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微小 RNA200a 通过调节 Rho/ROCK 通路促进与年龄相关的勃起功能障碍中的平滑肌细胞生长。

Micro RNA 200a contributes to the smooth muscle cells growth in aged-related erectile dysfunction via regulating Rho/ROCK pathway.

机构信息

Emergency & Intensive Care Unit Center, Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, People's Republic of China.

Health Management Center, Department of Infectious Diseases, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, People's Republic of China.

出版信息

Andrologia. 2022 Oct;54(9):e14503. doi: 10.1111/and.14503. Epub 2022 Jul 1.

Abstract

Aged-related erectile dysfunction (A-ED) is generally regarded as degeneration of penile erectile tissue due to age, male hormone deficiency and concomitant cardiovascular disease. Current pathological studies of A-ED are still limited. In this study, aged rats were divided into AE group (aged rats with ED) and YN group (young normal rats) for evaluating the roles of miRNA-200a and RhoA/ROCK signalling pathway in A-ED. Apo-morphine test, ICP measurement and pathological results were compared between these two groups. After transfection of miRNA-200a into Corpus cavernosum smooth muscle cells (CCSMCs), the expression of miRNA-200a, RhoA, ROCK1 and ROCK2 in the AE group were significantly increased. Additionally, miRNA-200a, RhoA, ROCK1 and ROCK2 were upregulated at a high level after transfecting the miRNA-200a mimics. Therefore, we speculated that miRNA-200a is a positive regulator, which may inhibit the growth of CCSMCs by activating the Rho/ROCK pathway in vitro.

摘要

年龄相关性勃起功能障碍(A-ED)通常被认为是由于年龄、男性激素缺乏和伴随的心血管疾病导致的阴茎勃起组织退化。目前对 A-ED 的病理研究仍然有限。在这项研究中,将老年大鼠分为 AE 组(有 ED 的老年大鼠)和 YN 组(年轻正常大鼠),以评估 miRNA-200a 和 RhoA/ROCK 信号通路在 A-ED 中的作用。对这两组进行了阿朴吗啡测试、ICP 测量和病理结果比较。在将 miRNA-200a 转染入海绵体平滑肌细胞(CCSMCs)后,AE 组的 miRNA-200a、RhoA、ROCK1 和 ROCK2 的表达显著增加。此外,转染 miRNA-200a 模拟物后,miRNA-200a、RhoA、ROCK1 和 ROCK2 的表达水平上调。因此,我们推测 miRNA-200a 是一种正调节剂,它可能通过激活 Rho/ROCK 通路在体外抑制 CCSMCs 的生长。

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