CD36 deficiency inhibits proliferation by cell cycle control in skeletal muscle cells.
CD36 deficiency inhibits proliferation by cell cycle control in skeletal muscle cells.
复制标题
DOI：
10.3389/fphys.2022.947325
复制
发表时间：
2022
影响因子：
4
通讯作者：
中科院分区：
文献类型：
--
作者：
与肥胖相关的肌肉功能障碍和相对肌肉萎缩影响越来越多的人。阐明骨骼肌细胞发育和生长的分子机制可能有助于维持肥胖症骨骼肌质量。脂肪酸转位酶（FAT/CD 36）作为一种长链脂肪酸转运蛋白，在脂质代谢和信号转导中起着重要作用。已知CD 36在肌源性分化中起作用，并且其是否影响骨骼肌细胞的增殖及其潜在机制尚不清楚。在这项研究中，使用C2 C12成肌细胞检测了CD 36缺乏对骨骼肌细胞活力和增殖的影响。结果表明，CD 36的缺失增强了PA对骨骼肌细胞增殖的抑制作用和促进凋亡的作用。有趣的是，CD 36的沉默通过以细胞周期蛋白D1/CDK 4依赖的方式阻止细胞周期从G 0/G1期进入S期来抑制细胞增殖。总之，我们证明了CD 36通过细胞周期控制参与骨骼肌细胞增殖，这些发现可能有助于治疗肥胖相关的肌肉萎缩。
Obesity-related muscular dysfunction and relative muscle atrophy affect an increasing number of people. Elucidating the molecular mechanisms of skeletal muscle cell development and growth may contribute to the maintenance of skeletal muscle mass in obesity. Fatty acid translocase (FAT/CD36), as a long-chain fatty acid transport protein, is crucial for lipid metabolism and signaling. CD36 is known to function in myogenic differentiation, and whether it affects the proliferation of skeletal muscle cells and the underlying mechanisms remain unclear. In this study, the effect of CD36 deficiency on skeletal muscle cell viability and proliferation was examined using C2C12 myoblasts. Results showed that the deletion of CD36 enhanced the inhibitory effect of PA on the proliferation and the promotion of apoptosis in skeletal muscle cells. Intriguingly, the silencing of CD36 suppressed cell proliferation by preventing the cell cycle from the G0/G1 phase to the S phase in a cyclin D1/CDK4-dependent manner. Overall, we demonstrated that CD36 was involved in skeletal muscle cell proliferation by cell cycle control, and these findings might facilitate the treatment of obesity-related muscle wasting.
登录
查看更多内容
肌遗传学寡脱氧核苷酸（MyODN）恢复了糖尿病麦芽脂质恶化的骨骼肌成肌细胞的分化。
影响因子：
4
作者：
Nakamura S;Yonekura S;Shimosato T;Takaya T
通讯作者：
Takaya T
影响因子：
5.2
作者：
Ustanina, Svetlana;Carvajal, Jaime;Braun, Thomas
通讯作者：
Braun, Thomas
影响因子：
3.7
作者：
Bhowmick R;Banik G;Chanda S;Chattopadhyay S;Chawla-Sarkar M
通讯作者：
Chawla-Sarkar M
影响因子：
7.7
作者：
Hu Z;Wang H;Lee IH;Modi S;Wang X;Du J;Mitch WE
通讯作者：
Mitch WE
影响因子：
6.1
作者：
Charytoniuk, Tomasz;Ilowska, Nicoletta;Konstantynowicz-Nowicka, Karolina
通讯作者：
Konstantynowicz-Nowicka, Karolina