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Condition: Diabetes

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Total 1499 results found since Jan 2013.

Negative regulation of Smad1 pathway and collagen IV expression by store-operated Ca2+ entry in glomerular mesangial cells.
Abstract Collagen IV (Col IV) is a major component of expanded glomerular extracellular matrix in diabetic nephropathy and Smad1 is a key molecule regulating Col IV expression in mesangial cells (MCs). The present study was conducted to determine if Smad1 pathway and Col IV protein abundance were regulated by store-operated Ca2+ entry (SOCE). In cultured human MCs, pharmacological inhibition of SOCE significantly increased the total amount of Smad1 protein. Activation of SOCE blunted high glucose-increased Smad1 protein content. Treating human MCs with angiotensin II at 1 µM for 15 min, or high glucose for 3 days...
Source: American Journal of Physiology. Renal Physiology - March 14, 2017 Category: Physiology Authors: Wu P, Ren Y, Ma Y, Wang Y, Jiang H, Chaudhari S, Davis ME, Zuckerman JE, Ma R Tags: Am J Physiol Renal Physiol Source Type: research

LNK deficiency aggregates palmitate-induced preadipocyte apoptosis.
Abstract LNK (SH2B3) is an intracellular adaptor protein that negatively regulates cellular proliferation or self-renewal of hematopoietic stem cells and some other progenitor cells. LNK is also recognized as a key regulator of insulin resistance and inflammatory responses in several tissues and organs. It is unknown the function of LNK in adipose tissue. We previously demonstrated that type 2 diabetes mellitus (T2DM) mouse model had elevated serum free fatty acids (FFAs) levels and increased preadipocyte apoptosis in visceral fat tissue, showing the occurrence of lipotoxicity. Here we show that, in contrast with ...
Source: Biochemical and Biophysical Research communications - May 16, 2017 Category: Biochemistry Authors: Du JY, Jin CC, Wang GH, Huang XQ, Cheng JD, Wen XJ, Zhao XM, Wang GL Tags: Biochem Biophys Res Commun Source Type: research

Reduced monocyte adhesion to aortae of diabetic plasminogen activator inhibitor-1 knockout mice
ConclusionThe findings suggest that PAI-1 is required for diabetes-induced monocyte adhesion via interactions with uPA/uPAR, and it also regulates TLR4 and TNF α expression in vascular EC. Inhibition of PAI-1 potentially reduces vascular inflammation under diabetic condition.
Source: Inflammation Research - May 26, 2017 Category: Research Source Type: research

MiR-31 is involved in the high glucose-suppressed osteogenic differentiation of human periodontal ligament stem cells by targeting Satb2.
In this study, we found that diabetic mice with increased miR-31 level in periodontal ligaments exhibited greater bone loss. In vitro, the high expression of miR-31 is associated with the impaired osteogenic differentiation ability of PDLSCs in high glucose environment. Furthermore, miR-31 inhibitors increased mineralized bone matrix formation and raised Runx2, Osx and OCN expression at both mRNA and protein levels. However, PDLSCs pretreated with miR-31 mimics decreased bone matrix formation and reduced Runx2, Osx and OCN expression level in high glucose microenvironment. Moreover, Satb2 was identified as a target of miR-...
Source: American Journal of Translational Research - June 2, 2017 Category: Research Tags: Am J Transl Res Source Type: research

Negative regulation of Smad1 pathway and collagen IV expression by store-operated Ca2+ entry in glomerular mesangial cells
Collagen IV (Col IV) is a major component of expanded glomerular extracellular matrix in diabetic nephropathy and Smad1 is a key molecule regulating Col IV expression in mesangial cells (MCs). The present study was conducted to determine if Smad1 pathway and Col IV protein abundance were regulated by store-operated Ca2+ entry (SOCE). In cultured human MCs, pharmacological inhibition of SOCE significantly increased the total amount of Smad1 protein. Activation of SOCE blunted high-glucose-increased Smad1 protein content. Treatment of human MCs with ANG II at 1 µM for 15 min, high glucose for 3 days, or TGF-β1 at ...
Source: AJP: Renal Physiology - June 4, 2017 Category: Urology & Nephrology Authors: Wu, P., Ren, Y., Ma, Y., Wang, Y., Jiang, H., Chaudhari, S., Davis, M. E., Zuckerman, J. E., Ma, R. Tags: RESEARCH ARTICLE 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

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

Effects of microRNA-211 on proliferation and apoptosis of lens epithelial cells by targeting SIRT1 gene in diabetic cataract mice.
Abstract Our study aimed at exploring the effects of microRNA-211 (miR-211) on the proliferation and apoptosis of lens epithelial cells in diabetic cataract mice by targeting NAD + -dependent histone deacetylase sirtulin 1 (SIRT1). Healthy male mice were assigned to normal and diabetic cataract groups. Blood glucose, lens turbidity and apoptosis were measured. Lens epithelial cells were classified into the normal, blank, negative control (NC), miR-211 mimics, miR-211 inhibitors, siRNA-SIRT1, and miR-211 inhibitors + siRNA-SIRT1 groups. MiR-211, Bcl-2, Bax, p53, and SIRT1 expressions of each group were detected. Ce...
Source: Bioscience Reports - July 5, 2017 Category: Biomedical Science Authors: Zeng K, Feng QG, Lin BT, Ma DH, Liu CM Tags: Biosci Rep Source Type: research

TXNDC5 Contributes to Rheumatoid Arthritis by Down ‐regulating IGFBP1 Expression
This study investigated whether TXNDC5 contributes to RA via the insulin signaling pathway. In the study, RA synovial fibroblast‐like cells (RASFs) transfected with an anti‐TXNDC5 small interfering RNA (siRNA) were analyzed with an Insulin Signaling Pathway RT2 Profiler PCR Array and an Insulin Resistance RT2 Profiler PCR Array. The PCR arrays detected significantly increased expression of insulin‐like growth factor binding protein 1 (IGFBP1) in RASFs with suppressed TXNDC5 expression. The result was verified using real‐time PCR and western blot analyses. Significantly elevated IGFBP1 expression and decreased IL‐...
Source: Clinical and Experimental Immunology - November 13, 2017 Category: Allergy & Immunology Authors: Jian Li, Bing Xu, Changsun Wu, Xinfeng Yan, Lei Zhang, Xiaotian Chang Tags: Original Article Source Type: research

Toll-Like Receptor 4 Reduces Occludin and Zonula Occludens 1 to Increase Retinal Permeability Both in vitro < b > < /b > and in vivo
In conclusion, these studies demonstrate that TLR4 in EC strongly regulates retinal permeability and neuronal and vasc ular changes following exposure to stressors such as I/R.J Vasc Res 2017;54:367-375
Source: Journal of Vascular Research - November 14, 2017 Category: Research Source Type: research

TXNDC5 Contributes to Rheumatoid Arthritis by Down-regulating IGFBP1 Expression.
This study investigated whether TXNDC5 contributes to RA via the insulin signaling pathway. In the study, RA synovial fibroblast-like cells (RASFs) transfected with an anti-TXNDC5 small interfering RNA (siRNA) were analyzed with an Insulin Signaling Pathway RT(2) Profiler PCR Array and an Insulin Resistance RT(2) Profiler PCR Array. The PCR arrays detected significantly increased expression of insulin-like growth factor binding protein 1 (IGFBP1) in RASFs with suppressed TXNDC5 expression. The result was verified using real-time PCR and western blot analyses. Significantly elevated IGFBP1 expression and decreased IL-6 secr...
Source: Clinical and Developmental Immunology - November 13, 2017 Category: Allergy & Immunology Authors: Li J, Xu B, Wu C, Yan X, Zhang L, Chang X Tags: Clin Exp Immunol Source Type: research

Slit2/Robo1 signaling is involved in angiogenesis of glomerular endothelial cells exposed to a diabetic-like environment
AbstractAbnormal angiogenesis plays a pathological role in diabetic nephropathy (DN), contributing to glomerular hypertrophy and microalbuminuria. Slit2/Robo1 signaling participates in angiogenesis in some pathological contexts, but whether it is involved in glomerular abnormal angiogenesis of early DN is unclear. The present study evaluated the effects of Slit2/Robo1 signaling pathway on angiogenesis of human renal glomerular endothelial cells (HRGECs) exposed to a diabetic-like environment or recombinant Slit2-N. To remove the effect of Slit2 derived from mesangial cells, human renal mesangial cells (HRMCs) grown in high...
Source: Angiogenesis - January 3, 2018 Category: Molecular Biology Source Type: research

Increased TRPC6 expression is associated with tubular epithelial cell proliferation and inflammation in diabetic nephropathy
Publication date: February 2018 Source:Molecular Immunology, Volume 94 Author(s): Yanqin Fu, Chongxian Wang, Dongming Zhang, Yaping Xin, Jun Li, Yuanyuan Zhang, Xiaojing Chu Although TRPC6 expression is shown to be significantly elevated in a rat model diabetic nephropathy (DN), its expression and role in human DN are unclear. We thus explored the role of TRPC6 in the pathophysiology of tubular epithelial cell injury following DN. HK-2 cells were cultured in a high-glucose medium to induce a DN cell model. Ad-TRPC6 and TRP6 siRNA were transfected to overexpress and knock down TRPC6. We found that TRPC6 expression was sign...
Source: Molecular Immunology - January 5, 2018 Category: Allergy & Immunology Source Type: research

Long Non-coding RNA BC168687 is Involved in TRPV1-mediated Diabetic Neuropathic Pain in Rats
Publication date: 15 March 2018 Source:Neuroscience, Volume 374 Author(s): Chenglong Liu, Congcong Li, Zeyu Deng, Errong Du, Changshui Xu Long noncoding RNAs (lncRNAs) participate in a diverse range of molecular and biological processes, and dysregulation of lncRNAs has been observed in the pathogenesis of various human diseases. We observed alterations in mechanical withdrawal thresholds (MWT) and thermal withdrawal latencies (TWL) in streptozotocin (STZ)-induced diabetic rats treated with small interfering RNA (siRNA) of lncRNA BC168687. We detected expression of transient receptor potential vanilloid type 1 (TRPV1) in ...
Source: Neuroscience - February 23, 2018 Category: Neuroscience Source Type: research

SIRT1 suppresses high glucose and palmitate-induced osteoclast differentiation via deacetylating p66Shc
In conclusion, this study confirms the role of DM in osteoclast differentiation in vitro. SIRT1 suppresses HG- and PA-induced osteoclast differentiation via p66Shc/ROS/NF-κB signaling.
Source: Molecular and Cellular Endocrinology - February 25, 2018 Category: Endocrinology Source Type: research