Cardiac protection induced by urocortin-2 enables the regulation of apoptosis and fibrosis after ischemia and reperfusion involving miR-29a modulation

Mayoral-González, Isabel; Calderón-Sánchez, Eva; Galeano-Otero, Isabel; Martín-Bórnez, Marta; Gutiérrez‐Carretero, Encarnación; Fernández‐Velasco, María; Doménech, Nieves; Crespo‐Leiro, María G.; Gómez, Ana M.; Ordoñez, Antonio; Hmadcha, Abdelkrim; Smani, Tarik

doi:10.1016/j.omtn.2022.01.003

Cited by 8 publications

(3 citation statements)

References 46 publications

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“…Another study determined that changes in the expression of miR-29a-3p was associated with sudden death in patients with coronary heart disease, apparently originated from M1 polarized pro-inflammatory monocytes, correlating with the increase in the level of pro-inflammatory cytokine IL-6 ( 30 ). Recently, we demonstrated that the overexpression of miR-29a-3p prevents changes in the expression of apoptotic and fibrotic genes induced by ischemia and reperfusion in rats ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

Predicted Value of MicroRNAs, Vascular Endothelial Growth Factor, and Intermediate Monocytes in the Left Adverse Ventricular Remodeling in Revascularized ST-Segment Elevation Myocardial Infarction Patients

Galeano-Otero

Bevilacqua

Guerrero-Márquez

et al. 2022

Front. Cardiovasc. Med.

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BackgroundPrimary percutaneous coronary intervention (PPCI) in patients with ST-segment elevation myocardial infarction (STEMI) improves the survival of patients; nevertheless, some patients develop left ventricular adverse remodeling (LVAR) a few months after the intervention. The main objective of this study was to characterize the role of pro-inflammatory cell populations, related cytokines, and microRNAs (miRNAs) released after PPCI as reliable prognostic biomarkers for LVAR in patients with STEMI.MethodsWe evaluated the level of pro-inflammatory subsets, before and after revascularization, 1 and 6 months after PPCI, using flow cytometry. We also performed a miRNA microarray in isolated peripheral blood mononuclear cells (PBMCs) and examined the levels of 27 cytokines in patients’ serum of patients by multiplex ELISA.ResultsWe observed that the levels of classical and intermediate monocytes increased 6 h after PPCI in patients who developed LVAR later. Multivariate regression analysis and ROC curves indicated that intermediate monocytes, after PPCI, were the best monocyte subset that correlated with LVAR. Within the 27 evaluated cytokines evaluated, we found that the increase in the level of vascular endothelial growth factor (VEGF) correlated with LVAR. Furthermore, the microarray analysis of PBMCs determined that up to 1,209 miRNAs were differentially expressed 6 h after PPCI in LVAR patients, compared with those who did not develop LVAR. Using RT-qPCR we confirmed a significant increase in miR-16, miR-21-5p, and miR-29a-3p, suggested to modulate the expression of different cytokines, 6 h post-PPCI in LVAR patients. Interestingly, we determined that the combined analysis of the levels of the intermediate monocyte subpopulation, VEGF, and miRNAs gave a better association with LVAR appearance. Similarly, combined ROC analysis provided high accurate specificity and sensibility to identify STEMI patients who will develop LVAR.ConclusionOur data suggest that the combined analysis of intermediate monocytes, VEGF, and miRNAs predicts LVAR in STEMI patients.

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Section: Discussionmentioning

confidence: 99%

Predicted Value of MicroRNAs, Vascular Endothelial Growth Factor, and Intermediate Monocytes in the Left Adverse Ventricular Remodeling in Revascularized ST-Segment Elevation Myocardial Infarction Patients

Galeano-Otero

Bevilacqua

Guerrero-Márquez

et al. 2022

Front. Cardiovasc. Med.

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“…On the contrary, in the RM‐1 mouse prostate cancer cell line, the presence of urocortin did not support apoptosis, while CRF had the opposite effect [ 31 ]. The cardioprotective actions of urocortin2 against ischemia–reperfusion (I/R) are well known, and at the same time, it decreases apoptosis in Wistar rats [ 32 ]. CRF also suppressed apoptosis in Y79 human retinoblastoma cells by inhibiting the proteolytic cleavage and activation of procaspase 3 [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Urocortin stimulates the ERK1/2 signaling pathway and the proliferation of HeLa cells via CRF receptor 1

et al. 2023

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Corticotropin‐releasing factor (CRF) stimulates adrenocorticotropic hormone (ACTH) secretion from the pituitary gland and is an essential regulator of the hypothalamic–pituitary–adrenocortical axis. Isoforms of CRF receptor are known to mediate the effects of urocortin stress ligands on the regulation of stress responses, anxiety, and feeding behavior; however, urocortin stress ligands also influence cell proliferation. In view of the tumor‐promoting capacity of prolonged stress, here we investigated (a) the effect of urocortin on cell proliferative signaling via extracellular signal‐regulated kinase 1/2, (b) the expression and cellular distribution of the specific CRF receptor isoforms, and (c) the intracellular localization of phosphorylated ERK1/2 in HeLa cells. Stimulation of cell proliferation was observed in the presence of 10 n m urocortin. Our data also suggest that MAP kinase MEK, the transcription factors E2F‐1 and p53, and PKB/Akt are involved in this process. These findings may have therapeutic relevance for the targeted treatment of various malignancies.

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“…As a post-transcriptional regulator of gene expression, microRNAs are a class of highly conserved, endogenous, single-stranded, non-coding small RNAs composed of approximately 22 nucleotides [ 5 ]. Since these small RNA molecules are only expressed in certain types of cells and tissues, it has been shown that abnormal expression of miR-29a-3p plays a role in a number of pathophysiological processes, including liver fibrosis [ 6 ], cardiac remodelling [ 7 ], pulmonary vascular remodelling [ 8 ], fibro-inflammatory processes [ 9 ], neurodegenerative events [ 10 ]. More significantly, earlier studies have revealed the dual function of miR-29a-3p in a number of malignancies, particularly hepatocellular carcinoma (HCC) [ 45 , 46 ].…”

Section: Introductionmentioning

confidence: 99%

MiR-29a-3p: a potential biomarker and therapeutic target in colorectal cancer

Cao

2022

Clin Transl Oncol

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Cancer is frequently caused by microRNAs, which control post-transcriptional levels of gene expression by binding to target mRNAs. MiR-29a-3p has recently been shown to play a twofold function in the majority of malignancies, including colorectal cancer (CRC), according to mounting evidence. Here, we not only briefly summarize such connection between miR-29a-3p and cancers, but aslo primarily evaluate the miR-29a-3p expression pattern, clinical applicability, and molecular mechanisms in CRC to provide a guide for future studies. This review established the diagnostic and prognostic value of miR-29a-3p abnormalty in a variety of clinical samples for CRC. Furthermore, current molecular mechanisms of miR-29a-3p for regulating cancerous biological processes such growth, invasion, metastasis, the epithelial-mesenchymal transformation process, and immunomodulation through its upstream regulatory factors and downstream targeted genes were briefly explored. More specifically, miR-29a-3p has been linked to a few medications that have been shown to have anticancer benefits. To sum up, miR-29a-3p is a promising biomarker and prospective therapeutic target for the diagnosis and prognosis of CRC, but further research is still needed to establish a theoretical basis for more practical applications.

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Cardiac protection induced by urocortin-2 enables the regulation of apoptosis and fibrosis after ischemia and reperfusion involving miR-29a modulation

Cited by 8 publications

References 46 publications

Predicted Value of MicroRNAs, Vascular Endothelial Growth Factor, and Intermediate Monocytes in the Left Adverse Ventricular Remodeling in Revascularized ST-Segment Elevation Myocardial Infarction Patients

Predicted Value of MicroRNAs, Vascular Endothelial Growth Factor, and Intermediate Monocytes in the Left Adverse Ventricular Remodeling in Revascularized ST-Segment Elevation Myocardial Infarction Patients

Urocortin stimulates the ERK1/2 signaling pathway and the proliferation of HeLa cells via CRF receptor 1

MiR-29a-3p: a potential biomarker and therapeutic target in colorectal cancer

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