Effects of miR-141-3p in Mice with Recurrent Spontaneous Abortion

Background and Purpose: To investigate miR-141-3p's role and regulatory mechanism in the pathogenesis of recurrent sponta-neous abortion (RSA).Methods: MiR-141-3p and CD163 expressions in the decidual tissues of 30 RSA patients and 30 early pregnancy people were detected, and the relationship between miR-141-3p and CD163 were confirmed. Isolation and purification of the human decidual macrophages (DMs) was conducted, and the normal pregnancy mouse model and RSA mouse model were constructed. Besides, CD163 expressions, M2 DMs' proportion, miR-141-3p levels, TNF-alpha, IL-6, and IL-8 levels were measured. Also CD163 relative optical density and the embryo absorption rate in the decidua tissue were calculated.Results: MiR-141-3p levels in RSA patients were significantly elevated compared to control people, while CD163 expressions were declined (p < 0.05). And CD163 was the target gene of miR-141-3p. miR-141-3p, IL-6, TNF-alpha, and IL-8 levels of human DMs in the miR-141-3p inhibitor + si-NC group were remarkably lower than the inhibitor NC + si-NC group, while CD163 expressions and M2 DMs' proportion were increased (p < 0.05). Furthermore, the embryo absorption rate, miR-141-3p, IL-6, TNF-alpha, and IL-8 levels of the RSA group were elevated compared to control mice, while CD163 expressions and M2 DMs' proportion were down-regulated (p < 0.05). After down-regulation of miR-141-3p, all indicators demonstrated the opposite trend. However, knocking down CD163 reversed the above trend. Conclusions: MiR-141-3p inhibited the polarization of M2 DMs and promoted the inflammation in the decidual tissue of RSA mice by targeting CD163.

Automated summary

This study investigates the role and regulatory mechanism of miR-141-3p in the pathogenesis of recurrent spontaneous abortion (RSA), and finds that miR-141-3p promotes inflammation in the decidual tissue of RSA mice by inhibiting CD163 and inhibiting the polarization of M2 macrophages.