MiR-136 contributes to pre-eclampsia through its effects on apoptosis and angiogenesis of mesenchymal stem cells

Liqin, JI; Zhang, Liping; Li, Yani; Guo, Li; Cao, Ni; Bai, Zhiying; Song, Yingchun; Xu, Zhen; Zhang, Juan; Liu, Chunhua; Ma, Xiaoxing

doi:10.1016/j.placenta.2017.01.102

Cited by 45 publications

(31 citation statements)

References 34 publications

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“…Ji et al (30) demonstrated that high level of miR-136-5p suppressed cell proliferation and promoted apoptosis of mesenchymal stem cells through targeting BCL2, which is a potential causal factor of preeclampsia. Zhang et al (31) demonstrated that miR-136-5p is involved in keratinocyte growth through targeting PPP2R2A, and may be a novel treatment target for the improvement of skin wound healing (31).…”

Section: Discussionmentioning

confidence: 99%

Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

et al. 2018

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Abstract. MicroRNAs (miRs) are involved in diverse physiological and developmental processes at the post-transcriptional level in cells. Previous studies have demonstrated that miR-136-5p is involved in certain types of cancer. However, the function of miR-136-5p in renal cell carcinoma (RCC) remains to be fully elucidated. In present study, miR-136-5p expression levels were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and MTT assays, CCK-8 assays, Transwell assays, wound healing assays and flow cytometry were performed to investigate the function of miR-136-5p in RCC. RT-qPCR revealed that the expression of miR-136 was significantly lower in RCC tissues and cells compared with adjacent non-tumor tissues and cells in vitro. miR-136-5pwas also demonstrated to be associated with RCC cell proliferation, viability, migration, invasion and apoptosis. miR-136-5p may therefore function as a tumor suppressor in RCC. Further studies are required to elucidate the molecular mechanisms and signaling pathways underlying these functions of miR-136-5p, to investigate the potential function of miR-136-5p as a biomarker for the early detection and prognosis of RCC, and its potential as a therapeutic target for the treatment of RCC.

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Section: Discussionmentioning

confidence: 99%

Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

et al. 2018

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“…miR-136 is highly expressed in pre-eclampsia and inhibits the formation of HUVEC capillaries via dysregulation of VEGF. In addition, the expression levels of miR-136 inversely correlates with VEGF [24]. In paclitaxel-resistant ovarian cancer cells, pre-miR-136 transfection significantly decreased angiogenesis and induced apoptosis, and regulation of miR-136 expression could resensitize paclitaxel-resistant cells [25].…”

Section: Discussionmentioning

confidence: 99%

Identification of potential molecular targets associated with proliferative diabetic retinopathy

Shao

et al. 2020

BMC Ophthalmol

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Background: This study aimed to identify and evaluate potential molecular targets associated with the development of proliferative diabetic retinopathy (DR). Methods: The microarray dataset "GSE60436" generated from fibrovascular membranes (FVMs) associated with proliferative DR was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) from the active FVMs and control or inactive FVMs and control were evaluated and co-DEGs were identified using VEEN analysis. Functional enrichment analysis, and protein-protein interactions (PPI) network and module analyses were performed on the upregulated and downregulated coDEGs. Finally, several predictions regarding microRNAs (miRNAs) and transcription factors (TFs) were made to construct a putative TF-miRNA-target network. Results: A total of 1475 co-DEGs were screened in active/inactive FVM samples, including 461 upregulated and 1014 downregulated genes, which were enriched for angiogenesis [Hypoxia Inducible Factor 1 Subunit Alpha (HIF1A) and Placental Growth Factor (PGF)] and visual perception, respectively. In the case of the upregulated co-DEGs, Kinesin Family Member 11 (KIF11), and BUB1 Mitotic Checkpoint Serine/Threonine Kinase (BUB1) exhibited the highest values in both the PPI network and module analyses, as well as the genes related to mitosis. In the case of downregulated co-DEGs, several G protein subunits, including G Protein Subunit Beta 3 (GNB3), exhibited the highest values in both the PPI network and module analyses. The genes identified in the module analysis were found to be from the signal transduction-related pathways. In addition, we were able to identify four miRNAs and five TFs, including miR-136 and miR-374. Conclusions: In brief, HIF1A, PGF, KIF11, G protein subunits, and miR-136, miR-374 may all be involved in angiogenesis, retinal endothelial cell proliferation, and visual signal transduction in proliferative DR. This study provides a number of novel insights that may aid the development of future studies dedicated to discovering novel therapeutic targets in proliferative DR.

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“…To study the mechanism of Exo UMSCs -mediated rejuvenation of OMSCs, the profiles of age-related miRNAs were screened from database (Miranda and TargetScan) and literatures [19,20] as most of the effects of exosome were carried out through exosomal miRNAs. Among these miRNAs, miR-136 was the most abundant in UMSCs as compared with OMSCs, and was increased more than 20-fold in OMSCs after cultured with Exo UMSCs , whereas no significant difference was observed for other miRNAs such as miR-106a, miR-155 and miR-29C among these groups (Fig 5a, Fig S6).…”

Section: Mirna-136 Was a Key Effecter Of Exo Umscs To Rejuvenate Omscsmentioning

confidence: 99%

Exosomes derived from human umbilical cord MSCs rejuvenate aged MSCs and enhance their functions for myocardial repair

Zhang

Zhu

et al. 2020

Preprint

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Backhround: Age and other cardiovascular risk factors have been reported to impair the activities of mesenchymal stem cells (MSCs), which will affect the efficacy of stem cell transplantation. The objective of the study is to investigate whether exosomes derived from human umbilical cord MSCs (UMSCs) could enhance the activities of bone marrow MSCs from old person (OMSCs), and improve their capacity for cardiac repair. Methods: Exosomes extracted from conditioned medium of UMSCs were used to treat OMSCs to generate OMSCsExo. The key molecule in the exosomes that have potential to rejuvenate aged MSCs were screened, and the role of OMSC was tested in the mouse model of mycardiac infarction(MI). Results: We found the activity of senescence-associated β-galactosidase and the expression of aging-related factors such as p53, p21, and p16 were significantly higher in OMSCs than those in UMSCs. After treatment with UMSC exosomes, these senescence phenotypes of OMSCs were remarkably reduced. The proliferation, migration, differentiation, anti-apoptotic and paracrine effect were increased in OMSCsExo. In vivo study, mice with cardiac infarction had significantly better cardiac function, less fibrosis, and more angiogenesis after they were injected with OMSCsExo as compared with those with OMSC. There was more miR-136 expression in UMSCs and OMSCsExo than in OMSCs. Upregulation of miR-136 by transfection of miR-136 mimic into OMSCs significantly attenuated the apoptosis and senescence of OMSCs. Apoptotic peptidase activating factor (Apaf1) was found to be the downstream gene that is negatively regulated by miR-136 via directly targeting at its 3’UTR. Conclusion: Our data suggest that exosomes from young MSCs can improve activities of aged MSCs and enhance their function for myocardial repair by transferring exosomal miR-136 and downregulating Apaf1.

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MiR-136 contributes to pre-eclampsia through its effects on apoptosis and angiogenesis of mesenchymal stem cells

Cited by 45 publications

References 34 publications

Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

Identification of potential molecular targets associated with proliferative diabetic retinopathy

Exosomes derived from human umbilical cord MSCs rejuvenate aged MSCs and enhance their functions for myocardial repair

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