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Specialty: Molecular Biology
Condition: Diabetes

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Total 188 results found since Jan 2013.

miR ‐29 contributes to normal endothelial function and can restore it in cardiometabolic disorders
Abstract We investigated the role of microRNAs (miRNA) in endothelial dysfunction in the setting of cardiometabolic disorders represented by type 2 diabetes mellitus (T2DM). miR‐29 was dysregulated in resistance arterioles obtained by biopsy in T2DM patients. Intraluminal delivery of miR‐29a‐3p or miR‐29b‐3p mimics restored normal endothelium‐dependent vasodilation (EDVD) in T2DM arterioles that otherwise exhibited impaired EDVD. Intraluminal delivery of anti‐miR‐29b‐3p in arterioles from non‐DM human subjects or rats or targeted mutation of Mir29b‐1/a gene in rats led to impaired EDVD and exacerbatio...
Source: EMBO Molecular Medicine - January 1, 2018 Category: Molecular Biology Authors: Michael E Widlansky, David M Jensen, Jingli Wang, Yong Liu, Aron M Geurts, Alison J Kriegel, Pengyuan Liu, Rong Ying, Guangyuan Zhang, Marc Casati, Chen Chu, Mobin Malik, Amberly Branum, Michael J Tanner, Sudhi Tyagi, Kristie Usa, Mingyu Liang Tags: Research Article Source Type: research

Melatonin protects diabetic heart against ischemia-reperfusion injury, role of membrane receptor-dependent cGMP-PKG activation
This study was designed to determine the role of melatonin membrane receptors in melatonin's cardioprotective actions against diabetic MI/R injury with a focus on cGMP and its downstream effector PKG. Streptozotocin-induced diabetic Sprague-Dawley rats and high-glucose medium-incubated H9c2 cardiomyoblasts were utilized to determine the effects of melatonin against MI/R injury. Melatonin treatment preserved cardiac function and reduced oxidative damage and apoptosis. Additionally, melatonin increased intracellular cGMP level, PKGIα expression, p-VASP/VASP ratio and further modulated myocardial Nrf-2-HO-1 and MAPK signalin...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - December 6, 2017 Category: Molecular Biology Source Type: research

Autophagy inhibits high glucose induced cardiac microvascular endothelial cells apoptosis by mTOR signal pathway
AbstractCardiac microvascular endothelial cells (CMECs) dysfunction is an important pathophysiological event in the cardiovascular complications induced by diabetes. However, the underlying mechanism is not fully clarified. Autophagy is involved in programmed cell death. Here we investigated the potential role of autophagy on the CMECs injury induced by high glucose. CMECs were cultured in normal or high glucose medium for 6, 12 and 24  h respectively. The autophagy of CMECs was measured by green fluorescence protein (GFP)-LC3 plasmid transfection. Moreover, the apoptosis of CMEC was determined by flow cytometry. Furtherm...
Source: Apoptosis - August 20, 2017 Category: Molecular Biology Source Type: research

Advanced glycation end products induce the apoptosis of and inflammation in mouse podocytes through CXCL9-mediated JAK2/STAT3 pathway activation.
In this study, we found that the serum and urine levels of C-X-C motif chemokine ligand 9 (CXCL9) were significantly elevated in patients with DN compared with healthy controls. Based on an in vitro model of mouse podocyte injury, AGEs decreased the proliferation of podocytes and increased the expression of CXCL9 and C-X-C motif chemokine receptor 3 (CXCR3), and promoted the activation of signal transducer and activator of transcription 3 (STAT3). The knockdown of CXCL9 by the transfection of mouse podoyctes with specific siRNA significantly increased the proliferation and decreased the apoptosis of the podoyctes. ...
Source: International Journal of Molecular Medicine - August 11, 2017 Category: Molecular Biology Authors: Yu J, Wu H, Liu ZY, Zhu Q, Shan C, Zhang KQ Tags: Int J Mol Med Source Type: research

(-)-Epigallocatechin-3-gallate attenuates myocardial injury induced by ischemia/reperfusion in diabetic rats and in H9c2 cells under hyperglycemic conditions.
In this study, we aimed to examine the effects of EGCG on diabetic cardiomyopathy during myocardial ischemia/reperfusion (I/R) injury. EGCG (100 mg/kg/day) was administered at week 6 for 2 weeks to diabetic rats following the induction of type 1 diabetes by streptozotocin (STZ). At the end of week 8, the animals were subjected to myocardial I/R injury. The EGCG-elicited structural and functional effects were analyzed. Additionally, EGCG (20 µM) was administered for 24 h to cultured cardiac H9c2 cells under hyperglycemic conditions (30 mM glucose) prior to hypoxia/reoxygenation (H/R) challenge, and its effec...
Source: International Journal of Molecular Medicine - July 19, 2017 Category: Molecular Biology Authors: Wu Y, Xia ZY, Zhao B, Leng Y, Dou J, Meng QT, Lei SQ, Chen ZZ, Zhu J Tags: Int J Mol Med Source Type: research

Insulin regulates titin pre-mRNA splicing through the PI3K-Akt-mTOR kinase axis in a RBM20-dependent manner
Publication date: September 2017 Source:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Volume 1863, Issue 9 Author(s): Chaoqun Zhu, Zhiyong Yin, Bihua Tan, Wei Guo Titin, a giant sarcomeric protein, is largely responsible for the diastolic properties of the heart. It has two major isoforms, N2B and N2BA due to pre-mRNA splicing regulated mainly by a splicing factor RNA binding motif 20 (RBM20). Mis-splicing of titin pre-mRNA in response to external stimuli may lead to altered ratio of N2B to N2BA, and thus, impaired cardiac contractile function. However, little is known about titin alternative splicing ...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - July 8, 2017 Category: Molecular Biology Source Type: research

Nogo receptor knockdown and ciliary neurotrophic factor attenuate diabetic retinopathy in streptozotocin-induced diabetic rats.
Authors: Guo X, Liu X Abstract Diabetic retinopathy (DR) is a common complication of diabetes mellitus (DM). We investigated whether Nogo receptor (NgR) knockdown and ciliary neurotrophic factor (CNTF) treatment, either alone or in combination, ameliorated diabetic retinopathy (DR) in diabetic rat model. STZ‑induced diabetic rats were administrated for a total of 12 weeks with 3 µM siRNA (5 µl) once every 6 weeks and/or 1 µg CNTF weekly. The retinal tissues were excised. We measured cell number in ganglion cell layer (GCL) using H&E staining and cell apoptosis using TUNEL assay. Bax, Bcl‑2, Caspase...
Source: Molecular Medicine Reports - June 29, 2017 Category: Molecular Biology Tags: Mol Med Rep 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

Catalase ameliorates diabetes ‐induced cardiac injury through reduced p65/RelA‐ mediated transcription of BECN1
Abstract Catalase is an antioxidative enzyme that converts hydrogen peroxide (H2O2) 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 auto...
Source: Journal of Cellular and Molecular Medicine - June 23, 2017 Category: Molecular Biology Authors: Xu Wang, Youli Tao, Yewei Huang, Kungao Zhan, Mei Xue, Ying Wang, Dandan Ruan, Yangzhi Liang, Xiaozhong Huang, Jianjun Lin, Zhiwei Chen, Lingchun Lv, Santie Li, Gen Chen, Yang Wang, Ruijie Chen, Weitao Cong, Litai Jin Tags: Original Article Source Type: research

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

Overexpressing STAMP2 attenuates adipose tissue angiogenesis and insulin resistance in diabetic ApoE −/−/LDLR−/− mouse via a PPARγ/CD36 pathway
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. Histological and morphological analysis demonstrated that STAMP2 gene overexpression reduced adipocyte size, angiogenesis in epididymal and brown adipose tissues. On aortic ring assay, microvessels sprouting from aortas were significantly inhibited after STAMP2 gene overexpression. The cellular effe...
Source: Journal of Cellular and Molecular Medicine - June 19, 2017 Category: Molecular Biology Authors: Feng Wang, Lu Han, Ran ‐ran Qin, Yao‐yuan Zhang, Di Wang, Zhi‐Hao Wang, Meng‐Xiong Tang, Yun Zhang, Ming Zhong, Wei Zhang Tags: Original Article 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

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 (H2S) 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 H2S donor. Firstly, we demonstrated that high glucose and palmitate decreased H2S production and CSE expression in RAECs. Then, the ...
Source: Journal of Cellular and Molecular Medicine - June 13, 2017 Category: Molecular Biology Authors: Ning Liu, Jichao Wu, Linxue Zhang, Zhaopeng Gao, Yu Sun, Miao Yu, Yajun Zhao, Shiyun Dong, Fanghao Lu, Weihua Zhang Tags: Original Article Source Type: research

Role of PARP-1 as a novel transcriptional regulator of MMP-9 in diabetic retinopathy
Publication date: Available online 3 May 2017 Source:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease Author(s): Manish Mishra, Renu A. Kowluru In diabetes, matrix metalloproteinase-9 (MMP-9) is activated, which damages mitochondria, resulting in accelerated capillary cell apoptosis. Regulation of MMP-9 is controlled by multiple transcription factors including nuclear factor-kB (NF-kB) and activator protein-1 (AP-1). Binding of these transcription factors, however, can be regulated by poly(ADP-ribose) polymerase-1 (PARP-1), which forms a strong initiation complex at the promoter region and facilitates mult...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - May 4, 2017 Category: Molecular Biology 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 overexp...
Source: Journal of Cellular and Molecular Medicine - April 26, 2017 Category: Molecular Biology Authors: Mengsi Hu, Rong Wang, Xiaobing Li, Minghua Fan, Jiangong Lin, Junhui Zhen, Liqun Chen, Zhimei Lv Tags: Original Article Source Type: research