Department of Thoracic Surgery, Fujian Medical University Union Hospital, No. 29 Xinquan Road, Gulou District, Fuzhou, People's Republic of China; Department of Thoracic Surgery, First Affiliated Hospital of Fujian Medical University, No. 20 Chazhong Road, Fuzhou, People's Republic of China.
Department of Thoracic Surgery, First Affiliated Hospital of Fujian Medical University, No. 20 Chazhong Road, Fuzhou, People's Republic of China.
Biochem Biophys Res Commun. 2020 Jul 23;528(2):299-304. doi: 10.1016/j.bbrc.2020.05.052. Epub 2020 May 27.
The pathogenesis of primary focal hyperhidrosis (PFH) is still not clear. PFH is thought to be a genetic disease. Whether activin A receptor type 1 (ACVR1) is involved in the pathogenesis of PFH is unknown. In this study, the expression of ACVR1 in sweat glands of patients with PAH was detected by western blot and immunofluorescence. The primary sweat gland cells obtained from primary axillary hyperhidrosis (PAH) patients were transfected with acvr1 vector. Cell proliferation, apoptosis and cell cycling of gland cells were measured after transfection with acvr1 vector. The mRNA and protein expression of aquaporin 5 (AQP5) and Na:K:2Cl Cotransporter 1 (NKCC1/SLC12A2) were detected. Our data showed that ACVR1 expression in axillary sweat gland tissue of PAH patients was significantly higher than that of normal control group. The function of ACVR1 was further investigated in the gland cells obtained from PAH patients. Compared with NC group, ACVR1 overexpression significantly promoted the proliferation of sweat gland cells and inhibited the apoptosis of sweat gland cells. Meanwhile, ACVR1 overexpression significantly reduced the percentage of cells in G0/G1 and G2/M phases, and increased the percentage of cells in S phase. In addition, ACVR1 overexpression significantly promoted the expression of AQP5 and NKCC1 at both mRNA and protein levels. Together, ACVR1 expression is related to PFH and ACVR1 overexpression can promote the proliferation of sweat gland cells and inhibit apoptosis by promoting the expression of AQP5 and NKCC1.
原发性局部多汗症(PFH)的发病机制尚不清楚。PFH 被认为是一种遗传病。ACVR1 是否参与 PFH 的发病机制尚不清楚。在这项研究中,通过 Western blot 和免疫荧光检测了 PFH 患者汗腺中 ACVR1 的表达。从原发性腋窝多汗症(PAH)患者中获得的原代汗腺细胞用 acvr1 载体转染。转染 acvr1 载体后,测量腺细胞的增殖、凋亡和细胞周期。检测水通道蛋白 5(AQP5)和 Na:K:2Cl 共转运蛋白 1(NKCC1/SLC12A2)的 mRNA 和蛋白表达。我们的数据表明,PAH 患者腋窝汗腺组织中 ACVR1 的表达明显高于正常对照组。进一步研究了从 PAH 患者获得的腺细胞中的 ACVR1 功能。与 NC 组相比,ACVR1 过表达显著促进了汗腺细胞的增殖并抑制了汗腺细胞的凋亡。同时,ACVR1 过表达显著降低了 G0/G1 和 G2/M 期细胞的百分比,增加了 S 期细胞的百分比。此外,ACVR1 过表达显著促进了 AQP5 和 NKCC1 在 mRNA 和蛋白水平的表达。总之,ACVR1 的表达与 PFH 有关,ACVR1 的过表达通过促进 AQP5 和 NKCC1 的表达可以促进汗腺细胞的增殖和抑制凋亡。