Lin Shaohui, Ma Shaojun, Lu Ping, Cai Wenwei, Chen Yi, Sheng Jing
Department of Geriatrics, Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai, China.
Int J Clin Exp Pathol. 2014 Apr 15;7(5):2199-208. eCollection 2014.
CTRP3, discovered as novel adipokines, is a member of the C1q tumor necrosis factor (TNF) related protein (CTRP) super-family. CTRP3 is found to function as adipokines that display diverse biological activities in metabolic and cardiovascular diseases. Recent study demonstrated that CTRP3 was protective against pathological cardiac remodeling in mice. Nevertheless, the effect of CTRP3 on vascular remodeling remains undefined. Our present study aimed to explore the effects of adipokine CTRP3 on the activation of adventitial fibroblasts (AFs) induced by TGF-β1. Immunofluorescent staining, real-time PCR and Western blot were conducted to evaluate the expression of α-smooth muscle-actin (α-SMA) and collagen I. The expression of CTGF was evaluated by enzymelinked immunosorbent assay (ELISA), while the proliferation and migration of adventitial fibroblasts were detected by using cell counting kit-8 (CCK-8) assay and Transwell technique, respectively. Functional analysis showed that CTRP3 inhibited TGF-β1 inducing AFs phenotypic conversion, collagen synthesis, proliferation and migration. The secretion of CTGF was also inhibited by CTRP3. Our findings suggest that CTRP3 may be beneficial to the prevention of cardiovascular diseases and provide a promising therapeutic strategy to attenuate vascular remodeling.
CTRP3作为一种新型脂肪因子被发现，是C1q肿瘤坏死因子（TNF）相关蛋白（CTRP）超家族的成员。CTRP3被发现作为脂肪因子在代谢和心血管疾病中发挥多种生物学活性。最近的研究表明，CTRP3对小鼠病理性心脏重塑具有保护作用。然而，CTRP3对血管重塑的影响仍不明确。我们目前的研究旨在探讨脂肪因子CTRP3对转化生长因子-β1（TGF-β1）诱导的外膜成纤维细胞（AFs）活化的影响。进行免疫荧光染色、实时聚合酶链反应（PCR）和蛋白质免疫印迹法以评估α-平滑肌肌动蛋白（α-SMA）和I型胶原的表达。通过酶联免疫吸附测定（ELISA）评估结缔组织生长因子（CTGF）的表达，而分别使用细胞计数试剂盒-8（CCK-8）测定法和Transwell技术检测外膜成纤维细胞的增殖和迁移。功能分析表明，CTRP3抑制TGF-β1诱导的AFs表型转化、胶原合成、增殖和迁移。CTRP3也抑制CTGF的分泌。我们的研究结果表明，CTRP3可能有助于预防心血管疾病，并为减轻血管重塑提供一种有前景的治疗策略。
