Identification of microRNAs and messenger RNAs involved in human umbilical cord mesenchymal stem cell treatment of ischemic cerebral infarction using integrated bioinformatics analysis

Qu, Yin-Meng; Sun, Xin; Yan, Xiaofeng; Jin, Hang; Guo, Zhen‐Ni; Yang, Yi

doi:10.4103/1673-5374.255998

Cited by 4 publications

(3 citation statements)

References 30 publications

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“…To identify the regulating miRNA in cerebral infarction, we performed microarray and found a significant decrease of miR-542-3p in ischemic tissues. And the low expression of miR-542-3p in ischemic brain tissue has been show in the previous study [ 44 ]. Interestingly, TLR4, which potentially binds with miR-542-3p, was increased in infarcted brain tissue.…”

Section: Discussionmentioning

confidence: 76%

RETRACTED ARTICLE: Mesenchymal stem cell-derived exosome miR-542-3p suppresses inflammation and prevents cerebral infarction

Cai

Zhou

et al. 2021

Stem Cell Res Ther

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Background Cerebral infarction ranks as the second leading cause of disability and death globally, and inflammatory response of glial cells is the main cause of brain damage during cerebral infarction. Methods Studies have shown that mesenchymal stem cells (MSCs) can secrete exosomes and contribute to cerebral disease. Here, we would explore the function of MSC-derived exosome in cerebral infarction. Results Microarray indicated a decrease of miR-542-3p and an increase of Toll-Like Receptor 4 (TLR4) in middle cerebral artery occlusion (MCAO) mice comparing with sham mice. And luciferase and RIP analysis indicated a binding of miR-542-3p and TLR4. Then, we injected AAV9-miR-542-3p into paracele of sham or MCAO mice. Functional analysis showed that AAV9-miR-542-3p inhibited infarction area and the number of degenerating neurons and suppressed inflammatory factors’ expression and inflammatory cell infiltration. As well, transfection of miR-542-3p mimics into HA1800 cells underwent oxygen and glucose deprivation (OGD). Similarly, overexpression of miR-542-3p alleviated OGD induced cell apoptosis, ROS, and activation of inflammation response. Moreover, miR-542-3p could be packaged into MSCs and secreted into HA1800 cells. The extractive exosome-miR-21-3p treatment relieved MCAO- or OGD-induced cerebral injury and inflammation through targeting TLR4. Conclusion These results confirmed that MSC-derived exosome miR-542-3p prevented ischemia-induced glial cell inflammatory response via inhibiting TLR4. These results suggest possible therapeutic strategies for using exosome delivery of miR-542-3p to cure cerebral ischemic injury.

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Section: Discussionmentioning

confidence: 76%

RETRACTED ARTICLE: Mesenchymal stem cell-derived exosome miR-542-3p suppresses inflammation and prevents cerebral infarction

Cai

Zhou

et al. 2021

Stem Cell Res Ther

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“…Almost immediately, we found that miR-26b was expressed to a greater extent in the adjacent tissues (Figure 1 H). StarBase v.3 was used to analyze miR-26b expression in liver hepatocellular carcinoma (LIHC) 31 , 32 , showing that miR-26b was expressed to a greater extent in the normal tissues compared to that in cancer tissues (Figure 1 I).…”

Section: Resultsmentioning

confidence: 99%

“…Numerous reports have demonstrated that miRNAs play a critical role in developing chemo-resistance based on their functions and targets 32 , 33 . miRNA-26b is encoded at 9p21.3, a vulnerable site in the genome, which has been reported to be missing in many HCC tumors and is downregulated in HCC cells 36 .…”

Section: Discussionmentioning

confidence: 99%

miR-26b enhances the sensitivity of hepatocellular carcinoma to Doxorubicin via USP9X-dependent degradation of p53 and regulation of autophagy

Chen¹,

Li²,

Liu³

et al. 2021

Int. J. Biol. Sci.

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Multi-drug resistance is a major challenge to hepatocellular carcinoma (HCC) treatment, and the over-expression or deletion of microRNA (miRNA) expression is closely related to the drug-resistant properties of various cell lines. However, the underlying molecular mechanisms remain unclear. CCK-8, EdU, flow cytometry, and transmission electron microscopy were performed to determine cell viability, proliferation, apoptosis, autophagic flow, and nanoparticle characterization, respectively. In this study, the results showed that the expression of miR-26b was downregulated following doxorubicin treatment in human HCC tissues. An miR-26b mimic enhanced HCC cell doxorubicin sensitivity, except in the absence of p53 in Hep3B cells. Delivery of the proteasome inhibitor, MG132, reversed the inhibitory effect of miR-26b on the level of p53 following doxorubicin treatment. Tenovin-1 (an MDM2 inhibitor) protected p53 from ubiquitination-mediated degradation only in HepG2 cells with wild type p53. Tenovin-1 pretreatment enhanced HCC cell resistance to doxorubicin when transfected with an miR-26b mimic. Moreover, the miR-26b mimic inhibited doxorubicin-induced autophagy and the autophagy inducer, rapamycin, eliminated the differences in the drug sensitivity effect of miR-26b. In vivo , treatment with sp94dr/miR-26b mimic nanoparticles plus doxorubicin inhibited tumor growth. Our current data indicate that miR-26b enhances HCC cell sensitivity to doxorubicin through diminishing USP9X-mediated p53 de-ubiquitination caused by DNA damaging drugs and autophagy regulation. This miRNA-mediated pathway that modulates HCC will help develop novel therapeutic strategies.

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Combined Analysis of Human and Experimental Rat Samples Identified Biomarkers for Ischemic Stroke

Chen,

Li,

Yang

et al. 2024

Mol Neurobiol

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Identification of microRNAs and messenger RNAs involved in human umbilical cord mesenchymal stem cell treatment of ischemic cerebral infarction using integrated bioinformatics analysis

Cited by 4 publications

References 30 publications

RETRACTED ARTICLE: Mesenchymal stem cell-derived exosome miR-542-3p suppresses inflammation and prevents cerebral infarction

RETRACTED ARTICLE: Mesenchymal stem cell-derived exosome miR-542-3p suppresses inflammation and prevents cerebral infarction

miR-26b enhances the sensitivity of hepatocellular carcinoma to Doxorubicin via USP9X-dependent degradation of p53 and regulation of autophagy

Combined Analysis of Human and Experimental Rat Samples Identified Biomarkers for Ischemic Stroke

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