Enhanced ITM2A expression inhibits chondrogenic differentiation of mesenchymal stem cells.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Mesenchymal stem cells (MSC) from bone marrow or adipose tissue (ASC) are broadly discussed as a cell population able to support cartilage regeneration and thus represent interesting candidates for cell-based tissue engineering in cartilage. ASC could represent an easily accessible and therefore particularly suitable source of cells. Their chondrogenic differentiation potential is, however, lower than that of MSC. The aim of this work was to characterise ASC in comparison to MSC in order to identify genes which may be involved in mechanisms causing the altered chondrogenic potential of ASC. Representational difference analysis was used to identify genes with higher expression in undifferentiated ASC than in MSC. Expression levels of identified genes were confirmed by real-time RT-PCR. Integral membrane protein 2A (ITM2A) was higher expressed in expanded ASC than in MSC in a donor-independent manner. During early chondrogenic differentiation in spheroid cultures ITM2A levels remained low in MSC and a transient down-regulation occurred in ASC correlating with successful chondrogenesis. Persisting ITM2A levels were found in non-differentiating ASC. Consistent with this finding, forced expression of ITM2A in the mouse mesenchymal stem cell line C3H10T1/2 prevented chondrogenic induction. In conclusion, ITM2A may in early stages of differentiation be associated with an inhibition of

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.