|Cancer||Cell death||Cell cycle||Cytoskeleton||Exo/endocytosis||Differentiation||Division||Organelles||Signalling||Stem cells||Trafficking|
Cell Biology International (2007) 31, 14281435 (Printed in Great Britain)
Signals in pathological CNS extracts of ALS mice promote hMSCs neurogenic differentiation in vitro
Cui‑Ping Zhaoa, Cheng Zhangab*, Yi‑Hua Wangc, Sheng‑Nian Zhoud, Chang Zhoua, Wan‑Yi Lib and Mei‑Juan Yub
aDepartment of Neurology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, PR China
bStem Cells and Tissue Engineering Research Center of Sun Yat-sen University, Guangzhou 510080, PR China
cDepartment of Neurosurgery, Affiliated Hospital, Yang Zhou University, Yangzhou 225000, PR China
dDepartment of Neurology, Qi-Lu Hospital, ShanDong University, Jinan 250012, PR China
The capability of MSCs to differentiate into neurons has been proven by many studies. Recently, other studies have cast doubt on MSCs neurogenic differentiation with non-physiological chemical inducing agents in vitro. This present study was designed to use conditioned medium to investigate whether signals from pathological condition of ALS were competent to induce a program of neurogenic differentiation in expanded cultures of hMSCs. Incubation of hMSCs with conditioned medium prepared from CNS extracts of ALS mice (SOD1-G93A ALS mice) resulted in a time-dependent morphological change from fibroblast-like into neuron-like, concomitant with increase in the expression of Nestin and subsequent β-tubulin III, NSE and GAP43. Moreover, signals in pathological CNS extracts of ALS mice were more effective in promoting hMSCs neurogenic differentiation than those in physiological extracts of normal adult mice. These results show that pathological condition of ALS is endowed with capacity to induce hMSCs neurogenic differentiation and hMSCs have shown a potential candidate in cellular therapy for ALS.
Key words: Differentiation, Mesenchyme, Stem cells, Amyotrophic lateral sclerosis.
*Corresponding author. Department of Neurology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, PR China. Fax: +86 020 87333122.
Received 9 January 2007/13 May 2007; accepted 6 June 2007doi:10.1016/j.cellbi.2007.06.003