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Source: J Cell Mol Med
Condition: Diabetes

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Total 22 results found since Jan 2013.

Overexpressing STAMP2 attenuates adipose tissue angiogenesis and insulin resistance in diabetic ApoE(-/-) /LDLR(-/-) mouse via a PPAR γ/CD36 pathway.
Overexpressing STAMP2 attenuates adipose tissue angiogenesis and insulin resistance in diabetic ApoE(-/-) /LDLR(-/-) mouse via a PPARγ/CD36 pathway. J Cell Mol Med. 2017 Jun 19;: Authors: Wang F, Han L, Qin RR, Zhang YY, Wang D, Wang ZH, Tang MX, Zhang Y, Zhong M, Zhang W Abstract The aim of this study was to investigate whether overexpression of STAMP2 improves insulin resistance by regulating angiogenesis in adipose tissues. The characteristics of diabetic mice were measured by serial metabolite and pathology tests. Samples were obtained from epididymal, subcutaneous and brown adipose tissues. Hist...
Source: J Cell Mol Med - June 19, 2017 Category: Molecular Biology Authors: Wang F, Han L, Qin RR, Zhang YY, Wang D, Wang ZH, Tang MX, Zhang Y, Zhong M, Zhang W Tags: J Cell Mol Med Source Type: research

Inhibition of P53/miR-34a improves diabetic endothelial dysfunction via activation of SIRT1.
Abstract Endothelial dysfunction contributes to diabetic macrovascular complications, resulting in high mortality. Recent findings demonstrate a pathogenic role of P53 in endothelial dysfunction, encouraging the investigation of the effect of P53 inhibition on diabetic endothelial dysfunction. Thus, high glucose (HG)-treated endothelial cells (ECs) were subjected to pifithrin-α (PFT-α)-a specific inhibitor of P53, or P53-small interfering RNA (siRNA), both of which attenuated the HG-induced endothelial inflammation and oxidative stress. Moreover, inhibition of P53 by PFT-α or P53-siRNA prohibited P53 acetylatio...
Source: J Cell Mol Med - February 22, 2019 Category: Molecular Biology Authors: Wu J, Liang W, Tian Y, Ma F, Huang W, Jia Y, Jiang Z, Wu H Tags: J Cell Mol Med Source Type: research

Endoplasmic reticulum stress-dependent autophagy inhibits glycated high-density lipoprotein-induced macrophage apoptosis by inhibiting CHOP pathway.
This study was designed to explore the inductive effect of glycated high-density lipoprotein (gly-HDL) on endoplasmic reticulum (ER) stress-C/EBP homologous protein (CHOP)-mediated macrophage apoptosis and its relationship with autophagy. Our results showed that gly-HDL caused macrophage apoptosis with concomitant activation of ER stress pathway, including nuclear translocation of activating transcription factor 6, phosphorylation of protein kinase-like ER kinase (PERK) and eukaryotic translation initiation factor 2α, and CHOP up-regulation, which were inhibited by 4-phenylbutyric acid (PBA, an ER stress inhibitor) and th...
Source: J Cell Mol Med - February 12, 2019 Category: Molecular Biology Authors: Tian H, Li Y, Kang P, Wang Z, Yue F, Jiao P, Yang N, Qin S, Yao S Tags: J Cell Mol Med Source Type: research

Diabetes aggravates myocardial ischaemia reperfusion injury via activating Nox2-related programmed cell death in an AMPK-dependent manner.
This study was designed to expose the crosstalk between oxidative stress and AMPK, a vital molecule that controls biological energy metabolism, in myocardial ischaemia reperfusion injury (I/RI) in diabetic rats. Diabetes was stimulated in rats using streptozotocin injection. Rats were separated on random into control, control + I/R, Diabetes, Diabetes + I/R, Diabetes + I/R + N-acetylcysteine and Diabetes + I/R + Vas2870 groups. Myocardial infarct size was determined, and the predominant Nox family isoforms were analysed. In vitro, the H9C2 cells were administered excess glucose and exposed to hypoxia/reoxygenat...
Source: J Cell Mol Med - April 28, 2020 Category: Molecular Biology Authors: Wang C, Zhu L, Yuan W, Sun L, Xia Z, Zhang Z, Yao W Tags: J Cell Mol Med Source Type: research

Tacrolimus ameliorates tubulointerstitial inflammation in diabetic nephropathy via inhibiting the NFATc1/TRPC6 pathway.
Abstract Tubulointerstitial inflammation is crucial for the progression of diabetic nephropathy (DN), and tubular cells act as a driving force in the inflammatory cascade. Emerging data suggested that tacrolimus (TAC) ameliorates podocyte injury and macrophage infiltration in streptozotocin (STZ) mice. However, the effect of TAC on tubulointerstitial inflammation remains unknown. We found that albuminuria and tubulointerstitial damage improved in db/db mice treated with TAC. Macrophage infiltration and expression of IL-6, TNF-α, fibronectin, collagen 1 and cleaved caspase 3 were inhibited as well. In addition, th...
Source: J Cell Mol Med - August 10, 2020 Category: Molecular Biology Authors: Zhang S, Wang H, Liu Y, Yang W, Liu J, Han Y, Liu Y, Liu F, Sun L, Xiao L Tags: J Cell Mol Med Source Type: research

Resveratrol-enhanced autophagic flux ameliorates myocardial oxidative stress injury in diabetic mice.
Abstract Autophagic dysfunction is observed in diabetes mellitus. Resveratrol has a beneficial effect on diabetic cardiomyopathy. Whether the resveratrol-induced improvement in cardiac function in diabetes is via regulating autophagy remains unclear. We investigated the mechanisms underlying resveratrol-mediated protection against heart failure in diabetic mice, with a focus on the role of sirtuin 1 (SIRT1) in regulating autophagic flux. Diabetic cardiomyopathy in mice was induced by streptozotocin (STZ). Long-term resveratrol treatment improved cardiac function, ameliorated oxidative injury and reduced apoptosis ...
Source: J Cell Mol Med - June 1, 2014 Category: Molecular Biology Authors: Wang B, Yang Q, Sun YY, Xing YF, Wang YB, Lu XT, Bai WW, Liu XQ, Zhao YX Tags: J Cell Mol Med Source Type: research

Lin28a protects against cardiac ischaemia/reperfusion injury in diabetic mice through the insulin-PI3K-mTOR pathway.
This study indicates that lin28a overexpression reduces IS, improves cardiac function, decreases cardiomyocyte apoptosis index and alleviates cardiomyocyte mitochondria impairment after cardiac I/R injury in diabetic mice. The mechanism responsible for the effects of lin28a is associated with the insulin-PI3K-mTOR dependent pathway. PMID: 25688987 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - February 16, 2015 Category: Molecular Biology Authors: Zhang M, Sun D, Li S, Pan X, Zhang X, Zhu D, Li C, Zhang R, Gao E, Wang H Tags: J Cell Mol Med Source Type: research

Long non-coding RNA MALAT1 regulates hyperglycaemia induced inflammatory process in the endothelial cells.
Abstract To examine whether the long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is altered in the endothelial cells in response to glucose and the significance of such alteration. We incubated human umbilical vein endothelial cells with media containing various glucose levels. We found an increase in MALAT1 expression peaking after 12 hrs of incubation in high glucose. This increase was associated with parallel increase in serum amyloid antigen 3 (SAA3), an inflammatory ligand and target of MALAT1 and was further accompanied by increase in mRNAs and proteins of inflamm...
Source: J Cell Mol Med - March 19, 2015 Category: Molecular Biology Authors: Puthanveetil P, Chen S, Feng B, Gautam A, Chakrabarti S Tags: J Cell Mol Med Source Type: research

LncRNA MALAT1 is dysregulated in diabetic nephropathy and involved in high glucose-induced podocyte injury via its interplay with β-catenin.
In this study, we found that MALAT1 levels were increased in kidney cortices from C57BL/6 mice with streptozocin (STZ)-induced diabetic nephropathy, and dynamically regulated in cultured mouse podocytes stimulated with high glucose, which showed a trend from rise to decline. The decline of MALAT1 levels was accompanied with β-catenin translocation to the nuclei and enhanced expression of serine/arginine splicing factor 1 (SRSF1), a MALAT1 RNA-binding protein. Further we showed early interference with MALAT1 siRNA partially restored podocytes function and prohibited β-catenin nuclear accumulation and SRSF1 overexpression....
Source: J Cell Mol Med - April 26, 2017 Category: Molecular Biology Authors: Hu M, Wang R, Li X, Fan M, Lin J, Zhen J, Chen L, Lv Z Tags: J Cell Mol Med Source Type: research

Hydrogen Sulphide modulating mitochondrial morphology to promote mitophagy in endothelial cells under high-glucose and high-palmitate.
Abstract Endothelial cell dysfunction is one of the main reasons for type II diabetes vascular complications. Hydrogen sulphide (H2 S) has antioxidative effect, but its regulation on mitochondrial dynamics and mitophagy in aortic endothelial cells under hyperglycaemia and hyperlipidaemia is unclear. Rat aortic endothelial cells (RAECs) were treated with 40 mM glucose and 200 μM palmitate to imitate endothelium under hyperglycaemia and hyperlipidaemia, and 100 μM NaHS was used as an exogenous H2 S donor. Firstly, we demonstrated that high glucose and palmitate decreased H2 S production and CSE expression in RAECs...
Source: J Cell Mol Med - June 13, 2017 Category: Molecular Biology Authors: Liu N, Wu J, Zhang L, Gao Z, Sun Y, Yu M, Zhao Y, Dong S, Lu F, Zhang W Tags: J Cell Mol Med Source Type: research

Catalase ameliorates diabetes-induced cardiac injury through reduced p65/RelA- mediated transcription of BECN1.
Abstract Catalase is an antioxidative enzyme that converts hydrogen peroxide (H2 O2 ) produced by superoxide dismutase from highly reactive superoxide (O2(-) ) to water and oxygen molecules. Although recent findings demonstrate that catalase, autophagy and the nuclear factor κB (NF-κB) signalling pathway are centrally involved in diabetic cardiomyopathy (DCM), the interplay between the three has not been fully characterized. Thus, the mechanism responsible for catalase-mediated protection against heart injury in diabetic mice was investigated in this study, as well as the role of NF-κB-p65 in the regulation of ...
Source: J Cell Mol Med - June 23, 2017 Category: Molecular Biology Authors: Wang X, Tao Y, Huang Y, Zhan K, Xue M, Wang Y, Ruan D, Liang Y, Huang X, Lin J, Chen Z, Lv L, Li S, Chen G, Wang Y, Chen R, Cong W, Jin L Tags: J Cell Mol Med Source Type: research

Allopurinol reduces oxidative stress and activates Nrf2/p62 to attenuate diabetic cardiomyopathy in rats.
Abstract Allopurinol (ALP) attenuates oxidative stress and diabetic cardiomyopathy (DCM), but the mechanism is unclear. Activation of nuclear factor erythroid 2-related factor 2 (Nrf2) following the disassociation with its repressor Keap1 under oxidative stress can maintain inner redox homeostasis and attenuate DCM with concomitant attenuation of autophagy. We postulated that ALP treatment may activate Nrf2 to mitigate autophagy over-activation and consequently attenuate DCM. Streptozotocin-induced type 1 diabetic rats were untreated or treated with ALP (100 mg/kg/d) for 4 weeks and terminated after heart functi...
Source: J Cell Mol Med - December 18, 2019 Category: Molecular Biology Authors: Luo J, Yan D, Li S, Liu S, Zeng F, Cheung CW, Liu H, Irwin MG, Huang H, Xia Z Tags: J Cell Mol Med Source Type: research

Inhibition of PHLPP1 ameliorates cardiac dysfunction via activation of the PI3K/Akt/mTOR signalling pathway in diabetic cardiomyopathy.
CONCLUSION: Our study indicated that PHLPP1 inhibition alleviated cardiac dysfunction via activating the PI3K/Akt/mTOR signalling pathway in DCM. Therefore, PHLPP1 may be a novel therapeutic target for human DCM. PMID: 32150791 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - March 8, 2020 Category: Molecular Biology Authors: Zhang M, Wang X, Liu M, Liu D, Pan J, Tian J, Jin T, Xu Y, An F Tags: J Cell Mol Med Source Type: research

Knockout of AKAP150 improves impaired BK channel-mediated vascular dysfunction through the Akt/GSK3 β signalling pathway in diabetes mellitus.
In this study, we investigated the regulation of impaired BK channel-mediated vascular dysfunction in diabetes mellitus. Using AKAP150 null mice (AKAP150-/- ) and wild-type (WT) control mice (C57BL/6J), diabetes was induced by intraperitoneal injection of streptozotocin. We found that knockout of AKAP150 reversed vascular remodelling and fibrosis in mice with diabetes and in AKAP150-/- diabetic mice. Impaired Akt/GSK3β signalling contributed to decreased BK-β1 expression in aortas from diabetic mice, and the silencing of AKAP150 increased Akt phosphorylation and BK-β1 expression in MOVAS cells treated with HG medium. Th...
Source: J Cell Mol Med - March 11, 2020 Category: Molecular Biology Authors: Zhu YR, Jiang XX, Ye P, Wang ZM, Zheng Y, Liu Z, Chen SL, Zhang DM Tags: J Cell Mol Med Source Type: research

HDAC6-mediated α-tubulin deacetylation suppresses autophagy and enhances motility of podocytes in diabetic nephropathy.
Abstract Histone deacetylase 6 (HDAC6) is the specific subtype of HDACs which preferentially located in the cytoplasm, and is crucial in insulin signalling. However, the role of HDAC6 in type 2 diabetic nephropathy (DN) remains undefined. In current study, we observed that HDAC6 was markedly activated in the kidneys of type 2 diabetic patients and db/db mice with albuminuria, along with the advanced glycation end products (AGE)-treated podocytes. Selective inhibition of HDAC6 activity protected kidneys from hyperglycaemia in db/db mice. Notably, overexpressing HDAC6 inhibited autophagy and promoted motility aside ...
Source: J Cell Mol Med - September 3, 2020 Category: Molecular Biology Authors: Liang T, Qi C, Lai Y, Xie J, Wang H, Zhang L, Lin T, Jv M, Li J, Wang Y, Zhang Y, Chen Z, Qiu X, Li R, Li Z, Ye Z, Liu S, Liang X, Shi W, Wang W Tags: J Cell Mol Med Source Type: research