is widely expressed in vertebrate embryos, and it takes part in the development of diverse structures such as limbs, kidneys, eyes, brains, etc. Renal tubular epithelial cell culture was performed, and mRNA and protein expression of some factors were detected. We recently demonstrated that ATRA up-regulated the LMX1B, and down-regulated the transforming growth factor-β1, collagen IV and fibronectin in a hypoxia/reoxygenation (H-R) injury system in renal tubular epithelial cells (RTEC). In conclusion, ATRA acts as a positive regulator of LMX1B in H-R RTEC.

Declaration of interest

This study was supported by the Nature Science Foundation of China (no. 81400719) and the sub-item of 985 Project Foundation of Sun Yat-Sen (The Hundred Talents Program Foundation; No. 88000-3311300).

Log in via your institution

Log in to Taylor & Francis Online

PDF download + Online access

  • 48 hours access to article PDF & online version
  • Article PDF can be downloaded
  • Article PDF can be printed
USD 65.00 Add to cart

Issue Purchase

  • 30 days online access to complete issue
  • Article PDFs can be downloaded
  • Article PDFs can be printed
USD 1,339.00 Add to cart

* Local tax will be added as applicable

Related Research

People also read lists articles that other readers of this article have read.

Recommended articles lists articles that we recommend and is powered by our AI driven recommendation engine.

Cited by lists all citing articles based on Crossref citations.
Articles with the Crossref icon will open in a new tab.