Departamento de Biologia Estrutural e Funcional, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), CEP 13083-862, Campinas, SP, Brazil.
Laboratório de Lípides (LIM10), Hospital das Clínicas (HCFMUSP) da Faculdade de Medicina da Universidade de São Paulo, CEP 01246-903, São Paulo, SP, Brazil.
Function (Oxf). 2024 Jul 11;5(4). doi: 10.1093/function/zqae024.
Cholesteryl ester transfer protein (CETP) increases the atherosclerosis risk by lowering HDL-cholesterol levels. It also exhibits tissue-specific effects independent of HDL. However, sexual dimorphism of CETP effects remains largely unexplored. Here, we hypothesized that CETP impacts the perivascular adipose tissue (PVAT) phenotype and function in a sex-specific manner. PVAT function, gene and protein expression, and morphology were examined in male and female transgenic mice expressing human or simian CETP and their non-transgenic counterparts (NTg). PVAT exerted its anticontractile effect in aortas from NTg males, NTg females, and CETP females, but not in CETP males. CETP male PVAT had reduced NO levels, decreased eNOS and phospho-eNOS levels, oxidative stress, increased NOX1 and 2, and decreased SOD2 and 3 expressions. In contrast, CETP-expressing female PVAT displayed increased NO and phospho-eNOS levels with unchanged NOX expression. NOX inhibition and the antioxidant tempol restored PVAT anticontractile function in CETP males. Ex vivo estrogen treatment also restored PVAT function in CETP males. Moreover, CETP males, but not female PVAT, show increased inflammatory markers. PVAT lipid content increased in CETP males but decreased in CETP females, while PVAT cholesterol content increased in CETP females. CETP male PVAT exhibited elevated leptin and reduced Prdm16 (brown adipocyte marker) expression. These findings highlight CETP sex-specific impact on PVAT. In males, CETP impaired PVAT anticontractile function, accompanied by oxidative stress, inflammation, and whitening. Conversely, in females, CETP expression increased NO levels, induced an anti-inflammatory phenotype, and preserved the anticontractile function. This study reveals sex-specific vascular dysfunction mediated by CETP.
胆固醇酯转移蛋白(CETP)通过降低高密度脂蛋白胆固醇(HDL-cholesterol)水平增加动脉粥样硬化风险。它还表现出独立于 HDL 的组织特异性效应。然而,CETP 效应的性别二态性在很大程度上仍未得到探索。在这里,我们假设 CETP 以性别特异性的方式影响血管周围脂肪组织(PVAT)表型和功能。检查了表达人类或类人 CETP 及其非转基因对应物(NTg)的雄性和雌性转基因小鼠的 PVAT 功能、基因和蛋白质表达以及形态。PVAT 在 NTg 雄性、NTg 雌性和 CETP 雌性的主动脉中发挥其抗收缩作用,但在 CETP 雄性中没有。CETP 雄性 PVAT 的 NO 水平降低,eNOS 和磷酸化 eNOS 水平降低,氧化应激增加,NOX1 和 2 增加,SOD2 和 3 表达减少。相比之下,表达 CETP 的雌性 PVAT 显示出增加的 NO 和磷酸化 eNOS 水平,而 NOX 表达不变。NOX 抑制和抗氧化剂 tempol 恢复了 CETP 雄性的 PVAT 抗收缩功能。体外雌激素处理也恢复了 CETP 雄性的 PVAT 功能。此外,CETP 雄性,而不是雌性 PVAT,表现出增加的炎症标志物。CETP 雄性的 PVAT 脂质含量增加,而 CETP 雌性的 PVAT 脂质含量减少,而 CETP 雌性的 PVAT 胆固醇含量增加。CETP 雄性 PVAT 表现出升高的瘦素和降低的 Prdm16(棕色脂肪细胞标志物)表达。这些发现强调了 CETP 对 PVAT 的性别特异性影响。在雄性中,CETP 损害了 PVAT 的抗收缩功能,同时伴有氧化应激、炎症和白化。相反,在雌性中,CETP 表达增加了 NO 水平,诱导了抗炎表型,并保持了抗收缩功能。本研究揭示了 CETP 介导的性别特异性血管功能障碍。