Overexpression of microRNA-202-3p in bone marrow mesenchymal stem cells improves cerebral ischemia-reperfusion injury by promoting angiogenesis and inhibiting inflammation

Yang, Guohua; Sun, Weiming; Le, Changhao; Liang, Dehuan; Lang, Simone

doi:10.18632/aging.202889

Cited by 18 publications

(20 citation statements)

References 37 publications

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“…Stem cell therapy is another promising treatment for IR-induced senescence. Multipotent mesenchymal stem cells (MSCs), being a category of adult stem cells springing from the mesoderm, with multi-directional differentiation and self-renewal potential, have recently emerged as a key player in regenerative medicine and clinical translational research [ 124 – 126 ]. Typically, MSCs have been extensively studied to inhibit premature senescence by protecting against the IR-induced pro-oxidative state, cell-cycle inhibition [ 93 ], and chronic fibrosis [ 127 ].…”

Section: Therapies That Target Cellular Senescence After Ir Injurymentioning

confidence: 99%

“…For instance, cell-cycle arrest of myocardiocytes after MI can be alleviated by MSC-EVs carrying miR-150-5p via downregulation of TXNIP [ 131 , 132 ], or by MSC-EVs targeting miR-497/Smad7/TGF-β pathway [ 133 ]. Yu et al also found that EVs carrying mi-202-3p could protect neurons from IR injury via downregulating TLR4-mediated inflammation response [ 124 ]. Xiao et al point that MSC-EVs reduce endothelial cell senescent burden and activate angiogenesis through miR-146a/Src pathway [ 134 ].…”

Section: Therapies That Target Cellular Senescence After Ir Injurymentioning

confidence: 99%

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Cellular senescence in ischemia/reperfusion injury

et al. 2022

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Ischemia/reperfusion (IR) injury, a main reason of mortality and morbidity worldwide, occurs in many organs and tissues. As a result of IR injury, senescent cells can accumulate in multiple organs. Increasing evidence shows that cellular senescence is the underlying mechanism that transforms an acute organ injury into a chronic one. Several recent studies suggest senescent cells can be targeted for the prevention or elimination of acute and chronic organ injury induced by IR. In this review, we concisely introduce the underlying mechanism and the pivotal role of premature senescence in the transition from acute to chronic IR injuries. Special focus is laid on recent advances in the mechanisms as well as on the basic and clinical research, targeting cellular senescence in multi-organ IR injuries. Besides, the potential directions in this field are discussed in the end. Together, the recent advances reviewed here will act as a comprehensive overview of the roles of cellular senescence in IR injury, which could be of great significance for the design of related studies, or as a guide for potential therapeutic target.

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Section: Therapies That Target Cellular Senescence After Ir Injurymentioning

confidence: 99%

Section: Therapies That Target Cellular Senescence After Ir Injurymentioning

confidence: 99%

Cellular senescence in ischemia/reperfusion injury

et al. 2022

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“…It has been reported that the transplantation of bone marrow mesenchymal stem cells (BMSCs) was able to induce the nerve function recovery after cerebral ischemia. 3 Additionally, a recent study indicated that BMSCs could alleviate the progression of CI/R injury through mediation of PI3K/Akt/mTOR signaling pathway. 4 More importantly, recent studies demonstrated that BMSCs-derived exosomes (BMSC-exos) were able to act as crucial mediators in the biological function of BMSCs.…”

Section: Introductionmentioning

confidence: 99%

Exosomal miR-133a-3p Derived from BMSCs Alleviates Cerebral Ischemia-Reperfusion Injury via Targeting DAPK2

Yang¹,

Xu²,

Lan³

et al. 2023

IJN

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Background: Cerebral ischemia-reperfusion (CI/R) injury is a subtype of complication after treatment of ischemic stroke. It has been reported that exosomes derived from BMSCs could play an important role in CI/R injury. However, whether BMSCs-derived exosomes could regulate CI/R injury via carrying miRNAs remains to be further explored. Methods: RNA sequencing was performed to identify the differentially expressed miRNAs. To mimic CI/R in vitro, SH-SY5Y cells were exposed to oxygen glucose deprivation/reoxygenation (OGD/R). The viability of SH-SY5Y cells was tested by CCK8 assay, and TUNEL staining was performed to detect the cell apoptosis. Results: MiR-133a-3p was identified to be reduced in exosomes derived from the plasma of patients with IS. Upregulation of miR-133a-3p significantly reversed OGD/R-induced SH-SY5Y cell growth inhibition. Consistently, BMSCs-derived exosomal miR-133a-3p could restore OGD/R-decreased SH-SY5Y cell proliferation via inhibiting apoptosis. Meanwhile, DAPK2 was a direct target of miR-133a-3p. In addition, OGD/R notably upregulated the level of DAPK2 and weakened the expressions of p-Akt and p-mTOR in SH-SY5Y cells, whereas exosomal miR-133a-3p derived from BMSCs notably reversed these phenomena. Exosomal miR-133a-3p derived from BMSCs could reverse OGD/R-induced cell apoptosis via inhibiting autophagy. Furthermore, exosomal miR-133a-3p derived from BMSCs markedly alleviated the symptom of CI/R injury in vivo. Conclusion: Exosomal miR-133a-3p derived from BMSCs alleviates CI/R injury via targeting DAPK2/Akt signaling. Thus, our study might shed new light on discovering new strategies against CI/R injury.

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“…MiR - 202 - 3p is present in many human diseases and is a new potential biomarker for the diagnosis of type 1 gastric neuroendocrine tumors ( 11 ). Its overexpression in bone marrow mesenchymal stem cells improves cerebral ischemia-reperfusion injury by promoting angiogenesis and inhibiting inflammation ( 12 ). Additionally, the overexpression of nuclear-enriched autosomal transcript 1 promotes the proliferation, migration, and invasion of endometrial cancer cells and inhibits apoptosis by targeting the miRNA - 202 - 3p /T-cell immunoglobulin and mucin domain 4 axis ( 13 ).…”

Section: Introductionmentioning

confidence: 99%

MiR-202-3p inhibits the proliferation and metastasis of lung adenocarcinoma cells by targeting RRM2

Cao¹,

Xue²,

Chen³

et al. 2022

Ann Transl Med

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Background: Lung adenocarcinoma (LUAD) is the most common type of lung cancer, and its pathogenesis is still unclear. The present study aimed to investigate the role of miR-202-3p and its downstream target gene, ribonucleotide reductase regulatory subunit M2 (RRM2), in the occurrence and development of LUAD and elucidate the correlation between RRM2 and the clinicopathological stage and prognosis of LUAD. Methods:The expression of miR-202-3p was analyzed using the CancerMIRNome database and quantitative polymerase chain reaction (qPCR). The effects of miR-202-3p and RRM2 on the proliferation, migration, and invasion of A549 cells were analyzed. A dual luciferase reporter assay was used to verify the targeting of miR-202-3p and RRM2. Additionally, the correlation between RRM2 expression and clinicopathology was analyzed. Results: (I) MiR-202-3p was lowly expressed in LUAD and the LUAD cell lines. qPCR confirmed that microRNA (miRNA) transfection was effective and sufficient for subsequent experiments. (II) MiR-202-3p inhibited the proliferation, invasion, and migration of LUAD cells. (III) There was a targeting relationship between miR-202-3p and RRM2, and miR-202-3p affected the expression of the RRM2 protein. RRM2 was highly expressed in lung cancer tissue. (IV) RRM2 was associated with the clinicopathological staging of lung cancer. The prognosis of patients with low RRM2 expression was better, and the prognostic sensitivity of RRM2 to lung cancer was high. RRM2 may exert its effects via the Notch pathway. (V) Si-RRM2 inhibited the expression of the RRM2 protein. RRM2 promoted the proliferation, migration, and invasion of LUAD cells. A miR-202-3p inhibitor restored the inhibitory effect of si-RRM2 on LUAD cells. Conclusions: MiR-202-3p was lowly expressed in lung cancer tissue. MiR-202-3p overexpression inhibited the proliferation and metastasis of lung cancer cells. RRM2 was highly expressed in lung cancer tissue and promoted the proliferation and metastasis of lung cancer cells. MiR-202-3p targeted and inhibited RRM2, thereby reducing the proliferation and metastasis of LUAD cells. LUAD patients with low RRM2 expression had a better prognosis, and the expression level of RRM2 was correlated with the clinical characteristics of lung cancer patients.

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Overexpression of microRNA-202-3p in bone marrow mesenchymal stem cells improves cerebral ischemia-reperfusion injury by promoting angiogenesis and inhibiting inflammation

Cited by 18 publications

References 37 publications

Cellular senescence in ischemia/reperfusion injury

Cellular senescence in ischemia/reperfusion injury

Exosomal miR-133a-3p Derived from BMSCs Alleviates Cerebral Ischemia-Reperfusion Injury via Targeting DAPK2

MiR-202-3p inhibits the proliferation and metastasis of lung adenocarcinoma cells by targeting RRM2

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