SMOC2 promoted vascular smooth muscle cell proliferation, migration, and extracellular matrix degradation by activating BMP/TGF‐β1 signaling pathway

Abstract

A widespread degenerative condition of the aorta, abdominal aortic aneurysm (AAA), severely endangers the health of middle-aged and elderly people. SPARC related modular calcium binding2 (SMOC2) is upregulated in the carotid arteries of rats with atherosclerotic lesions, but its function in AAA is still unknown. Therefore, the aim of this research was to evaluate the function of SMOC2 in AAA. The results showed that in the AAA tissues, SMOC2 expression was upregulated compared with healthy controls. Overexpression of SMOC2 promoted vascular smooth muscle cells (VSMCs) proliferation, migration, and extracellular matrix (ECM) degradation. In contrast, silence of SMOC2 inhibited VSMCs proliferation, migration, and ECM degradation. Overexpression of SMOC2 promoted BMP and TGF-β1 expression and silence of SMOC2 had an opposite effect. Besides, inhibition of BMP or TGF-β1 suppressed VSMCs cell proliferation, migration, and ECM degradation. Moreover, inhibition BMP or TGF-β1 reversed the promotive effects of SMOC2 overexpression on VSMCs proliferation, migration, and ECM degradation. SMOC2 may affecte the formation of AAA by upregulating BMP and TGF-β1 to regulate the proliferation, migration, and ECM degradation of VSMCs.

FTO Positively Regulates Odontoblastic Differentiation via SMOC2 in Human Stem Cells from the Apical Papilla under Inflammatory Microenvironment

“…Prior extensive in vivo studies have substantiated the essential role of SMOC2 in root dentin formation [28][29][30][31][32]. Additionally, in vitro analyses have underscored the intricate interactions between SMOC2 and signaling molecules such as transforming growth factor-β1, Runx2, and bone morphogenetic proteins, pivotal for odonto/osteogenic differentiation [33,52]. Furthermore, pronounced expression of SMOC2 in the apical papilla growing region of developing mouse and human teeth, followed by a decrease in expression in adult teeth, has been reported [53,54].…”

SMOC2, OGN, FCN3, and SERPINA3 could be biomarkers for the evaluation of acute decompensated heart failure caused by venous congestion

“…Additionally, mouse studies have demonstrated that SMOC2 knockdown can ameliorate cardiac function impairment and cardiac fibrosis, potentially through the inhibition of the ILK/p38 signaling pathway 34 . Furthermore, the overexpression of SMOC2 has been observed to enhance vascular smooth muscle cell proliferation, migration, and extracellular matrix breakdown, pointing to its significant role in cardiovascular pathophysiology 35 .…”