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MicroRNA - Europe PMC

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Last Updated: 23 April 2022

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p53 inhibition attenuates cisplatin-induced acute kidney injury through microRNA-142-5p regulating SIRT7/NF-κB.

The key reason of chronic kidney injury induced by cisplatin is epithelial cell apoptosis. With cisplatin therapy, MiR-142-5p was down-regulated in human renal tubular epithelial cells. The overexpression of miR-142-5p attenuated the cisplatin-induced cell apoptosis in HK-2 cells and miR-142-5p inhibition exacerbated miR-142-5p's inhibition of miR-142-5p also exacerbated miR-142-5p apoptosis in HK-2 cells, causing miR-142-5p's apoptosis in HK-2 cell apoptosisplatin-induced apoptosisplatin-142-5platin-142-5platin-142-5platin-induced apoptosisplatin-induced apoptosisplatin-142-5platin-142-5platin-142-5platin-142-5platin-142-5platin-142-5platin-142-5platin-142-5platin-142-5platin-induced apoptosisplatin-induced apoptosisplatin-142-5platin-142-5platin-142-5platin-142-5platin-142-5platin-142 In addition, we reported that SIRT7 inhibition delayed cisplatin-induced HK-2 cell apoptosis in cisplatin-induced apoptosis and reduced the expression of nuclear factor kappa B. For repressing SIRT7/NF-B, our results showed that p53 inhibition could attenuate cisplatin-induced acute kidney injury by up-regulating miR-142-5p to repress SIRT7/NF-B.

Source link: https://europepmc.org/article/MED/35220863


MicroRNA-122-5p ameliorates tubular injury in diabetic nephropathy via FIH-1/HIF-1α pathway.

Diabetes kidney disease affects approximately one-third of diabetes patients, but the exact molecular cause of DKD remains unclear, and there is still a lack of effective drugs. In STZ-induced diabetic nephropathy mice, we observed a significant rise in microRNA-122-5p in renal tubular cells. Moreover, miR-122-5p inhibition promoted cell death and serve tubular injury, as well as DN progression after STZ therapy in mice, while miR-122-5p mimicry demonstrated kidney protective effects in this model. miR-122-5p. com's direct target of miR-122-5p.

Source link: https://europepmc.org/article/MED/35166173


microRNA-455-5p alleviates neuroinflammation in cerebral ischemia/reperfusion injury.

Neuroinflammation is a key pathophysiological factor that contributes to brain injury after cerebral ischemia/reperfusion. After ischemic stroke, microRNA 455-5p downregulation has been identified as a potential biomarker and therapeutic target for neuronal injury in patients of ischemia. mouse models of cerebral ischemia/reperfusion injury were developed in this study by transient occlusion of the middle cerebral artery for 1 hour followed by reperfusion. The results revealed that cerebral ischemia/reperfusion reduced miR-455-5p expression in both the brain tissue and the peripheral blood. MiR-455-5p reduced C-C and protein levels, stymied microglia development, and reduced the production of the inflammatory factors tumor necrosis factor- and interleukin-1, as well as reduced the production of the inflammatory factors tumor necrosis factor- and interleukin-1. MiR-455-5p is a potential biomarker and therapeutic target for cerebral ischemia/reperfusion disease treatment, as well as reducing the neuroinflammatory response by inhibiting C-C chemokine receptor type 5 expression and reducing the neuroinflammatory response, according to these findings.

Source link: https://europepmc.org/article/MED/35017437


MicroRNA is a potential target for therapies to improve the physiological function of skeletal muscle after trauma.

MicroRNAs can influence the activity of ion channels in several organs. The miR-142a-3p overexpression reduced cell membrane permeability, increased potassium current density, and decreased calcium current density, according to the study. MiR-142a-3p reduced sodium channel current density, according to Knockdown. The miR-142a-3p expression change in C2C12 cells affected ion channel currents, suggesting that it could play a role in muscle cell electrophysiology.

Source link: https://europepmc.org/article/MED/34916449


MicroRNA biomarkers in frontotemporal dementia and to distinguish from Alzheimer's disease and amyotrophic lateral sclerosis.

Frontotemporal lobar degeneration is a group of progressive brain disorders that are mostly related to atrophy of the prefrontal and anterior temporal lobes. Frontotemporal lobar degeneration is thought to be related to frontotemporal dementia. Frontotemporal dementia's early detection is vital in planning treatment plans and interventions for these patients. Moreover, miR-223-3p regulation and downregulation of miR-15a-5p, both in blood serum and cerebrospinal fluid, resulted in characteristic behavioral-variant frontotemporal dementia in healthy controls. Frontotemporal lobar degeneration and frontotemporal dementia, respectively, from healthy controls, were deregulated by miR-132-3p in frontal and temporal cortical tissue. MiR-223-3p, MiR-15a-5p, miR-22-3p, central fluid, and miR-124 in cerebrospinal fluid are among the potential best miRNA biofluid biomarker candidates for behavioral-variant frontotemporal dementia candidates. No miRNAs were found to distinguish between behavioral-variant frontotemporal dementia and primary progressive aphasia subtypes.

Source link: https://europepmc.org/article/MED/34916411


MicroRNA hsa-miR-657 promotes retinoblastoma malignancy by inhibiting peroxisome proliferator-activated receptor alpha expression.

In retinoblastoma, our study was designed to investigate the possibility of an interaction between microRNA miR-657 and the peroxisome proliferator-activated receptor alpha. Using RT-qPCR, miR-657 and PPARA were evaluated in retinoblastoma tissues and cells. miR-657 enhanced the retinoblastoma tumorigenesis by specifically inhibiting PPARA expression, implying that miR-657, which aims to boost cell growth, aids in retinoblastoma formation. This research provides new insight into the miR-657- and PPARA-mediated mechanisms underlying retinoblastoma progression, as well as the possibility of therapeutic intervention, suggesting that the interaction between miR-657 and PPARA may be a good target for therapeutic intervention.

Source link: https://europepmc.org/article/MED/35324527


Identification of dynamic microRNA associated with systemic defence against Helicoverpa armigera infestation in Cajanus scarabaeoides.

Introduction Helicoverpa armigera is a significant insect pest of many crops, including pigeonpea. Gene regulatory mechanisms governing this plant's systemic immune response to pod borer infection are yet to be understood. Helicoverpa armigera infested and undamaged adjacent leaves of Cajanus scarabaeoides were compared to gain insight into the plant-insect interactions and the identification of cellular defense mediators. The majority of the miRNA found in the adjacent leaves was found to target genes involved in the defense pathways and plant immune responses, according to a new review. Conclusion The miRNA response in the unfed leaves demonstrated the signs of induced metabolic changes and signal transduction for the induction of defense pathway genes. In C. scarabaeoides, miRNAs were instrumental in presenting pod borer resistance and raising a systemic defense reaction against pod borer infestation. This report details the involvement of miRNAs in delivering pod borer resistance and building a systemic defense mechanism against pod borer infestation.

Source link: https://europepmc.org/article/MED/35452179


Downregulated long intergenic non-coding RNA 00,174 represses malignant biological behaviors of lung cancer cells by regulating microRNA-584-3p/ribosomal protein S24 axis.

The precise regulatory framework of LINC00174 in lung cancer formation remains largely unknown. The constructs transforming LINC00174, miR-584-3p, or RPS24 expression were transplanted into LC cells to investigate the malignant phenotypes of LC cells. The silenced miR-584-3p elevation on LC cells could resurrect the repressive effects of reduced LINC00174 on the cell growth of LC cells, as RPS24 overexpression reversed the repressive effects of miR-584-3p elevation on LC cells. Repressed LINC00174 may help LC cells have malignant phenotypes by changing the miR-584-3p/RPS24 axis, thereby removing the miR-584-3p/RPS24 axis.

Source link: https://europepmc.org/article/MED/35451652


microRNA-15b-5p encapsulated by M2 macrophage-derived extracellular vesicles promotes gastric cancer metastasis by targeting BRMS1 and suppressing DAPK1 transcription.

Background Extracellular vesicles derived from tumor-associated macrophages have been implicated in gastric cancer progression and metastasis by the exchange of molecular cargo RNAs. MiR-15b-5p was detected as an expression, and miR-15b-5p's downstream genes were investigated. In vivo, a lung metastasis model in nude mice was developed to determine the effects of miR-15b-5p on tumor metastasis. Results miR-15b-5p was upregulated in GC tissues and cells, as well as M2 macrophage-derived EVs. MiR-15b-5p could be transferred from M2 macrophage-derived EVs into GC cells, where it attacked BRMS1 by binding to its 3'UTR. By blocking the BRMS1/DAPK1 axis, in vitro experiments showed that orthotopic implantation of miR-15b-5p overexpressing GC cells in nude mice resulted in tumor formation and enhanced tumor metastasis. Conclusions Overall, M2 macrophage-derived EVs' miR-15b-5p constitutes a molecular mechanism implicated in GC metastasis, and may therefore be considered as a new therapeutic target for its therapy.

Source link: https://europepmc.org/article/MED/35449111

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions