Neuronal differentiation of human mesenchymal stem cells: changes in the expression of the Alzheimer's disease-related gene seladin-1

Benvenuti, Susanna; Saccardi, Riccardo; Luciani, Paola; Urbani, Serena; Deledda, Cristiana; Cellai, Ilaria; Francini, Fabio; Squecco, Roberta; Rosati, Fabiana; Danza, Giovanna; Gelmini, Stefania; Greeve, Isabell; Rossi, Matteo; Maggi, Roberto; Serio, Mario; Peri, Alessandro (2006). Neuronal differentiation of human mesenchymal stem cells: changes in the expression of the Alzheimer's disease-related gene seladin-1. Experimental cell research, 312(13), pp. 2592-604. San Diego, Calif.: Elsevier 10.1016/j.yexcr.2006.04.016

Full text not available from this repository. (Request a copy)

Seladin-1 (SELective Alzheimer's Disease INdicator-1) is an anti-apoptotic gene, which is down-regulated in brain regions affected by Alzheimer's disease (AD). In addition, seladin-1 catalyzes the conversion of desmosterol into cholesterol. Disruption of cholesterol homeostasis in neurons may increase cell susceptibility to toxic agents. Because the hippocampus and the subventricular zone, which are affected in AD, are the unique regions containing stem cells with neurogenic potential in the adult brain, it might be hypothesized that this multipotent cell compartment is the predominant source of seladin-1 in normal brain. In the present study, we isolated and characterized human mesenchymal stem cells (hMSC) as a model of cells with the ability to differentiate into neurons. hMSC were then differentiated toward a neuronal phenotype (hMSC-n). These cells were thoroughly characterized and proved to be neurons, as assessed by molecular and electrophysiological evaluation. Seladin-1 expression was determined and found to be significantly reduced in hMSC-n compared to undifferentiated cells. Accordingly, the total content of cholesterol was decreased after differentiation. These original results demonstrate for the first time that seladin-1 is abundantly expressed by stem cells and appear to suggest that reduced expression in AD might be due to an altered pool of multipotent cells.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Head Organs and Neurology (DKNS) > Clinic of Neurology

UniBE Contributor:

Greeve, Isabell

ISSN:

0014-4827

ISBN:

16762343

Publisher:

Elsevier

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:50

Last Modified:

17 Mar 2015 21:52

Publisher DOI:

10.1016/j.yexcr.2006.04.016

PubMed ID:

16762343

Web of Science ID:

000239294700018

URI:

https://boris.unibe.ch/id/eprint/20963 (FactScience: 4775)

Actions (login required)

Edit item Edit item
Provide Feedback