| First Author | Aristorena M | Year | 2014 |
| Journal | J Cell Sci | Volume | 127 |
| Issue | Pt 12 | Pages | 2723-35 |
| PubMed ID | 24777481 | Mgi Jnum | J:214668 |
| Mgi Id | MGI:5603677 | Doi | 10.1242/jcs.143644 |
| Citation | Aristorena M, et al. (2014) Expression of endoglin isoforms in the myeloid lineage and their role during aging and macrophage polarization. J Cell Sci 127(Pt 12):2723-35 |
| abstractText | Endoglin plays a crucial role in pathophysiological processes such as hereditary hemorrhagic telangiectasia (HHT), preeclampsia and cancer. Endoglin expression is upregulated during the monocyte-to-macrophage transition, but little is known about its regulation and function in these immune cells. Two different alternatively spliced isoforms of endoglin have been reported, L-endoglin and S-endoglin. Although L-endoglin is the predominant variant, here, we found that there was an increased expression of the S-endoglin isoform during senescence of the myeloid lineage in human and murine models. We performed a stable isotope labelling of amino acids in cell culture (SILAC) analysis of both L-endoglin and S-endoglin transfectants in the human promonocytic cell line U937. Analysis of differentially expressed protein clusters allowed the identification of cellular activities affected during aging. S-endoglin expression led to decreased cellular proliferation and a decreased survival response to granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced apoptosis, as well as increased oxidative stress. Gene expression and functional studies suggested that there was a non-redundant role for each endoglin isoform in monocyte biology. In addition, we found that S-endoglin impairs the monocytic differentiation into the pro-inflammatory M1 phenotype and contributes to the compromised status of macrophage functions during aging. |
