Journal
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
Volume 24, Issue 3, Pages 385-392Publisher
AMER SOC NEPHROLOGY
DOI: 10.1681/ASN.2012101031
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Funding
- National Institutes of Health (NIH) [CA125550, CA-155370, CA-151925, DK 081576, DK 055001]
- Metastasis Research Center at the MD Anderson Cancer Center
- Cancer Prevention and Research Institute of Texas
- NIH Research Training Grant in Gastroenterology at the Beth Israel Deaconess Medical Center [2T32DK007760-11]
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Hypoxia is associated with tissue injury and fibrosis but its functional role in fibroblast activation and tissue repair/regeneration is unknown. Using kidney injury as a model system, we demonstrate that injured epithelial cells produce an increased number of exosomes with defined genetic information to activate fibroblasts. Exosonnes released by injured epithelial cells promote proliferation, a-smooth muscle actin expression, F-actin expression, and type I collagen production in fibroblasts. Fibroblast activation is dependent on exosomes delivering TGF-beta 1 mRNA among other yet to be identified moieties. This study suggests that TGF-beta 1 mRNA transported by exosomes constitutes a rapid response to initiate tissue repair/regenerative responses and activation of fibroblasts when resident parenchyma is injured. The results also inform potential utility of exosome-targeted therapies to control tissue fibrosis. J Am Soc Nephrol 24: 385-392, 2013. doi: 10.1681/ASN.2012101031
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