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Tensin-3 Regulates Integrin-Mediated Proliferation and Differentiation of Tonsil-Derived Mesenchymal Stem Cells. | LitMetric

Tensin-3 Regulates Integrin-Mediated Proliferation and Differentiation of Tonsil-Derived Mesenchymal Stem Cells.

Cells

Department of Otorhinolaryngology, Head and Neck Surgery, Pusan National University School of Medicine and Biomedical Research Institute, Pusan National University Hospital, Busan 49241, Korea.

Published: December 2019

AI Article Synopsis

  • Human palatine tonsils can be a source of multipotent mesenchymal stem cells (TMSCs), which proliferate faster than those from bone marrow (BMSCs) or adipose tissue (ADSCs).
  • The study found that tensin-3 (TNS3) is expressed at higher levels in TMSCs compared to BMSCs and ADSCs, and silencing TNS3 leads to reduced cell growth and alters key signaling pathways.
  • TNS3 appears to influence TMSC proliferation and differentiation by regulating the expression of active integrin beta-1 (ITGβ1), with its inhibition affecting adipogenic and other cell lineage differentiations.

Article Abstract

Human palatine tonsils are potential tissue source of multipotent mesenchymal stem cells (MSCs). The proliferation rate of palatine tonsil-derived MSCs (TMSCs) is far higher than that of bone marrow-derived MSCs (BMSCs) or adipose tissue-derived MSCs (ADSCs). In our previous study, we had found through DNA microarray analysis that tensin-3 (TNS3), a type of focal adhesion protein, was more highly expressed in TMSCs than in both BMSCs and ADSCs. Here, the role of TNS3 in TMSCs and its relationship with integrin were investigated. TNS3 expression was significantly elevated in TMSCs than in other cell types. Cell growth curves revealed a significant decrease in the proliferation and migration of TMSCs treated with siRNA for TNS3 (siTNS3). siTNS3 treatment upregulated p16 and p21 levels and downregulated SOX2 expression and focal adhesion kinase, protein kinase B, and c-Jun N-terminal kinase phosphorylation. siTNS3 transfection significantly reduced adipogenic differentiation of TMSCs and slightly decreased osteogenic and chondrogenic differentiation. Furthermore, TNS3 inhibition reduced active integrin beta-1 (ITGβ1) expression, while total ITGβ1 expression was not affected. Inhibition of ITGβ1 expression in TMSCs by siRNA showed similar results observed in TNS3 inhibition. Thus, TNS3 may play an important role in TMSC proliferation and differentiation by regulating active ITGβ1 expression.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7017379PMC
http://dx.doi.org/10.3390/cells9010089DOI Listing

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