AI Article Synopsis
- Mesenchymal stem cells (MSCs) can modify immune reactions, and issues with them are linked to various diseases, including preeclampsia (PE).
- The study found that increased levels of miR-30a in MSCs during PE inhibit critical inflammatory signaling pathways and reduce the production of pro-inflammatory molecules like IL-6 and COX2.
- Overall, miR-30a appears to contribute to immune dysfunction at the maternal-fetal interface in PE, affecting MSCs' ability to regulate inflammation in macrophages.
Article Abstract
Mesenchymal stem cells (MSCs) possess the ability to modulate the immune response, and their abnormalities are related to several diseases. We previously reported that miR-30a expression significantly increased in the maternal-fetal interface during preeclampsia (PE), but the effects of miR-30a on the immunoregulatory characteristics of MSCs are unclear. In this study, we determined that miR-30a over-expression inhibited the IL-1β-elicited activation of the nuclear factor κB (NF-κB) and JNK signaling pathways and the production of IL-6, cyclooxygenase 2 (COX2) and IL-8 by targeting transforming growth factor-β-activated kinase 1 binding protein 3 (TAB3) in MSCs. Moreover, the over-expression of miR-30a also impaired MSCs' anti-inflammatory effects on macrophages. These data demonstrated that miR-30a in MSCs may participate in the immune dysregulation of the maternal-fetal interface during PE.
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| http://dx.doi.org/10.1016/j.febslet.2015.11.001 | DOI Listing |
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