Key result
Elevated periostin drives adventitial remodeling in atherosclerosis by activating fibroblasts and inducing TGF-β1 and MCP1.
Why the study?
Cues implicated in adventitial remodeling during atherosclerosis are far from fully understood, motivating exploration of periostin's role.
Periostin is elevated in the adventitia during atherosclerosis and drives adventitial remodeling by activating fibroblasts and integrin-related signaling pathways.
POSTN activation of adventitial fibroblasts in mice leaves open its role in human atherosclerosis and any therapeutic targeting.
Background and aims: Adventitial remodeling is an important pathological process of atherosclerosis, but cues implicated in adventitial remodeling are far from fully understood. Periostin (POSTN), a matricellular protein, has been demonstrated to have multiple roles in cardiovascular diseases. The aim of the study was to explore the function of POSTN in adventitial remodeling during atherosclerosis. Methods: An atherosclerosis model was constructed based on ApoE-/- mice fed a high-fat and high-cholesterol diet. The expression of POSTN in the adventitia of mouse atherosclerotic vascular specimens was detected by immunohistochemical staining. The roles of POSTN in regulating adventitial fibroblast activation were assessed by cell contractility and activation marker α-smooth muscle actin (α-SMA) expression evaluation in adventitial fibroblasts overexpressing POSTN. In addition, we performed quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting to examine the expression of the proinflammatory chemokines transforming growth factor-β1 (TGF-β1) and monocyte chemotactic protein 1 (MCP1), as well as some extracellular matrix (ECM)-related proteins, in POSTN-overexpressing adventitial fibroblasts. Finally, the integrin-related signaling pathway was detected upon POSTN overexpression in adventitial fibroblasts. Results: POSTN was highly expressed in the adventitia of atherosclerotic aortae in the mouse atherosclerosis model and promoted the activation and contraction of adventitial fibroblasts. Meanwhile, POSTN also induced adventitial fibroblasts to express TGF-β1, monocyte chemotactic protein-1 (MCP1), and ECM-related proteins and activated the phosphorylation of focal adhesion kinase (FAK) and Src. Conclusions: Our results revealed that POSTN is elevated in adventitia during atherosclerosis and contributes to the adventitial remodeling of atherosclerosis by activating adventitial fibroblasts.
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Wang et al. (2022) studied Atherosclerosis. Periostin (POSTN) overexpression was evaluated on Adventitial fibroblast activation and contraction. Periostin is elevated in the adventitia during atherosclerosis and contributes to adventitial remodeling by activating adventitial fibroblasts and inducing TGF-β1 and MCP1 expression.
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