Follistatin is a crucial chemoattractant for mouse decidualized endometrial stromal cell migration by JNK signalling

Guole Liu, Yan Qi, Jiandong Wu, Francis Lin, Zhonghui Liu, Xueling Cui
In: Journal of Cellular and Molecular Medicine · 2022 · vol. 27(1) , pp. 127–140 · doi:10.1111/jcmm.17648 · PMID:36528873 · W4311860700
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Follistatin, not activin A, significantly attracts mouse decidualized endometrial stromal cells by upregulating MMP9 and Ezrin via JNK signaling, aiding decidualization and tissue remodeling.

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Abstract

Follistatin (FST) and activin A as gonadal proteins exhibit opposite effects on follicle-stimulating hormone (FSH) release from pituitary gland, and activin A-FST system is involved in regulation of decidualization in reproductive biology. However, the roles of FST and activin A in migration of decidualized endometrial stromal cells are not well characterized. In this study, transwell chambers and microfluidic devices were used to assess the effects of FST and activin A on migration of decidualized mouse endometrial stromal cells (d-MESCs). We found that compared with activin A, FST exerted more significant effects on adhesion, wound healing and migration of d-MESCs. Similar results were also seen in the primary cultured decidual stromal cells (DSCs) from uterus of pregnant mouse. Simultaneously, the results revealed that FST increased calcium influx and upregulated the expression levels of the migration-related proteins MMP9 and Ezrin in d-MESCs. In addition, FST increased the level of phosphorylation of JNK in d-MESCs, and JNK inhibitor AS601245 significantly attenuated FST action on inducing migration of d-MESCs. These data suggest that FST, not activin A in activin A-FST system, is a crucial chemoattractant for migration of d-MESCs by JNK signalling to facilitate the successful uterine decidualization and tissue remodelling during pregnancy.

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