Suppression of microRNA-205-5p in human mesenchymal stem cells improves their therapeutic potential in treating diabetic foot disease

Zhu, Lingyan; Wang, Gongxian; Fischbach, Shane; Xiao, Xianmin

doi:10.18632/oncotarget.17012

Cited by 24 publications

(36 citation statements)

References 40 publications

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“…The recent evidence showed that the dysregulated miR‐205 expression occurred in the early stage of DM . Regulating miR‐205 in mesenchymal stem cells might improve the therapeutic effects on diabetic foot disease, one severe complication of DM . This might be the first study indicating the regulatory effect of BAI on miR‐205.…”

Section: Discussionmentioning

confidence: 78%

Retracted: Baicalin prevents tumor necrosis factor‐α−induced apoptosis and dysfunction of pancreatic β‐cell line Min6 via upregulation of miR‐205

You

Wang

et al. 2018

J of Cellular Biochemistry

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Baicalin (BAI), one major flavonoid from Scutellaria baicalensis, possesses anticancer and anti-inflammatory properties. However, the effect of BAI on diabetes mellitus has not been investigated. This study explored the antidiabetic effect of BAI on pancreatic β-cell line Min6. Min6 cells were treated with tumor necrosis factor-α (TNF-α) to mimic β-cell destruction in type 1 diabetes mellitus. The effects of BAI on viability and apoptosis of Min6 cells were analyzed by the cell counting kit-8 assay and Annexin V-fluoresceine isothiocyanate/propidium iodide staining method. The insulin secretion of Min6 cells was determined using radioimmunoassay. Expression of apoptosis-associated proteins and inducible nitric oxide synthase (iNOS), and activation of phosphatidylinositol 3'-kinase/protein kinase B (PI3K/AKT) and nuclear factor ΚB (NF-κB) pathways were analyzed by Western blot analysis. Relative microRNA-205 (miR-205) expression was determined by quantitative real time polymerase chain reaction. TNF-α treatment inhibited cell growth and insulin secretion, but promoted iNOS expression. All of these effects were reversed by BAI treatment. BAI promoted viability; suppressed apoptosis; regulated caspase-3, B-cell lymphoma 2 and Bcl-2-associated X protein; decreased iNOS level; and increased insulin production. BAI protected Min6 cells by upregulating miR-205. Besides, the Min6 cell-protective effect of BAI was PI3K/AKT pathway and NF-κB pathway dependent. BAI activated the PI3K/AKT pathway and inhibited the NF-κB pathway by regulating miR-205. In conclusion, BAI protected Min6 cells from TNF-α-induced injury by upregulating miR-205, which acts, at least in part, via activation of the PI3K/AKT pathway and inactivation of the NF-κB pathway.

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Section: Discussionmentioning

confidence: 78%

Retracted: Baicalin prevents tumor necrosis factor‐α−induced apoptosis and dysfunction of pancreatic β‐cell line Min6 via upregulation of miR‐205

You

Wang

et al. 2018

J of Cellular Biochemistry

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“…These injuries are associated with impaired endothelial cell tube formation (24). Several studies have reported that the dysregulation of miRNA in diabetic endothelial cells influences their functions (25,26). Therefore, targeting and regulating miRNA in an advanced pathway is a strategy for overcoming HG-induced endothelial injury.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR‑17‑5p protects against high glucose‑induced endothelial cell injury by targeting E2F1‑mediated suppression of autophagy and promotion of apoptosis

Yao

Xue

2018

Int J Mol Med

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E2 promoter binding factor 1 (E2F1) has been reported to have an important regulatory role in cell survival during hyperglycemic conditions; however, the mechanisms remain to be fully elucidated. Bioinformatics analyses have suggested that microRNA (miR)‑17‑5p targets the 3'untranslated region (3'UTR) of E2F1. The aim of the present study was to characterize the protective effect of miR‑17‑5p/E2F1 on human umbilical vein endothelial cells (HUVECs) under high glucose (HG) conditions, to confirm the regulatory effect of miR‑17‑5p on E2F1/AMP‑activated protein kinase α2 (AMPKα2)‑mediated apoptosis and E2F1/mammalian target of rapamycin complex 1 (mTORC1)‑mediated autophagy. Bifluorescein experiments were performed to characterize the interaction between miR‑17‑5p and E2F1. The Cell Counting Kit‑8 assay, flow cytometry, immunofluorescence, and reverse transcription‑quantitative polymerase chain reaction and western blot analyses were used to detect cell viability, apoptosis, autophagy, and relative mRNA and protein expression, respectively. The results showed that HG induced the downregulation of miR‑17‑5p and upregulation of E2F1 during HUVEC injury. The downregulation of E2F1 inhibited HG‑induced HUVEC dysfunction by suppressing mTORC1‑mediated inhibition of autophagy and AMPKα2‑mediated promotion of apoptosis. The results suggested that inhibiting the expression of E2F1 protected against HG‑induced HUVEC injury via the activation of autophagy. The overexpression of miR‑17‑5p inhibited E2F1‑mediated HUVEC injury under HG conditions, which was reversed following transfection with an E2F1‑overexpression vector. The bifluorescein experiments showed that miR‑17‑5p targeted the 3'UTR of E2F1. Taken together, the results suggested that the expression of miR‑17‑5p inhibited HG‑induced endothelial cell injury by targeting E2F1.

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“…In another study the suppression of miRNA‐205‐5P, as a VEGF antagonizing miRNA in MSCs, was performed. Consequently, it enhanced VEGF and the pro‐angiogenic effects of MSCs which improved MSC therapeutic efficacy in the treatment of diabetic foot disease …”

Section: Methods To Enhance the Efficacy Of Msc‐based Wound Therapymentioning

confidence: 99%

“…Consequently, it enhanced VEGF and the pro-angiogenic effects of MSCs which improved MSC therapeutic efficacy in the treatment of diabetic foot disease. 76…”

Section: Genetic Modificationsmentioning

confidence: 99%

A review on different methods to increase the efficiency of mesenchymal stem cell‐based wound therapy

Shojaei

Rahmati

Dehkordi

2019

Wound Repair Regeneration

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Mesenchymal stem cells (MSCs) accelerate wound healing but the harsh environment of wound site limits the engraftment, retention, and survival rate of transplanted cells. There are multiple approaches that amplify the therapeutic potential of MSCs. The MSCs derived from medical waste material, provide comparable regenerative abilities compared to traditional sources. The application of different scaffolds increases MSC delivery and migration into the wound. The spheroid culture of MSC increases the paracrine effects of the entrapped cells and the secretion of pro‐angiogenic and anti‐inflammatory cytokines. The MSC pretreating and preconditioning enhances the cell migration, proliferation, and survival rate, which lead to higher angiogenesis, re‐epithelialization, wound closure, and granulation tissue formation. Moreover, genetic modification has been performed in order to increase MSC angiogenesis, differentiation potential, as well as the cell life span. Herein, we review the results of aforementioned approaches and provide information accommodating to the continued development of MSC‐based wound therapy in the future.

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Suppression of microRNA-205-5p in human mesenchymal stem cells improves their therapeutic potential in treating diabetic foot disease

Cited by 24 publications

References 40 publications

Retracted: Baicalin prevents tumor necrosis factor‐α−induced apoptosis and dysfunction of pancreatic β‐cell line Min6 via upregulation of miR‐205

Retracted: Baicalin prevents tumor necrosis factor‐α−induced apoptosis and dysfunction of pancreatic β‐cell line Min6 via upregulation of miR‐205

Overexpression of miR‑17‑5p protects against high glucose‑induced endothelial cell injury by targeting E2F1‑mediated suppression of autophagy and promotion of apoptosis

A review on different methods to increase the efficiency of mesenchymal stem cell‐based wound therapy

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