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MFGE8 is down-regulated in cardiac fibrosis and attenuates endothelial-mesenchymal transition through Smad2/3-Snail signalling pathway.
In conclusion, our experiments indicate that MFGE8 might play a protective role in TGF-β1-induced EndMT and might be a potential therapeutic target for cardiac fibrosis. PMID: 32945126 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - September 16, 2020 Category: Molecular Biology Authors: Wang B, Ge Z, Wu Y, Zha Y, Zhang X, Yan Y, Xie Y Tags: J Cell Mol Med Source Type: research

HIF-1 α-induced up-regulation of microRNA-126 contributes to the effectiveness of exercise training on myocardial angiogenesis in myocardial infarction rats.
In conclusion, we revealed that HIF-1α, whose expression experiences up-regulation during ET, could function as an upstream regulator to miR-126, resulting in angiogenesis promotion through the PI3K/AKT/eNOS and MAPK signalling pathway and subsequent improvement of the MI heart function. PMID: 32939968 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - September 15, 2020 Category: Molecular Biology Authors: Song W, Liang Q, Cai M, Tian Z Tags: J Cell Mol Med Source Type: research

Knockdown of endogenous RNF4 exacerbates ischaemia-induced cardiomyocyte apoptosis in mice.
Abstract RNF4, a poly-SUMO-specific E3 ubiquitin ligase, is associated with protein degradation, DNA damage repair and tumour progression. However, the effect of RNF4 in cardiomyocytes remains to be explored. Here, we identified the alteration of RNF4 from ischaemic hearts and oxidative stress-induced apoptotic cardiomyocytes. Upon myocardial infarction (MI) or H2 O2 /ATO treatment, RNF4 increased rapidly and then decreased gradually. PML SUMOylation and PML nuclear body (PML-NB) formation first enhanced and then degraded upon oxidative stress. Reactive oxygen species (ROS) inhibitor was able to attenuate the elev...
Source: J Cell Mol Med - July 27, 2020 Category: Molecular Biology Authors: Qiu F, Han Y, Shao X, Paulo P, Li W, Zhu M, Tang N, Guo S, Chen Y, Wu H, Zhao D, Liu Y, Chu W Tags: J Cell Mol Med Source Type: research

Inhibition of TGF β-activated protein kinase 1 ameliorates myocardial ischaemia/reperfusion injury via endoplasmic reticulum stress suppression.
Inhibition of TGFβ-activated protein kinase 1 ameliorates myocardial ischaemia/reperfusion injury via endoplasmic reticulum stress suppression. J Cell Mol Med. 2020 May 07;: Authors: Zeng J, Jin Q, Ruan Y, Sun C, Xu G, Chu M, Ji K, Wu L, Li L Abstract Transforming growth factor β-activated protein kinase 1 (TAK1) involves in various biological responses and is a key regulator of cell death. However, the role of TAK1 on acute myocardial ischaemia/reperfusion (MI/R) injury is unknown. We observed that TAK1 activation increased significantly after MI/R and hypoxia/reoxygenation (H/R), and we hypothesiz...
Source: J Cell Mol Med - May 6, 2020 Category: Molecular Biology Authors: Zeng J, Jin Q, Ruan Y, Sun C, Xu G, Chu M, Ji K, Wu L, Li L Tags: J Cell Mol Med Source Type: research

Silencing of ATP2B1-AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA-mediated NF- κB signalling pathway.
This study aimed to investigate the effect of long intergenic non-protein-coding RNA (lincRNA) ATPase plasma membrane Ca2+ transporting 1 antisense RNA 1 (ATP2B1-AS1) against MI by targeting nuclear factor-kappa-B inhibitor alpha (NFKBIA) and mediating the nuclear factor-kappa-B (NF-κB) signalling pathway. An MI mouse model was established and idenepsied by cardiac function evaluation. It was determined that ATP2B1-AS1 was highly expressed, while NFKBIA was poorly expressed and NF-κB signalling pathway was activated in MI mice. Cardiomyocytes were extracted from mice and introduced with a series of mouse ATP2B1-AS1 vecto...
Source: J Cell Mol Med - March 9, 2020 Category: Molecular Biology Authors: Song KY, Zhang XZ, Li F, Ji QR Tags: J Cell Mol Med Source Type: research

Mineralocorticoid receptor deficiency improves the therapeutic effects of mesenchymal stem cells for myocardial infarction via enhanced cell survival.
Abstract The poor survival of stem cells seriously limits their therapeutic efficacy for myocardial infarction (MI). Mineralocorticoid receptor (MR) activation plays an important role in the pathogenesis of multiple cardiovascular diseases. Here, we examined whether MR silencing in bone marrow derived mesenchymal stem cells (MSCs) could improve MSCs' survival and enhance their cardioprotective effects in MI. MSCs from male Sprague-Dawley rats were transfected with adenoviral small interfering RNA to silence MR (siRNA-MR). MR silencing decreased hypoxia-induced MSCs' apoptosis, as demonstrated by Annexin V/7-AAD st...
Source: J Cell Mol Med - December 13, 2018 Category: Molecular Biology Authors: Xie X, Shen Y, Chen J, Huang Z, Ge J Tags: J Cell Mol Med Source Type: research

Microglial Mincle receptor in the PVN contributes to sympathetic hyperactivity in acute myocardial infarction rat.
Abstract Malignant ventricular arrhythmias (VAs) following myocardial infarction (MI) is a lethal complication resulting from sympathetic nerve hyperactivity. Numerous evidence have shown that inflammation within the paraventricular nucleus (PVN) participates in sympathetic hyperactivity. Our aim was to explore the role of Macrophage-inducible C-type lectin (Mincle) within the PVN in augmenting sympathetic activity following MI,and whether NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome/IL-1β axis is involved in this activity. MI was induced by coronary artery ligation. Mincle expression l...
Source: J Cell Mol Med - October 24, 2018 Category: Molecular Biology Authors: Wang Y, Yin J, Wang C, Hu H, Li X, Xue M, Liu J, Cheng W, Wang Y, Li Y, Shi Y, Tan J, Li X, Liu F, Liu Q, Yan S Tags: J Cell Mol Med Source Type: research

Heat-shock transcription factor 1 is critically involved in the ischaemia-induced cardiac hypertrophy via JAK2/STAT3 pathway.
Abstract Cardiac hypertrophy after myocardial infarction (MI) is an independent risk factor for heart failure. Regression of cardiac hypertrophy has emerged as a promising strategy in the treatment of MI patients. Here, we have been suggested that heat-shock transcription factor 1 (HSF1) is a novel repressor of ischaemia-induced cardiac hypertrophy. Ligation of left anterior descending coronary was used to produce MI in HSF1-deficient heterozygote (KO), HSF1 transgenic (TG) mice and their wild-type (WT) littermates, respectively. Neonatal rat cardiomyocytes (NRCMs) were treated by hypoxia to mimic MI in vitro. The...
Source: J Cell Mol Med - July 11, 2018 Category: Molecular Biology Authors: Yuan L, Qiu L, Ye Y, Wu J, Wang S, Wang X, Zhou N, Zou Y Tags: J Cell Mol Med Source Type: research

miR-21 promotes cardiac fibroblast-to-myofibroblast transformation and myocardial fibrosis by targeting Jagged1.
This study aimed to investigate the role of miR-21 in the regulation of CMT and myocardial fibrosis. Primary rat CFs were isolated from young SD rats and treated with TGF-β1, miR-21 sponge or Jagged1 siRNA. Cell proliferation, invasion and adhesion were detected. MI model was established in male SD rats using LAD ligation method and infected with recombinant adenovirus. The heart function and morphology was evaluated by ultrasonic and histological analysis. We found that TGF-β1 induced the up-regulation of miR-21 and down-regulation of Jagged1 in rat CFs. Luciferase assay showed that miR-21 targeted 3'-UTR of Jagged1 in ...
Source: J Cell Mol Med - May 28, 2018 Category: Molecular Biology Authors: Zhou XL, Xu H, Liu ZB, Wu QC, Zhu RR, Liu JC Tags: J Cell Mol Med Source Type: research

Suppressive effect of epigallocatechin-3-O-gallate on endoglin molecular regulation in myocardial fibrosis in vitro and in vivo.
In conclusion, epigallocatechin-3-O-gallate (EGCG) attenuated the endoglin expression and myocardial fibrosis by anti-inflammatory effect in vitro and in vivo, the novel suppressive effect was mediated through JNK/AP-1 pathway. PMID: 27306149 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - June 15, 2016 Category: Molecular Biology Authors: Lin CM, Chang H, Wang BW, Shyu KG Tags: J Cell Mol Med Source Type: research

Acute hyperglycaemia enhances oxidative stress and aggravates myocardial ischaemia/reperfusion injury: role of thioredoxin-interacting protein.
This study aimed to investigate whether or not hyperglycaemia enhances Txnip expression in myocardial ischaemia/reperfusion (MI/R) and consequently exacerbates MI/R injury. Rats were subjected to 30 min. of left coronary artery ligation followed by 4 hrs of reperfusion and treated with saline or high glucose (HG, 500 g/l, 4 ml/kg/h intravenously). In vitro study was performed on cultured rat cardiomyocytes subjected to simulated ischaemia/reperfusion (SI/R) and incubated with HG (25 mM) or normal glucose (5.6 mM) medium. In vivo HG infusion during MI/R significantly impaired cardiac function, aggravated myocardial in...
Source: J Cell Mol Med - January 11, 2013 Category: Molecular Biology Authors: Su H, Ji L, Xing W, Zhang W, Zhou H, Qian X, Wang X, Gao F, Sun X, Zhang H Tags: J Cell Mol Med Source Type: research