Suppression of microRNA-320 Induces Cerebral Protection Against Ischemia/Reperfusion Injury by Targeting HMGB1/NF-κB Axis DOI Creative Commons

Shufang Liang,

Wei Cao, Yu Zhuang

et al.

Physiological Research, Journal Year: 2024, Volume and Issue: 1/2024, P. 127 - 138

Published: March 6, 2024

MicroRNAs have been shown to potentially function in cerebral ischemia/reperfusion (IR) injury. This study aimed examine the expression of microRNA-320 (miR-320) IR injury and its involvement mitochondrial function, oxidative stress, inflammatory responses by targeting HMGB1/ NF-κB axis. Sprague-Dawley rats were subjected middle artery occlusion simulate The miR-320 was assessed using qRT-PCR. Neurological infarct volume, cytokines evaluated relevant methods, including staining, fluorometry, ELISA. HMGB1 analyzed through Western blotting. levels miR-320, HMGB1, neurological deficits, infarction significantly higher after induction. Intracerebral overexpression resulted substantial increased elevated 8-isoprostane, NF-κBp65, TNF-α, IL-1β, ICAM-1, VCAM-1, expression. It also promoted loss membrane potential ROS while reducing MnSOD GSH levels. Downregulation inhibition activity reversed outcomes MiR-320 plays a negative role regulating inflammatory/oxidative reactions induced enhancing modulating function.

Language: Английский

Alterations in Apoptotic Pathways and Expression of miR-134, miR-181, and miR-497 Induced by Wharton’s Jelly-Derived Mesenchymal Stem Cells in a Rat Model of Ischemic Brain Injury DOI Creative Commons
Tahereh Alizamir, Ali Fathi Jouzdani,

Fatemeh Attari

et al.

IBRO Neuroscience Reports, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

Citations

0
Identification and characterization of biomarkers associated with endoplasmic reticulum protein processing in cerebral ischemia-reperfusion injury DOI Creative Commons

Liang-da Li,

Yue Zhou,

Shan-fen Shi

et al.

PeerJ, Journal Year: 2024, Volume and Issue: 12, P. e16707 - e16707

Published: Jan. 2, 2024

Background Cerebral ischemia (CI), ranking as the second leading global cause of death, is frequently treated by reestablishing blood flow and oxygenation. Paradoxically, this reperfusion can intensify tissue damage, to CI-reperfusion injury. This research sought uncover biomarkers pertaining protein processing in endoplasmic reticulum (PER) during Methods We utilized Gene Expression Omnibus (GEO) dataset GSE163614 discern differentially expressed genes (DEGs) single out PER-related DEGs. The functions pathways these DEGs were identified via Ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) enrichment analyses. Core pinpointed through protein-protein interaction (PPI) networks. Subsequent this, with diagnostic relevance distinguished using external validation datasets. A single-sample gene-set analysis (ssGSEA) was undertaken pinpoint strong associations hypoxia apoptosis, suggesting their potential roles primary inducers apoptosis hypoxic conditions ischemia-reperfusion injuries. Results Our study demonstrated that genes, specifically ADCY5, CAMK2A, PLCB1, NTRK2, DLG4, markedly down-regulated models, exhibiting a robust association apoptosis. Conclusion data indicates DLG4 could be pivotal responsible for triggering environments

Language: Английский

Citations

3
Hydrogen sulfide in health and diseases: cross talk with noncoding RNAs DOI
Qing-Bo Lu, Yi Ding, Xiao Fu

et al.

AJP Cell Physiology, Journal Year: 2023, Volume and Issue: 324(4), P. C856 - C877

Published: March 7, 2023

Hydrogen sulfide (H2S) is previously described as a potentially lethal toxic gas. However, this gasotransmitter also endogenously generated by the actions of cystathionine-β-synthase (CBS), cystathionine-γ-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3-MST) in mammalian systems, thus belonging to family gasotransmitters after nitric oxide (NO) carbon monoxide (CO). The physiological or pathological significance H2S has been extensively expanded for decades. Growing evidence revealed that exerts cytoprotective functions cardiovascular, nervous, gastrointestinal systems modulating numerous signaling pathways. With continuous advancement microarray next-generation sequencing technologies, noncoding RNAs (ncRNAs) have gained recognition key players human health diseases due their considerable potential predictive biomarkers therapeutic targets. Coincidentally, ncRNAs are not independent regulators but interact with each other during development progression diseases. Specifically, might serve downstream mediators act on H2S-generating enzymes govern endogenous production. purpose review summarize interactive regulatory roles initiation various explore benefits. This will highlight importance cross talk between disease therapy.

Language: Английский

Citations

5
miR-188-5p silencing improves cerebral ischemia/reperfusion injury by targeting Lin28a DOI
Dan Hou,

Chaoying Pei,

Dan Yu

et al.

Metabolic Brain Disease, Journal Year: 2023, Volume and Issue: 38(7), P. 2327 - 2338

Published: Aug. 12, 2023

Language: Английский

Citations

4
MiR-122 overexpression alleviates oxygen–glucose deprivation-induced neuronal injury by targeting sPLA2-IIA DOI Creative Commons
Yuanfang Yu, Li Pan, Mengyuan Chen

et al.

Frontiers in Neurology, Journal Year: 2024, Volume and Issue: 15

Published: May 10, 2024

Background Ischemic stroke (IS) is a neurological disease with significant disability and mortality. MicroRNAs were proven to be associated cerebral ischemia. Previous studies have demonstrated miR-122 downregulation in both animal models of IS the blood patients. Nonetheless, role mechanism miR-122-5p remain unclear. Methods We established primary human mouse astrocytes, along HT22 hippocampal neuronal cells, through oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. To assess impact miR-122, we employed CCK8 assays, flow cytometry, RT-qPCR, western blotting, ELISA evaluate cell viability, apoptosis, reactive oxygen species (ROS) generation, cytokine expression. A dual-luciferase reporter gene assay was investigate interaction between sPLA2-IIA. Results Overexpression resulted decreased reduced cleaved caspase-3 expression, increased viability astrocytes cells subjected OGD/R. RT-qPCR analyses decrease mRNA levels interleukin (IL)-6 tumor necrosis factor (TNF)-α following overexpression. Moreover, overexpression reversed OGD/R-induced ROS 8-OHdG formation astrocytes. Additionally, protein expression inducible nitric oxide synthase (iNOS). Furthermore, found that attaches 3′-UTR sPLA2-IIA, thereby downregulate its Conclusion Our study demonstrates miR-122-mediated inhibition sPLA2-IIA attenuates injury by suppressing alleviating post-ischemic inflammation, reducing production. Thus, miR-122/sPLA2-IIA axis may represent promising target for

Language: Английский

Citations

1
MicroRNA Nobel Prize: Timely Recognition and High Anticipation of Future Products—A Prospective Analysis DOI Open Access
Sarfaraz K. Niazi,

Matthias Magoola

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(23), P. 12883 - 12883

Published: Nov. 29, 2024

MicroRNAs (miRNAs) maintain cellular homeostasis by blocking mRNAs binding with them to fine-tune the expression of genes across numerous biological pathways. The 2024 Nobel Prize in Medicine and Physiology for discovering miRNAs was long overdue. We anticipate a deluge research work involving repeat history prizes awarded on other RNAs. Although miRNA therapies are included several complex diseases, realization that regulate their roles addressing hundreds diseases expected; but advancement drug discovery tools, we even faster entry new drugs. To promote this, provide details current science, logic, intellectual property, formulations, regulatory process anticipation many more researchers will introduce novel based discussion advice provided this paper.

Language: Английский

Citations

1
miR-135a-5p alleviates cerebral ischemia-reperfusion injury by inhibiting pyroptosis mediated through the DDX3X/NLRP3 pathway DOI
Bin Liu, Xin Jiang, Yunfei Zhang

et al.

Experimental Neurology, Journal Year: 2024, Volume and Issue: 385, P. 115127 - 115127

Published: Dec. 22, 2024

Language: Английский

Citations

1
MicroRNAs in the Regulation of NADPH Oxidases in Vascular Diabetic and Ischemic Pathologies: A Case for Alternate Inhibitory Strategies? DOI Creative Commons

Sean Wallace,

Patrick J. Pagano, Damir Kračun

et al.

Antioxidants, Journal Year: 2022, Volume and Issue: 12(1), P. 70 - 70

Published: Dec. 29, 2022

Since their discovery in the vasculature, different NADPH oxidase (NOX) isoforms have been associated with numerous complex vascular processes such as endothelial dysfunction, inflammation, arterial remodeling, and dyslipidemia. In turn, these often underlie cardiovascular metabolic pathologies including diabetes mellitus type II, cardiomyopathy, systemic pulmonary hypertension atherosclerosis. Increasing attention has directed toward miRNA involvement II its co-morbidities search for predictive stratifying biomarkers therapeutic targets. Owing to challenges of generating isoform-selective NOX inhibitors (NOXi), development specific NOXis suitable purposes hindered. that vein, differential regulation by a particular or combina-tion thereof could at some point become reasonable approach targeting under circumstances. Whereas administration miRNAs chronically, even acutely, patients poses own set difficulties, miRNA-mediated NOXs vasculature is worth surveying. this review, distinct focus on role was made context ischemic injury models.

Language: Английский

Citations

6
Effect of dexmedetomidine on tourniquet-induced skeletal muscle injury DOI Open Access
Wenjie Cheng, Zhe Wu, Jizheng Zhang

et al.

Revista da Associação Médica Brasileira, Journal Year: 2023, Volume and Issue: 69(2), P. 228 - 232

Published: Feb. 1, 2023

The aim of this study was to investigate whether dexmedetomidine could reduce tourniquet-induced skeletal muscle injury.C57BL6 male mice were randomly assigned sham, ischemia/reperfusion, and groups. Mice in the ischemia/reperfusion groups received normal saline solution intraperitoneally, respectively. sham group underwent same procedure as group, with exception tourniquet application. Subsequently, ultrastructure gastrocnemius observed, its contractile force examined. In addition, Toll-like receptor 4 nuclear factor-κB expression within muscles detected by Western blot.Dexmedetomidine alleviated myocyte damage increased contractility muscles. Moreover, significantly inhibited 4/nuclear muscle.Taken together, these results demonstrate that administration attenuated structural functional impairment muscle, partly through inactivation pathway.

Language: Английский

Citations

1
MicroRNA-323-5p Involved in Dexmedetomidine Preconditioning Impart Neuroprotection DOI Creative Commons
Hyunyoung Seong, Daun Jeong,

Eung Hwi Kim

et al.

Medicina, Journal Year: 2023, Volume and Issue: 59(9), P. 1518 - 1518

Published: Aug. 23, 2023

Background and Objectives: Cerebral ischemia is one of the major preoperative complications. Dexmedetomidine a well-known sedative–hypnotic agent that has potential organ-protective effects. We examine miRNAs associated with preconditioning effects dexmedetomidine in cerebral ischemia. Materials Methods: Transient infarcts were induced mice via reperfusion after temporary occlusion side middle artery. A subset these was exposed to prior infarction miRNA profiling whole brain performed. administered miRNA-323-5p mimic/inhibitor oxygen–glucose deprivation/reoxygenation astrocytes. Additionally, we miR-323-5p mimic inhibitor intracerebroventricular injection 2 h induction artery occlusion. Results: The infarct volume significantly lower dexmedetomidine-preconditioned mice. Analysis samples revealed an increased expression five decreased three dexmedetomidine-pretreated group. viability cells attenuated dexmedetomidine-treated groups. Transfection anti-miR-323-5p contributed astrocyte viability. When injected intraventricularly, reduced when preconditioned compared negative control. Conclusions: protective effect against transient neuronal ischemia–reperfusion injury eight specific profiled. Also, downregulation cell under ischemic conditions both vivo vitro. Our findings suggest as therapeutic infarction.

Language: Английский

Citations

1