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Coronary heart disease (CHD) is one of the most vital reasons for death and disability all over the world. miRNA, as a plasma index, is quite valuable for disease screening and prognosis prediction in CHD. Mining the molecular mechanism behind miRNA is also helpful for us to find molecular therapeutic strategies. In this research, we found that the expression of plasma miR-30c-5p in CHD patients was obviously lower than that in the control group (CG), which had a high differential value for CHD. We also discovered that miR-30c-5p was obviously correlated with clinical characteristics of CHD patients such as age, NYHA grade, smoking history, hypertension, hyperlipidemia, etc. In prognosis analysis, the miR-30c-5p expression in patients with poor prognosis was dramatically lower than that in those with good one, and the AUC for predicting poor prognosis of CHD was not lower than 0.850. In addition, we also induced myocardial ischemia/reperfusion (I/R) injury model of H9C2 cells through hypoxia/reoxygenation, and found that H9C2 cells also had abnormally down-regulated miR-30c-5p and up-regulated BCL2-like 11 (BCL2L11). Up-regulating miR-30c-5p or down-regulating BCL2L11 were helpful to improve proliferation and apoptosis of I/R injury model. Mechanically, BCL2L11 was also negatively regulated by miR-30c-5p, and up-regulating the former could cancel the in vitro protective effect of up-regulating the latter on H9C2 cell I/R injury model. In vivo research, up-regulating miR-30c-5p or down-regulating BCL2L11 can improve myocardial injury, histopathological changes and apoptosis in rat I/R model., Competing Interests: None., (AJTR Copyright © 2021.)

Coronary heart disease (CHD) is a fatal disease associated with coronary atherosclerosis. Although triptolide (TTL) has been reported to protect against CHD, the mechanism has not yet been determined. This study intended to explore its molecular regulation mechanism in CHD. It is shown in this study that TTL contributed to the proliferation and migration of in vitro cell models of CHD (endothelial cells) and the inhibition of apoptosis, and had an improvement effect on apoptosis factors and endoplasmic reticulum stress (ERS). From its mechanisms, TTL evidently downregulates miR-24-3p which is elevated in CHD, and evidently upregulates BCL2-like 11 (BCL2L11) which is suppressed in CHD, as well as affects the activation of peroxisome proliferator-activated receptors (PPARs)-Peroxisome proliferator activated receptor-γ co-activator-1α (PGC-1α) pathway of nuclear receptor transcription factors. In addition, miR-24-3p-BCL2L11-PPARs-PGC1α axis regulates protective effects of TTL against CHD., Competing Interests: None., (AJTR Copyright © 2020.)

Endometriosis is a benign disease but manifests with malignant features and limited treatment options. Women with endometriosis should not be ignored or patronized by the medical profession and society. In this regard, a major cultural change and searching for the optimum therapeutic regimen from multiple perspectives is needed in China even in the whole world. Long non-coding RNAs are crucial for various human diseases while its potential functions and mechanisms are largely unknown in endometriosis. LINC00261 was significantly downregulated in endometriosis tissues and our study indicated that it suppresses proliferation and invasion of endometriosis cells functionally in vitro . Insights of the mechanism of competitive endogenous RNAs were obtained from bioinformatic analysis, RIP, RNA pull-down and luciferase assays, which further confirmed that LINC00261 functions as a molecular sponge to regulate BCL2L11 expression by binding to miR-132-3p directly. These data defined LINC00261/miR-132-3p/BCL2L11 regulatory networks may be a novel therapeutic target for endometriosis., Competing Interests: None.

Abnormal maternal trophoblast invasion is a common finding in preeclampsia pregnancy. A hypoxic environment develops in the placenta after the 10th week of pregnancy and exerts a major influence over trophoblast activity. In the present study, we investigated expression of miR-222 and apoptosis-related BCL2L11 in preeclampsia placenta and in primary placenta mesenchymal stem cells (MSCs) under hypoxia. The results demonstrate that miR-222 is upregulated in the placenta of preeclampsia patients, along with the downregulation of BCL2L11 in both mRNA and protein levels. In vitro results demonstrate that miR-222 is upregulated either in preeclampsia placenta tissues or in the MSCs under hypoxia. Western blotting showed downregulation of BCL2L11 in the trophoblasts under hypoxia, along with an increased MSC apoptosis. miR-222 was also confirmed to downregulate BCL2L11 expression via targeting the 3' untranslated region (UTR) of the BCL2L11 gene. miR-222 inhibitor transfection markedly ameliorated expression and transcriptional activity of BCL2L11 . Altogether, the present study found that upregulation of miR-222 promotes apoptosis of mesenchymal stem cells in preeclampsia patients in response to hypoxia, via targeting BCL2L11. This suggests that a key regulatory role of miR-222 is in preeclampsia progression., Competing Interests: None., (IJCEP Copyright © 2018.)

Growing evidence indicates that miR-106a is involved in tumor growth and metastasis of cancers, but the participation of miR-106a in endometrial adenocarcinoma (EC) is not clear. BCL2L11 is a member of the BCL-2 family and is located in the outer membrane of mitochondria, where this protein acts as a key regulator of excitotoxic apoptosis, apoptosis-inducing factor translocation, and mitochondrial depolarization. To identify a novel therapeutic target in EC, we studied the roles of miR-106a in the proliferation, apoptosis, and metastasis of EC. The expression levels of miR-106a were measured in tumor tissues of EC by quantitative real-time PCR, and lentiviral transduction was used to verify the function of miR-106a by silencing. Subcutaneous injection of EC cell lines into athymic mice was used to research EC tumor formation. Bioinformatics tools and a luciferase assay were applied to assess the relation between miR-106a and its target. The protein level of the miR-106a target was measured by western blotting. MiR-106a expression was higher in EC tissues compared with their healthy counterparts. Inhibition of expression of miR-106a reduced EC cell migration and invasion in vitro as well as in vivo tumor growth. BCL2L11 mRNA contains a binding site for miR-106a in the 3'untranslated region. BCL2L11 was found to be one of miR-106a targets. Altogether, our data suggest that miR-106a inhibits proliferation and invasiveness and induces cell cycle arrest and apoptosis in EC cells by targeting BCL2L11 , and therefore miR-106a may serve as a prognostic marker of EC.