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1.400038 重庆,陆军军医大学(第三军医大学)第一附属医院妇产科
2.401147 重庆,中国科学院大学重庆医院(重庆市人民医院)妇产科
[常青,E-mail:cqli99@126.comCHANG Qing, E-mail: cqli99@126.com
收稿:2021-11-30,
修回:2022-02-24,
纸质出版:2022-06-30
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严小丽, 陈诚, 王丹, 等. 孕酮通过RhoA/ROCK信号通路促进子宫平滑肌收缩的机制研究[J]. 陆军军医大学学报, 2022,44(12):1199-1206.
Xiaoli YAN, Cheng CHEN, Dan WANG, et al. Mechanism of progesterone promoting uterine smooth muscle contraction through RhoA/ROCK signaling pathway[J]. Journal of Army Medical University, 2022, 44(12): 1199-1206.
严小丽, 陈诚, 王丹, 等. 孕酮通过RhoA/ROCK信号通路促进子宫平滑肌收缩的机制研究[J]. 陆军军医大学学报, 2022,44(12):1199-1206. DOI: 10.16016/j.2097-0927.202111235.
Xiaoli YAN, Cheng CHEN, Dan WANG, et al. Mechanism of progesterone promoting uterine smooth muscle contraction through RhoA/ROCK signaling pathway[J]. Journal of Army Medical University, 2022, 44(12): 1199-1206. DOI: 10.16016/j.2097-0927.202111235.
目的
2
探讨孕酮通过RhoA/ROCK信号通路影响子宫平滑肌收缩的作用机制。
方法
2
收集临产与未临产人子宫平滑肌组织各5例,采用Western blot和免疫组化检测肌球蛋白轻链20磷酸化(phosphorylation of myosin light chain 20
p-MLC20)、ROCK1、ROCK2的表达;分离培养子宫平滑肌细胞并经免疫荧光技术鉴定,激光共聚焦显微镜检测细胞内游离Ca
2+
浓度([Ca
2+
]
i);孕酮受体拮抗剂米非司酮及孕酮(P4)干预子宫平滑肌细胞,Western blot检测细胞中p-MLC20及ROCK1、ROCK2的表达,以及ROCK抑制剂Y-27632与孕酮干预后子宫平滑肌细胞中p-MLC20的表达。
结果
2
与未临产组织相比,临产子宫平滑肌组织中p-MLC20、ROCK1、ROCK2表达明显上升(
P
<
0.05);孕酮诱导子宫平滑肌细胞后,细胞内ROCK1、ROCK2、p-MLC20水平增加(
P
<
0.05);Y-27632与孕酮干预子宫平滑肌细胞后,细胞内p-MLC20水平下降(
P
<
0.05)。
结论
2
孕酮通过RhoA/ROCK信号通路调控p-MLC20水平,促进子宫平滑肌细胞收缩。
Objective
2
To investigate the mechanism of progesterone affecting the contractions of uterine smooth muscle through RhoA/ROCK signaling pathway.
Methods
2
The tissues of uterine smooth muscle were collected from 5 cases in labor and another 5 of non-labor
respectively. The expression levels of phosphorylation of myosin light chain (p-MLC20)
ROCK1 and ROCK2 were detected by Western blotting and immunohistochemical (IHC) assay. Uterine smooth muscle cells were isolated and cultured
and then identified by im
munofluorescence assay. Laser confocal microscopy was used to measure the concentration of intracellular free Ca
2+
([Ca
2+
]
i) in the cells. In addition
the uterine smooth muscle cells were treated with progesterone+progesterone receptor antagonist
mifepristone
and with progesterone+ROCK inhibitor
Y-27632
respectively. Western blotting was performed to determine the expression of p-MLC20
ROCK1 and ROCK2 in the corresponding groups.
Results
2
As compared with the non-labor group
the expression of p-MLC20
ROCK1 and ROCK2 in the uterine smooth muscle tissues were significantly increased in the labor group (
P
<
0.05). Progesterone induced the elevation of p-MLC20
ROCK1 and ROCK2 levels in the cultured uterine smooth muscle cells (
P
<
0.05)
while after the intervention of Y-27632+progesterone
the p-MLC20 level was greatly decreased (
P
<
0.05).
Conclusion
2
Progesterone regulates p-MLC20 level through RhoA/ROCK signaling pathway and thus promotes the contractions of uterine smooth muscle cells.
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