Down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows

Chen, Kunlin; Fu, Yuanyuan; Shi, Min-Yan; Li, Huixia

doi:10.1007/s11626-016-0045-x

Cited by 19 publications

(10 citation statements)

References 47 publications

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“…Furthermore, the inhibition of miRNA counteracted the negative effects of the overloading HP on these factors and enhanced those of a low cyclic pressure. Additionally, it has been reported that the transient transfection of miR-34a, miR-146a, and miR-181a down-regulated the expression of antioxidant enzymes with a simultaneous decrease of mitochondrial intracellular ROS levels in PBMC of Holstein cows, in HUVEC lines, and in primary OA chondrocytes and synoviocytes [29,30,56,57]. According to this evidence, in this study, the silencing of miR-34a and miR-181a reduced the production of mitochondrial superoxide anion and the mRNA levels of SOD-2 and NRF2 in OA chondrocytes, increasing the activity of low cyclic HP and limiting the effects of static continuous loading.…”

Section: Discussionmentioning

confidence: 99%

Hydrostatic Pressure Regulates Oxidative Stress through microRNA in Human Osteoarthritic Chondrocytes

Cheleschi

Barbarino

Gallo

et al. 2020

IJMS

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Hydrostatic pressure (HP) modulates chondrocytes metabolism, however, its ability to regulate oxidative stress and microRNAs (miRNA) has not been clarified. The aim of this study was to investigate the role of miR-34a, miR-146a, and miR-181a as possible mediators of HP effects on oxidative stress in human osteoarthritis (OA) chondrocytes. Chondrocytes were exposed to cyclic low HP (1–5 MPa) and continuous static HP (10 MPa) for 3~h. Metalloproteinases (MMPs), disintegrin and metalloproteinase with thrombospondin motif (ADAMTS)-5, type II collagen (Col2a1), miR-34a, miR-146a, miR-181a, antioxidant enzymes, and B-cell lymphoma 2 (BCL2) were evaluated by quantitative real-time polymerase chain reaction qRT-PCR, apoptosis and reactive oxygen species ROS production by cytometry, and β-catenin by immunofluorescence. The relationship among HP, the studied miRNA, and oxidative stress was assessed by transfection with miRNA specific inhibitors. Low cyclical HP significantly reduced apoptosis, the gene expression of MMP-13, ADAMTS5, miRNA, the production of superoxide anion, and mRNA levels of antioxidant enzymes. Conversely, an increased Col2a1 and BCL2 genes was observed. β-catenin protein expression was reduced in cells exposed to HP 1–5 MPa. Opposite results were obtained following continuous static HP application. Finally, miRNA silencing enhanced low HP and suppressed continuous HP-induced effects. Our data suggest miRNA as one of the mechanisms by which HP regulates chondrocyte metabolism and oxidative stress, via Wnt/β-catenin pathway.

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Section: Discussionmentioning

confidence: 99%

Hydrostatic Pressure Regulates Oxidative Stress through microRNA in Human Osteoarthritic Chondrocytes

Cheleschi

Barbarino

Gallo

et al. 2020

IJMS

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“…The bta-miR-181a is known to be involved in various cellular biological processes including cell proliferation and apoptosis 57 . The impact of bta-miR-181a in peripheral blood mononuclear cells (PBMC) subjected to HS showed that inhibiting the miRNA would reverse the HS damage and improve the viability of PBMCs in Holstein cows 58 . The involvement of miRNAs in stress response is well known and EV-coupled miRNAs are differentially expressed in response to metabolic stress 30 .…”

Section: Discussionmentioning

confidence: 99%

Extracellular vesicles shuttle protective messages against heat stress in bovine granulosa cells

Gebremedhn

Gad

Aglan

et al. 2020

Sci Rep

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Elevated summer temperature is reported to be the leading cause of stress in dairy and beef cows, which negatively affects various reproductive functions. Follicular cells respond to heat stress (HS) by activating the expression of heat shock family proteins (HSPs) and other antioxidants. HS is reported to negatively affect the bi-directional communication between the follicular cells and the oocyte, which is partly mediated by follicular fluid extracellular vesicles (EVs) released from surrounding cells. As carriers of bioactive molecules (DNA, RNA, protein, and lipids), the involvement of EVs in mediating the stress response in follicular cells is not fully understood. Here we used an in vitro model to decipher the cellular and EV-coupled miRNAs of bovine granulosa cells in response to HS. Moreover, the protective role of stress-related EVs against subsequent HS was assessed. For this, bovine granulosa cells from smaller follicles were cultured in vitro and after sub-confluency, cells were either kept at 37 °C or subjected to HS (42 °C). Results showed that granulosa cells exposed to HS increased the accumulation of ROS, total oxidized protein, apoptosis, and the expression of HSPs and antioxidants, while the viability of cells was reduced. Moreover, 14 and 6 miRNAs were differentially expressed in heat-stressed granulosa cells and the corresponding EVs, respectively. Supplementation of stress-related EVs in cultured granulosa cells has induced adaptive response to subsequent HS. However, this potential was not pronounced when the cells were kept under 37 °C. Taking together, EVs generated from granulosa cells exposed to HS has the potential to shuttle bioactive molecules to recipient cells and make them robust to subsequent HS.

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“…The gene expression of miR-34a and miR-181a is induced by the oxidative stress stimulus as demonstrated in different studies from human cardiac and carcinoma cell lines and in OA chondrocytes [4,46,47]. Moreover, the inhibition of miR-34a and of miR-181a decreased the expression of antioxidant enzymes with a concomitant reduction of mitochondrial intracellular ROS levels in primary mesangial cells, in PBMC of Holstein cows and in HUVEC lines [48,49]. According to the current literature, transfection of our OA cells with miR-34a and miR-181a specific inhibitors significantly down-regulated the expression of antioxidant enzymes as well as the production of mitochondrial superoxide anion, particularly preventing their induction by visfatin.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-34a and MicroRNA-181a Mediate Visfatin-Induced Apoptosis and Oxidative Stress via NF-κB Pathway in Human Osteoarthritic Chondrocytes

Cheleschi

Tenti

Mondanelli

et al. 2019

Cells

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Current evidence suggests a complex interaction between adipokines and microRNA (miRNA) in osteoarthritis (OA) pathogenesis. The present study explored the role of miR-34a and miR-181a in regulating apoptosis and oxidative stress induced by visfatin in human OA chondrocytes. Chondrocytes were transfected with miR-34a and miR-181a inhibitors and stimulated with visfatin for 24 h, in the presence of nuclear factor (NF)-κB inhibitor (BAY-11-7082, 2 h pre-incubation). Apoptosis and reactive oxygen species (ROS) production were detected by cytometry, miRNA, antioxidant enzymes, nuclear factor erythroid (NRF)2 and B-cell lymphoma (BCL)2 expressions by quantitative real time polymerase chain reaction (real time PCR) and western blot. P50 NF-κB subunit was measured by immunofluorescence. Visfatin significantly induced apoptosis and superoxide anion production, increased miR-34a, miR-181a, superoxide dismutase (SOD)-2, catalase (CAT), NRF2 and decreased BCL2 gene and protein expression in OA chondrocytes. All the visfatin-caused effects were suppressed by using miR-34a and miR-181a inhibitors. Pre-incubation with BAY-11-7082 counteracted visfatin-induced expression of miRNA, BCL2, SOD-2, CAT and NRF2. Inhibition of miR-34a and miR-181a significantly reduced the activation of p50 NF-κB. Visfatin confirms its ability to induce apoptosis and oxidative stress in human OA chondrocytes; these effects appeared mediated by miR-34a and miR-181a via NF-κB pathway. We highlight the relevance of visfatin as potential therapeutic target for OA treatment.

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Down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows

Cited by 19 publications

References 47 publications

Hydrostatic Pressure Regulates Oxidative Stress through microRNA in Human Osteoarthritic Chondrocytes

Hydrostatic Pressure Regulates Oxidative Stress through microRNA in Human Osteoarthritic Chondrocytes

Extracellular vesicles shuttle protective messages against heat stress in bovine granulosa cells

MicroRNA-34a and MicroRNA-181a Mediate Visfatin-Induced Apoptosis and Oxidative Stress via NF-κB Pathway in Human Osteoarthritic Chondrocytes

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