Effect of MicroRNA-126a-3p on Bone Marrow Mesenchymal Stem Cells Repairing Blood-brain Barrier and Nerve Injury after Intracerebral Hemorrhage

Wang, Chunyan; Cao, Jingwei; Duan, Shanshan; Xu, Ran; Yu, Hongli; Huo, Xin; Qian, Yuanyuan

doi:10.1016/j.jstrokecerebrovasdis.2020.104748

Cited by 25 publications

(29 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MiRNA based treatments had the characteristics of delayed MSC senescence and multidimensional targets. Given the significant function of miRNA-126 in promoting angiogenesis, the miRNA-126 transfected MSCs were injected into the collagenase-induced ICH rats, leading to decreased brain water content and improved neurological score (Wang et al, 2020). In addition, the CX3CR1 overexpressed MSCs increased the viability and migration ability of transplanted MSCs, and improved the sensory and motor functions of the collagenase induced mice ICH model .…”

Section: Preconditioning Treatmentsmentioning

confidence: 99%

Mesenchymal Stem Cells Transplantation in Intracerebral Hemorrhage: Application and Challenges

Gong

Hao

Wang

2021

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Intracerebral hemorrhage (ICH) is one of the leading causes of death and long-term disability worldwide. Mesenchymal stem cell (MSC) therapies have demonstrated improved outcomes for treating ICH-induced neuronal defects, and the neural network reconstruction and neurological function recovery were enhanced in rodent ICH models through the mechanisms of neurogenesis, angiogenesis, anti-inflammation, and anti-apoptosis. However, many key issues associated with the survival, differentiation, and safety of grafted MSCs after ICH remain to be resolved, which hinder the clinical translation of MSC therapy. Herein, we reviewed an overview of the research status of MSC transplantation after ICH in different species including rodents, swine, monkey, and human, and the challenges for MSC-mediated ICH recovery from pathological microenvironment have been summarized. Furthermore, some efficient strategies for the outcome improvement of MSC transplantation were proposed.

show abstract

Section: Preconditioning Treatmentsmentioning

confidence: 99%

Mesenchymal Stem Cells Transplantation in Intracerebral Hemorrhage: Application and Challenges

Gong

Hao

Wang

2021

Front. Cell. Neurosci.

View full text Add to dashboard Cite

show abstract

“…growth. [6] Therefore, elucidating the molecular mechanism of ox-LDL-induced EC injury is of great value for exploring the occurrence and development of AS and inventing effective drugs.…”

mentioning

confidence: 99%

Exosomal miR‐512‐3p derived from mesenchymal stem cells inhibits oxidized low‐density lipoprotein‐induced vascular endothelial cells dysfunction via regulating Keap1

Chen

Zhou

Zhang

et al. 2021

J Biochem & Molecular Tox

View full text Add to dashboard Cite

Atherosclerosis (AS) is a prevalent chronic inflammatory vascular disease.Upregulated oxidized low-density lipoprotein (ox-LDL) in the serum has been found to induce endothelial cells (ECs) apoptosis by increasing oxidative stress and promoting inflammatory response, which are essential mechanisms of AS development. Mesenchymal stem cells (MSCs), which secrete exosomes to transport microRNAs (miRNAs) and regulate cell functions, have become a research focus in recent years. The results of this study manifested that MSCs-derived exosomes were phagocytosed by EC. In addition, miR-512-3p enriched by MSCs-derived exosomes markedly inhibited ox-LDL-mediated EC damage, namely, accelerated EC proliferation, inhibited Caspase-3 activation and cell apoptosis, inhibited the levels of inflammatory cytokines (tumor necrosis factor-α, interleukin (IL)-1β, and IL-6) and oxidative factor MDA, and increased the contents of SOD and GSH-PX. Mechanistically, Keleh-like ECH-associated protein 1 (Keap1) was proved to be a functional target of miR-512-3p. Furthermore, silencing Keap1 limited ox-LDL-mediated EC cell dysfunction, while over-expressing Keap1 mitigated the exosomal miR-512-3pmediated protective effect in Ox-LDL-induced EC. The above results confirmed that miR-512-3p shuttled by MSCs-derived exosomes protected EC against ox-LDL by targeting Keap1.

show abstract

“…GDNF transfected MSCs express neural cell-specific biomarkers including NSE, MAP2, and GFAP after implantation into ICH rats which leads to better behavioral performance than parental MSCs [187]. Moreover, overexpression of microRNA-126a-3p in BM-MSCs appears to repair the blood-brain barrier by differentiating to CD31 + endothelial cells and upregulating ZO-1 and claudin-5 (both tight junction proteins) after ICH in rats [188].…”

Section: Stem Cell Therapymentioning

confidence: 99%

Central Nervous System Tissue Regeneration after Intracerebral Hemorrhage: The Next Frontier

Zhang

Xue

Yong

2021

Cells

View full text Add to dashboard Cite

Despite marked advances in surgical techniques and understanding of secondary brain injury mechanisms, the prognosis of intracerebral hemorrhage (ICH) remains devastating. Harnessing and promoting the regenerative potential of the central nervous system may improve the outcomes of patients with hemorrhagic stroke, but approaches are still in their infancy. In this review, we discuss the regenerative phenomena occurring in animal models and human ICH, provide results related to cellular and molecular mechanisms of the repair process including by microglia, and review potential methods to promote tissue regeneration in ICH. We aim to stimulate research involving tissue restoration after ICH.

show abstract

Effect of MicroRNA-126a-3p on Bone Marrow Mesenchymal Stem Cells Repairing Blood-brain Barrier and Nerve Injury after Intracerebral Hemorrhage

Cited by 25 publications

References 28 publications

Mesenchymal Stem Cells Transplantation in Intracerebral Hemorrhage: Application and Challenges

Mesenchymal Stem Cells Transplantation in Intracerebral Hemorrhage: Application and Challenges

Exosomal miR‐512‐3p derived from mesenchymal stem cells inhibits oxidized low‐density lipoprotein‐induced vascular endothelial cells dysfunction via regulating Keap1

Central Nervous System Tissue Regeneration after Intracerebral Hemorrhage: The Next Frontier

Contact Info

Product

Resources

About