miR‑16‑2‑3p inhibits cell proliferation and migration and induces apoptosis by targeting PDPK1 in�maxillary primordium mesenchymal cells

Abstract

MicroRNAs (miRNAs) post-transcriptionally regulate gene expression by targeting the 3' untranslated region (UTR) of target genes, and serve diverse roles in cell proliferation, differentiation and apoptosis. However, the association between miR-16-2-3p and 3-phosphoinositide-dependent protein kinase-1 (PdPK1) in nonsyndromic cleft lip (NScL) remains unclear. In the present study, a luciferase activity assay indicated that miR-16-2-3p negatively regulated PdPK1 in maxillary primordium mesenchymal cells (MPMcs). In addition, it was confirmed that the expression levels of miR-16-2-3p was markedly increased in cleft lip tissues compared with those in adjacent normal lip tissues. A negative correlation between miR-16-2-3p and PdPK1 in cleft lip tissues was observed. Furthermore, miR-16-2-3p inhibited cell proliferation and migration, and induced apoptosis of MPMcs via repressing PdPK1. Finally, miR-16-2-3p exerted its suppressive role in MPMcs by inhibiting the PdPK1/protein kinase B signaling pathway. These results indicate that miR-16-2-3p may inhibit cell proliferation and migration, and promote apoptosis in MPMcs through repression of PdPK1 and may be a potential target for future clinical prevention and treatment of NScL.

Sedentary and Trained Older Men Have Distinct Circulating Exosomal microRNA Profiles at Baseline and in Response to Acute Exercise

“…In contrast, all four downregulated miRNA species target components of IGF1 signaling (Peng et al, 2013;Xu et al, 2013;Gao et al, 2014;Xu et al, 2014;Liu et al, 2018), suggesting that the exercise-induced exomiR signature in trained older adults activates IGF1 signaling. Except for miR-34b-3p (Hermeking, 2010), the majority of differentially regulated miRNAs at 3hPost vs. Pre target components of IGF1 signaling (Peng et al, 2013;Ye et al, 2015;Meier et al, 2016;Ntoumou et al, 2017;Yan et al, 2017;Zhu et al, 2018;Han et al, 2019), suggesting that they may also modulate the IGF1 pathway.…”

Expansion of plasma MicroRNAs over the first month following human stroke

“…Many prior stroke studies describe dysregulation of miR-16 (which implies the lead miR-16-5p strand), 8 but we only found downregulation of the passenger strand miR-16-2-3p similar to a study in hyperacute stroke. 11 MiR-16-2-3p is associated with apoptosis and suppression of cell proliferation, 44 , 45 so decreased miR-16-2-3p could reflect a response to either prolong cell life or promote inflammation/repair. MiR-19a-3p decreased within 72 hrs post-stroke in human whole blood consistent with our findings in plasma at later time points.…”

Extracellular vesicle microRNA cargoes from intermittent hypoxia-exposed cardiomyocytes and their effect on endothelium

“…For example, previous ndings revealed a pivotal role for miR-125b-5p in regulating cardiomyocyte survival during acute myocardial infarction [26] and EVs-derived miR125b-5p under hypoxia-conditioned facilitated ischemic cardiac repair by ameliorating cardiomyocyte apoptosis [27]. Moreover, recent researches indicated miR-22-3p was a key molecule in regulating vascular smooth muscle cell proliferation and migration by targeting HMGB1 [28] and a promising therapeutic target for atherosclerosis treatment [29]. EV miR-23a-3p from mesenchymal stem cells attenuated myocardial injury through suppressing DMT1 expression [30].…”