Human Umbilical Cord Mesenchymal Stem Cells Infected with Adenovirus Expressing HGF Promote Regeneration of Damaged Neuron Cells in a Parkinson's Disease Model. (3rd September 2014)

• Record Type: Journal Article
• Authors: Liu, Xin-Shan; Li, Jin-Feng; Wang, Shan-Shan; Wang, Yu-Tong; Zhang, Yu-Zhen; Yin, Hong-Lei; Geng, Shuang; Gong, Hui-Cui; Han, Bing; Wang, Yun-Liang
• Other Names: Duan Shiwei Academic Editor.
• Is Part Of: BioMed research international. Volume 2014(2014)
• Publication Date: 2014-09-03
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Life sciences -- Periodicals; 610.5
• DOI: 10.1155/2014/909657
• Languages: English
• ISSNs: 2314-6133

Abstract

Abstract : Parkinson's disease (PD) is a neurodegenerative movement disorder that is characterized by the progressive degeneration of the dopaminergic (DA) pathway. Mesenchymal stem cells derived from human umbilical cord (hUC-MSCs) have great potential for developing a therapeutic agent as such. HGF is a multifunctional mediator originally identified in hepatocytes and has recently been reported to possess various neuroprotective properties. This study was designed to investigate the protective effect of hUC-MSCs infected by an adenovirus carrying the HGF gene on the PD cell model induced by MPP+ on human bone marrow neuroblastoma cells. Our results provide evidence that the cultural supernatant from hUC-MSCs expressing HGF could promote regeneration of damaged PD cells at higher efficacy than the supernatant from hUC-MSCs alone. And intracellular free Ca 2+ obviously decreased after treatment with cultural supernatant from hUC-MSCs expressing HGF, while the expression of CaBP-D28k, an intracellular calcium binding protein, increased. Therefore our study clearly demonstrated that cultural supernatant of MSC overexpressing HGF was capable of eliciting regeneration of damaged PD model cells. This effect was probably achieved through the regulation of intracellular Ca 2+ levels by modulating of CaBP-D28k expression.