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J. Biol. Chem., Vol. 283, Issue 41, 27927-27936, October 10, 2008

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β 1 Integrin-mediated Effects of Tenascin-R Domains EGFL and FN6-8 on Neural Stem/Progenitor Cell Proliferation and Differentiation in Vitro^*

Hong Liao¹², Wenhui Huang¹, Melitta Schachner^¶, Yue Guan, Jingjing Guo, Jun Yan, Jing Qin, Xianshu Bai, and Luyong Zhang^||3

From the Neurobiology Laboratory, New Drug Screening Centre and the ^||Jiangsu Center for Pharmacodynamic Research and Evaluation, China Pharmaceutical University, Nanjing 210038, China, the Zentrum für Molekulare Neurobiologie, University of Hamburg, D-20251 Hamburg, Germany, and the ^¶Keck Centre for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, New Jersey 08854

Neural stem/progenitor cells (NSCs) have the capacity for self-renewal and differentiation into major classes of central nervous system cell types, such as neurons, astrocytes, and oligodendrocytes. The determination of fate of NSCs appears to be regulated by both intrinsic and extrinsic factors. Mounting evidence has shown that extracellular matrix molecules contribute to NSC proliferation and differentiation as extrinsic factors. Here we explore the effects of the epidermal growth factor-like (EGFL) and fibronectin type III homologous domains 6-8 (FN6-8) of the extracellular matrix molecule tenascin-R on NSC proliferation and differentiation. Our results show that domain FN6-8 inhibited NSC proliferation and promoted NSCs differentiation into astrocytes and less into oligodendrocytes or neurons. The EGFL domain did not affect NSC proliferation, but promoted NSC differentiation into neurons and reduced NSC differentiation into astrocytes and oligodendrocytes. Treatment of NSCs with β 1 integrin function-blocking antibody resulted in attenuation of inhibition of the effect of FN6-8 on NSC proliferation. The influence of EGFL or FN6-8 on NSCs differentiation was inhibited byβ 1 integrin antibody application, implicatingβ 1 integrin in proliferation and differentiation induced by EGFL and FN6-8 mediated triggering of NSCs.

Received for publication, June 23, 2008

^* This work was supported by grants from the National Natural Science Foundation of China (30670793), Natural Science Foundation of Jiang Su Province (BK2006150), International Coorperation Projects of Jiang Su Province (BZ2006050), Pharmacodynamics Research and Evaluation Fund of Jiang Su Province, and Initial Fund of China Pharmaceutical University (to H. L.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains Figs. S1-S3.

¹ Both authors contributed equally to this work.

² To whom correspondence may be addressed: 1 Shen Nong Rd., Nanjing 210038, China. Tel.: 86-25-85391036; Fax: 86-25-85303260; E-mail: liaohong56{at}hotmail.com.

³ To whom correspondence may be addressed: 1 Shen Nong Rd., Nanjing 210038, China. Tel.: 86-25-83271500; Fax: 86-25-85303260; E-mail: lyzhang{at}cpu.edu.cn.

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