BMC cardiovascular disorders · 2025
Osteocalcin deficiency attenuates neointima formation after vascular injury in rat.
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Yi Ming, Li Yan, Sun Jinghao, Si Jin, Liu Huirong, Li Jing
Аннотация
BACKGROUND: The bone-specific protein osteocalcin (OCN) is an established marker of vascular calcification and vascular smooth muscle cell (VSMC) osteogenic trans-differentiation. Recent studies have revealed the regulatory function of externally administered OCN on atherosclerosis and vascular remodeling. However, the role of OCN in VSMCs involved in cell migration and neointima formation has not been clearly described.
METHODS: Rat carotid-artery balloon-injury was performed to induce neointima formation. OCN expression was detected in injured carotid arteries by western blot and immunofluorescence staining. Rat primary cultured VSMCs were treated with tumor necrosis factor-α (TNF-α) and platelet-derived growth factor-BB (PDGF-BB). OCN overexpression was induced by virus infection. VSMC migration was detected by scratched wound-healing assay. The ratio of intima to media thickness and vascular cell adhesion molecule-1 (VCAM-1) expression were compared between wild type (WT) rat and OCN knockout (OCN-/-) rat after vascular injury. Blood pressure and vascular stiffness were detected between WT rat and OCN-/- rat by rat tail blood pressure test and small animal ultrasound.
RESULTS: OCN was significantly up-regulated in balloon-injured carotid arteries of rat and enhanced in VSMCs treated by the TNF-α and PDGF-BB. With OCN overexpression, VSMC proliferation and migration were simultaneously aggravated. OCN-/- rats maintained normal carotid artery architecture and function under physiological condition. After carotid artery injury, OCN-/- rats exhibited significantly reduced neointimal thickness and VCAM-1 expression of injured vessels compared to WT rats.
CONCLUSIONS: OCN participates in the pathological processes of vascular neointima formation and promotes inflammatory response of VSMC to vascular injury, but deletion of OCN does not affect vascular integrity under physiological condition, suggesting that OCN may provide new insights into the mechanism of intima hyperplasia.
METHODS: Rat carotid-artery balloon-injury was performed to induce neointima formation. OCN expression was detected in injured carotid arteries by western blot and immunofluorescence staining. Rat primary cultured VSMCs were treated with tumor necrosis factor-α (TNF-α) and platelet-derived growth factor-BB (PDGF-BB). OCN overexpression was induced by virus infection. VSMC migration was detected by scratched wound-healing assay. The ratio of intima to media thickness and vascular cell adhesion molecule-1 (VCAM-1) expression were compared between wild type (WT) rat and OCN knockout (OCN-/-) rat after vascular injury. Blood pressure and vascular stiffness were detected between WT rat and OCN-/- rat by rat tail blood pressure test and small animal ultrasound.
RESULTS: OCN was significantly up-regulated in balloon-injured carotid arteries of rat and enhanced in VSMCs treated by the TNF-α and PDGF-BB. With OCN overexpression, VSMC proliferation and migration were simultaneously aggravated. OCN-/- rats maintained normal carotid artery architecture and function under physiological condition. After carotid artery injury, OCN-/- rats exhibited significantly reduced neointimal thickness and VCAM-1 expression of injured vessels compared to WT rats.
CONCLUSIONS: OCN participates in the pathological processes of vascular neointima formation and promotes inflammatory response of VSMC to vascular injury, but deletion of OCN does not affect vascular integrity under physiological condition, suggesting that OCN may provide new insights into the mechanism of intima hyperplasia.
Предметные рубрики MeSH
AnimalsNeointimaCarotid Artery InjuriesCell MovementMuscle, Smooth, VascularDisease Models, AnimalMyocytes, Smooth MuscleMaleOsteocalcinRats, Sprague-DawleyCells, CulturedVascular Cell Adhesion Molecule-1BecaplerminVascular StiffnessCell ProliferationRatsCarotid Intima-Media ThicknessTumor Necrosis Factor-alpha