Down-Regulation of miR-301a-3p Reduces Burn-Induced Vascular Endothelial Apoptosis by potentiating hMSC-Secreted IGF-1 and PI3K/Akt/FOXO3a Pathway

Liu, Lingying; Yin, Hui; Hao, Xingxia; Song, Haixing; Chai, Jiake; Duan, Huijuan; Yang, Chonglin; Yang, Longlong; Wu, Yushou; Han, Shaofang; Wang, Xiaoteng; Yue, Xiaotong; Chi, Yunfei; Liu, Wei; Wang, Qiong; Wang, Hongyu; Bai, Hailiang; Shi, Xiuxiu; Li, Shaozeng

doi:10.1016/j.isci.2020.101383

Cited by 13 publications

(6 citation statements)

References 46 publications

(54 reference statements)

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“…Hence, miR-21 may reverse the bacterial infection-induced pathological process of atherosclerosis ( 18 ). In addition, severe burns inhibit miR-301a-3p expression, which suppresses the apoptosis of HUVECs and stabilizes endothelial barrier permeability ( 19 ). miR-301a-3p expression is upregulated in obesity-related inflammation, and miR-301a decreases the production of proinflammatory cytokines in 3T3-L1 cells ( 20 ).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑301a‑3p increases oxidative stress, inflammation and apoptosis in ox‑LDL‑induced HUVECs by targeting KLF7

Jiang¹,

Lv²

2021

Exp Ther Med

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Arteriosclerotic cardiovascular disease is an inflammatory disease of ischemia or endothelial dysfunction caused by atherosclerosis, thereby causing high mortality. The viability and apoptosis of human umbilical vein endothelial cells (HUVECs) following oxidized low-density lipoprotein (ox-LDL) induction or transfection was detected by Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis. MicroRNA (miR)-301a-3p and Krueppel-like factor 7 (KLF7) mRNA expression was determined by reverse transcription-quantitative PCR (RT-qPCR). The levels of monocyte chemoattractant protein-1 (MCP-1) and IL-6, activities of reactive oxygen species and superoxide dismutase and lactate dehydrogenase leakage were analyzed by respective commercial assay kits. The protein expression of IL-6, MCP-1, Bcl2, Bax, poly (ADP-ribose) polymerase (PARP), cleaved PARP, pro-caspase3 and cleaved caspase-3 was detected by western blotting. miR-301a-3p expression is highly expressed in ox-LDL-induced HUVECs. miR-301a-3p is also a target of KLF7. Inhibition of miR-301a-3p suppressed oxidative stress, inflammation and apoptosis in ox-LDL-induced HUVECs, which was reversed by KLF7 inhibition. In conclusion, miR-301a-3p promotes oxidative stress, inflammation and apoptosis in ox-LDL-induced HUVECs via decreasing KLF7 expression.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑301a‑3p increases oxidative stress, inflammation and apoptosis in ox‑LDL‑induced HUVECs by targeting KLF7

Jiang¹,

Lv²

2021

Exp Ther Med

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“…It is well-known that endothelial injury plays an important role in the development of many cardiovascular diseases (Lerman and Zeiher, 2005 ). Moreover, miR-301a-3p has also been reported to induce HUVECs apoptosis and increase endothelial barrier permeability (Liu et al, 2020 ). Therefore, it might be assumed that the mitochondria-localized miR-301a-3p could rapidly re-enter into the cytosol and regulate its target genes, thus affecting endothelial function under oxidative stress conditions.…”

Section: Discussionmentioning

confidence: 99%

RNA-Binding Protein MSI2 Binds to miR-301a-3p and Facilitates Its Distribution in Mitochondria of Endothelial Cells

Guo

Gao

Wang

et al. 2021

Front. Mol. Biosci.

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Numerous miRNAs have been detected in mitochondria, which play important roles in many physiological and pathophysiological processes. However, the dynamic changes of miRNA distribution in mitochondria and their mechanisms in reactive oxygen species (ROS)-induced endothelial injury remain unclear. Therefore, miRNA levels in whole cells and mitochondria of H2O2-treated endothelial cells were analyzed by small RNA sequencing in the present study. The results showed that H2O2 significantly reduced the relative mitochondrial distribution of dozens of miRNAs in human umbilical vein endothelial cells (HUVECs). Among the high-abundance miRNAs, miR-301a-3p has the most significant changes in the redistribution between cytosol and mitochondria confirmed by absolute quantitative polymerase chain reaction (qPCR). To unravel the mechanism of miR-301a-3p distribution in mitochondria, RNA pull-down followed by label-free quantitative proteomic analysis was performed, and RNA-binding protein Musashi RNA binding protein 2 (MSI2) was found to specifically bind to miR-301a-3p. Western blotting and immunofluorescence colocalization assay showed that MSI2 was located in mitochondria of various cell types. H2O2 significantly downregulated MSI2 expression in whole endothelial cells, promoted the distribution of MSI2 in cytosol and decreased its distribution in the mitochondria. Moreover, overexpression of MSI2 increased the mitochondrial distribution of miR-301a-3p, whereas inhibition of MSI2 decreased its distribution in mitochondria. Thus, MSI2 might be responsible for the distribution of miR-301a-3p between cytosol and mitochondria in endothelial cells. Our findings revealed for the first time that MSI2 was involved in the regulation of miRNA distribution in mitochondria and provided valuable insight into the mechanism of mitochondrial distribution of miRNAs.

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“…It has been demonstrated stem cells secrete a variety of cytokines and growth factors, such as EGF, IL, LIF, FGF2, TGF-β, and IGF-1, that regulate the physiological conditions of recipient cells [33][34][35][36]. The beneficial effects of these factors on IVM have been demonstrated in several species, such as human [37,38], cow [39], horse [40], pig [41], and mouse [38].…”

Section: Discussionmentioning

confidence: 99%

Effects of Human Endothelial Progenitor Cell and Its Conditioned Medium on Oocyte Development and Subsequent Embryo Development

Lee

2020

IJMS

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Human endothelial progenitor cells (EPCs) secrete numerous growth factors, and they have been applied to regenerative medicine for their roles in angiogenesis as well as neovascularization. Angiogenesis is one of the essential factors for the maturation of ovarian follicles; however, the physiological function of EPCs or their derivatives on in vitro culture systems has not been fully understood. The aim of this study was to evaluate the effectiveness of EPCs and their conditioned medium (EPC-CM) on oocyte development and subsequent embryo development. In the results, the oocyte development and subsequent embryo development were significantly improved in EPCs and the EPC-CM group. In addition, markedly increased levels of growth factors/cytokines, such as basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF), insulin growth factor-1 (IGF-1), interleukin-10 (IL-10), and epidermal growth factor (EGF), were observed in medium from the EPC-CM group. Additionally, EPC-CM after in vitro maturation (IVM) had significantly decreased reactive oxygen species (ROS) levels compared to those of other groups. Transcriptional levels of growth factor receptor-related genes (FGFR2, IGF1R) and anti-apoptotic-related gene (BCL2) were significantly upregulated in cumulus cells/oocytes from the EPC-CM group compared with those from the control. Furthermore, the expression levels of cumulus expansion-related genes (PTGS2, TNFAIP6, HAS2) and oocyte-maturation-related factors (GDF9, BMP15) were significantly enhanced in the EPC-CM group. Consequently, the present study provides the first evidence that EPC-CM contains several essential growth factors for oocyte development by regulating genes involved in oocyte maturation.

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Down-Regulation of miR-301a-3p Reduces Burn-Induced Vascular Endothelial Apoptosis by potentiating hMSC-Secreted IGF-1 and PI3K/Akt/FOXO3a Pathway

Cited by 13 publications

References 46 publications

MicroRNA‑301a‑3p increases oxidative stress, inflammation and apoptosis in ox‑LDL‑induced HUVECs by targeting KLF7

MicroRNA‑301a‑3p increases oxidative stress, inflammation and apoptosis in ox‑LDL‑induced HUVECs by targeting KLF7

RNA-Binding Protein MSI2 Binds to miR-301a-3p and Facilitates Its Distribution in Mitochondria of Endothelial Cells

Effects of Human Endothelial Progenitor Cell and Its Conditioned Medium on Oocyte Development and Subsequent Embryo Development

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