Loss of expression of miR-335 is implicated in hepatic stellate cell migration and activation

Journal Article · Fri Jul 15 00:00:00 EDT 2011 · Experimental Cell Research

DOI:https://doi.org/10.1016/J.YEXCR.2011.05.001· OSTI ID:22212157

Chen, Chao ^[1]; Wu, Chao-Qun ^[2]; Zhang, Zong-Qi ^[3]; Yao, Ding-Kang; Zhu, Liang ^[1]

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1. Department of Gastroenterology, Changzheng Hospital, Second Military Medical University, No.415 Fengyang Road, Shanghai 200003 (China)
2. Genetics Institute, Fudan University, No. 220 Handan Road, Shanghai 200433 (China)
3. Department of Cardiology, No. 3 Hospital, Shanghai Jiao Tong University Medical school, No.280 Mohe Road, Shanghai 201900 (China)

Activation and migration of resident stellate cells (HSCs) within the hepatic space of Disse play an important role in hepatic fibrosis, which accounts for the increased numbers of activated HSCs in areas of inflammation during hepatic fibrosis. Currently, microRNAs have been found to play essential roles in HSC differentiation, proliferation, apoptosis, fat accumulation and collagen production. However, little is known about microRNA mediated HSC activation and migration. In this study, the miRNA expression profiles of quiescent HSCs, partially activated HSCs and fully activated HSCs were compared in pairs. Gene ontology (GO) and GO-Map network analysis indicated that the activation of HSCs was regulated by microRNAs. Among them miR-335 was confirmed to be significantly reduced during HSC activation by qRT-PCR, and restoring expression of miR-335 inhibited HSC migration and reduced {alpha}-SMA and collagen type I. Previous study revealed that tenascin-C (TNC), an extracellular matrix glycoprotein involved in cell migration, might be a target of miR-335. Therefore, we further studied the TNC expression in miR-335 over-expressed HSCs. Our data showed that exogenous TNC could enhance HSC migration in vitro and miR-335 restoration resulted in a significant inhibition of TNC expression. These results demonstrated that miR-335 restoration inhibited HSC migration, at least in part, via downregulating the TNC expression.

• OSTI ID: 22212157
• Journal Information: Experimental Cell Research, Vol. 317, Issue 12; Other Information: Copyright (c) 2011 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
APOPTOSIS
CELL PROLIFERATION
COLLAGEN
FIBROSIS
GENES
GLYCOPROTEINS
IN VITRO
INFLAMMATION
LIVER
NETWORK ANALYSIS
POLYMERASE CHAIN REACTION