Therapeutic Potentials of MicroRNA-126 in Cerebral Ischemia

Ebrahimi, Vahid; Rastegar-Moghaddam, Seyed Hamidreza; Mohammadipour, Abbas

doi:10.1007/s12035-022-03197-4

Cited by 16 publications

(8 citation statements)

References 68 publications

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“…Despite extensive basic and clinical research spanning decades, the morbidity and mortality rates associated with cerebral I/R remain elevated, making it a significant global cause of death. 28 The current study’s findings underscore the relationship between increased phosphorylation of RhoA at Ser188 and the neuroprotective effects of H 2 S against rat cerebral I/R injury. Key findings include the following: (1) in vivo, H 2 S-promoted RhoA phosphorylation at Ser188; (2) H 2 S-mediated RhoA phosphorylation at Ser188 inhibited the activity of the RhoA/ROCK pathway; and (3) H 2 S-mediated RhoA phosphorylation at Ser188 was associated with neuroprotection against cerebral I/R injury.…”

Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 55%

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Hydrogen Sulfide Protects against Rat Ischemic Brain Injury by Promoting RhoA Phosphorylation at Serine 188

Chen,

et al. 2024

ACS Omega

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The protective role of hydrogen sulfide against cerebral ischemia-reperfusion injury involves the inhibition of the RhoA-/Rho-associated coiled-coil kinase (ROCK) pathway. However, the specific mechanism remains elusive. This study investigates the impact of hydrogen sulfide on RhoA phosphorylation at serine 188 (Ser188) in vivo, aiming to test the hypothesis that hydrogen sulfide exerts neuroprotection by enhancing RhoA phosphorylation at Ser188, subsequently inhibiting the RhoA/ROCK pathway. Recombinant RhoA wild -pEGFP-N1 and RhoA S188A -pEGFP-N1 plasmids were constructed and administered via stereotaxic injection into the rat hippocampus. A rat global cerebral ischemia-reperfusion model was induced by bilateral carotid artery ligation to elucidate the neuroprotective mechanisms of hydrogen sulfide. Both RhoA wild -pEGFP-N1 and RhoA S188A -pEGFP-N1 plasmids expressed RhoA wild and RhoA S188A proteins, respectively, in rat hippocampal tissues, alongside the intrinsic RhoA protein. Systemic administration of the exogenous hydrogen sulfide donor sodium hydrosulfide led to an increase in Ser188 phosphorylation of transfected RhoA wild and intrinsic RhoA protein within the hippocampus. However, this effect was not observed in tissues transfected with RhoA S188A . Sodium hydrosulfide-mediated RhoA phosphorylation correlated with decreased RhoA and ROCK 2 activity in rat hippocampal tissues. Furthermore, sodium hydrosulfide administration reduced cerebral ischemia-reperfusion-induced neuronal damage and apoptosis in rat hippocampal tissues transfected with RhoA wild . However, this neuroprotective effect was attenuated in rats transfected with RhoA S188A . These findings suggest that the neuroprotective mechanism of hydrogen sulfide against cerebral ischemia/reperfusion injury involves increased RhoA phosphorylation at Ser188. Promoting this phosphorylation may represent a potential intrinsic therapeutic target for ischemic stroke.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 55%

Hydrogen Sulfide Protects against Rat Ischemic Brain Injury by Promoting RhoA Phosphorylation at Serine 188

Chen,

et al. 2024

ACS Omega

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“…By blocking an increase in MMPs levels and stopping the decline in junctional proteins, such as occludin, claudin‐5, and zonula occludens‐1 (ZO‐1), it lessens the breakdown of the blood‐brain barrier. Furthermore, miR‐126 promotes neurogenesis and angiogenesis following a stroke 200 . When exosomes formed from ADSCs‐miR‐126 derived exosomes were administered systemically to stroke rats, the expression of vWF and DCX was dramatically elevated, and recovery from function was enhanced 201 .…”

Section: Engineered Mscs In Strokementioning

confidence: 99%

Therapeutic gene delivery by mesenchymal stem cell for brain ischemia damage: Focus on molecular mechanisms in ischemic stroke

Saleh,

Majeed,

Margiana

et al. 2024

Cell Biochemistry & Function

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Cerebral ischemic damage is prevalent and the second highest cause of death globally across patient populations; it is as a substantial reason of morbidity and mortality. Mesenchymal stromal cells (MSCs) have garnered significant interest as a potential treatment for cerebral ischemic damage, as shown in ischemic stroke, because of their potent intrinsic features, which include self‐regeneration, immunomodulation, and multi‐potency. Additionally, MSCs are easily obtained, isolated, and cultured. Despite this, there are a number of obstacles that hinder the effectiveness of MSC‐based treatment, such as adverse microenvironmental conditions both in vivo and in vitro. To overcome these obstacles, the naïve MSC has undergone a number of modification processes to enhance its innate therapeutic qualities. Genetic modification and preconditioning modification (with medications, growth factors, and other substances) are the two main categories into which these modification techniques can be separated. This field has advanced significantly and is still attracting attention and innovation. We examine these cutting‐edge methods for preserving and even improving the natural biological functions and therapeutic potential of MSCs in relation to adhesion, migration, homing to the target site, survival, and delayed premature senescence. We address the use of genetically altered MSC in stroke‐induced damage. Future strategies for improving the therapeutic result and addressing the difficulties associated with MSC modification are also discussed.

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“…It is worth noting that miR-210 is recognized as one of the key regulators of neonatal hypoxia–ischemia [ 249 ]; its overexpression, along with that of miR-130a, increases BBB permeability by inhibiting the expression of occludin and β-catenin [ 250 , 251 ]. Overexpression of miR-126-3p/-5p and miR-98 in the ischemic brain of mice suppresses the effects of pro-inflammatory cytokines and adhesion molecules, preserving the integrity of the cerebral endothelium and thus reducing the negative consequences of stroke [ 252 , 253 , 254 ]. A similar effect is observed with overexpression of miR-152-3p, which reduces the degree of neurological deficit and disruption of BBB integrity in experimental ischemia by inhibiting apoptosis of endothelial cells through negative modulation of the MAP3K2/JNK/c-Jun pathway [ 255 ].…”

Section: Peculiarities Of Epigenetic Regulation In Bbb Dysfunctionmentioning

confidence: 99%

The Role of microRNAs in Epigenetic Regulation of Signaling Pathways in Neurological Pathologies

Tregub,

Ibrahimli,

Averchuk

et al. 2023

IJMS

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In recent times, there has been a significant increase in researchers’ interest in the functions of microRNAs and the role of these molecules in the pathogenesis of many multifactorial diseases. This is related to the diagnostic and prognostic potential of microRNA expression levels as well as the prospects of using it in personalized targeted therapy. This review of the literature analyzes existing scientific data on the involvement of microRNAs in the molecular and cellular mechanisms underlying the development of pathologies such as Alzheimer’s disease, cerebral ischemia and reperfusion injury, and dysfunction of the blood–brain barrier.

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Therapeutic Potentials of MicroRNA-126 in Cerebral Ischemia

Cited by 16 publications

References 68 publications

Hydrogen Sulfide Protects against Rat Ischemic Brain Injury by Promoting RhoA Phosphorylation at Serine 188

Hydrogen Sulfide Protects against Rat Ischemic Brain Injury by Promoting RhoA Phosphorylation at Serine 188

Therapeutic gene delivery by mesenchymal stem cell for brain ischemia damage: Focus on molecular mechanisms in ischemic stroke

The Role of microRNAs in Epigenetic Regulation of Signaling Pathways in Neurological Pathologies

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