| First Author | Feng SK | Year | 2021 |
| Journal | Mol Cell Endocrinol | Volume | 534 |
| Pages | 111373 | PubMed ID | 34174367 |
| Mgi Jnum | J:344652 | Mgi Id | MGI:6751528 |
| Doi | 10.1016/j.mce.2021.111373 | Citation | Feng SK, et al. (2021) Deficiency of Omentin-1 leads to delayed fracture healing through excessive inflammation and reduced CD31(hi)Emcn(hi) vessels. Mol Cell Endocrinol 534:111373 |
| abstractText | Fracture healing is a complicated process affected by many factors, such as inflammatory responses and angiogenesis. Omentin-1 is an adipokine with anti-inflammatory properties, but whether omentin-1 affects the fracture healing process is still unknown. Here, by using global omentin-1 knockout (omentin-1(-/-)) mice, we demonstrated that omentin-1 deficiency resulted in delayed fracture healing in mice, accompanied by increased inflammation and osteoclast formation, and decreased production of platelet-derived growth factor-BB (PDGF-BB) and osteogenesis-promoting vessels that are strongly positive for CD31 and Endomucin (CD31(hi)Emcn(hi)) in the fracture area. In vitro, omentin-1 treatment suppressed the ability of the tumor necrosis factor-alpha (TNF-alpha)-activated macrophages to stimulate multi-nuclear osteoclast formation, resulting in a significant increase in the generation of mono-nuclear preosteoclasts and PDGF-BB, a pro-angiogenic protein that is abundantly secreted by preosteoclasts. PDGF-BB significantly augmented endothelial cell proliferation, tube formation and migration, whereas direct treatment with omentin-1 did not induce obvious effects on angiogenesis activities of endothelial cells. Our study suggests a positive role of omentin-1 in fracture healing, which may be associated with the inhibition of inflammation and stimulation of preosteoclast PDGF-BB-mediated promotion of CD31(hi)Emcn(hi) vessel formation. |
