| First Author | Korf-Klingebiel M | Year | 2015 |
| Journal | Nat Med | Volume | 21 |
| Issue | 2 | Pages | 140-9 |
| PubMed ID | 25581518 | Mgi Jnum | J:216795 |
| Mgi Id | MGI:5609664 | Doi | 10.1038/nm.3778 |
| Citation | Korf-Klingebiel M, et al. (2015) Myeloid-derived growth factor (C19orf10) mediates cardiac repair following myocardial infarction. Nat Med 21(2):140-9 |
| abstractText | Paracrine-acting proteins are emerging as a central mechanism by which bone marrow cell-based therapies improve tissue repair and heart function after myocardial infarction (MI). We carried out a bioinformatic secretome analysis in bone marrow cells from patients with acute MI to identify novel secreted proteins with therapeutic potential. Functional screens revealed a secreted protein encoded by an open reading frame on chromosome 19 (C19orf10) that promotes cardiac myocyte survival and angiogenesis. We show that bone marrow-derived monocytes and macrophages produce this protein endogenously to protect and repair the heart after MI, and we named it myeloid-derived growth factor (MYDGF). Whereas Mydgf-deficient mice develop larger infarct scars and more severe contractile dysfunction compared to wild-type mice, treatment with recombinant Mydgf reduces scar size and contractile dysfunction after MI. This study is the first to assign a biological function to MYDGF, and it may serve as a prototypical example for the development of protein-based therapies for ischemic tissue repair. |
