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Condition: Diabetes Type 1

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Total 127 results found since Jan 2013.

High glucose-induced hyperosmolarity contributes to COX-2 expression and angiogenesis: implications for diabetic retinopathy
Conclusions: Glucose-related hyperosmolarity seems to be able to promote angiogenesis and retinopathy through activation of TonEBP and possibly increasing expression of AQP1 and COX-2. Osmolarity signaling may be a target for therapy.
Source: Cardiovascular Diabetology - January 29, 2016 Category: Cardiology Authors: Rosalinda MadonnaGaia GiovannelliPamela ConfaloneFrancesca RennaYong-Jian GengRaffaele De Caterina Source Type: research

PKCδ inhibition normalizes the wound-healing capacity of diabetic human fibroblasts
Abnormal fibroblast function underlies poor wound healing in patients with diabetes; however, the mechanisms that impair wound healing are poorly defined. Here, we evaluated fibroblasts from individuals who had type 1 diabetes (T1D) for 50 years or more (Medalists, n = 26) and from age-matched controls (n = 7). Compared with those from controls, Medalist fibroblasts demonstrated a reduced migration response to insulin, lower VEGF expression, and less phosphorylated AKT (p-AKT), but not p-ERK, activation. Medalist fibroblasts were also functionally less effective at wound closure in nude mice. Activation of the δ isoform o...
Source: Journal of Clinical Investigation - January 26, 2016 Category: Biomedical Science Authors: Mogher Khamaisi, Sayaka Katagiri, Hillary Keenan, Kyoungmin Park, Yasutaka Maeda, Qian Li, Weier Qi, Thomas Thomou, Danielle Eschuk, Ana Tellechea, Aris Veves, Chenyu Huang, Dennis Paul Orgill, Amy Wagers, George L. King Source Type: research

Human umbilical cord matrix-derived stem cells exert trophic effects on {beta}-cell survival in diabetic rats and isolated islets RESEARCH ARTICLE
ABSTRACT Human umbilical cord matrix-derived stem cells (uMSCs), owing to their cellular and procurement advantages compared with mesenchymal stem cells derived from other tissue sources, are in clinical trials to treat type 1 (T1D) and type 2 diabetes (T2D). However, the therapeutic basis remains to be fully understood. The immunomodulatory property of uMSCs could explain the use in treating T1D; however, the mere immune modulation might not be sufficient to support the use in T2D. We thus tested whether uMSCs could exert direct trophic effects on β-cells. Infusion of uMSCs into chemically induced diabetic rats preve...
Source: DMM Disease Models and Mechanisms - December 4, 2015 Category: Biomedical Science Authors: Zhou, Y., Hu, Q., Chen, F., Zhang, J., Guo, J., Wang, H., Gu, J., Ma, L., Ho, G. Tags: RESEARCH ARTICLE Source Type: research

Silencing of angiotensin II type-1 receptor inhibits high glucose-induced epithelial-mesenchymal transition in human renal proximal tubular epithelial cells via inactivation of mTOR/p70S6K signaling pathway.
Abstract The epithelial-mesenchymal transition (EMT) plays a significant role in renal tubulointerstitial fibrosis (TIF), which is one of hallmark pathological feature of diabetic nephropathy (DN). Angiotensin II via its type-1 receptor AT1R is involved in the development of TIF. The purpose of our study was aimed to investigate the effect of silencing of AT1R on EMT and elucidate the possible mechanism underling these effects. EMT was induced by high glucose (HG) in human proximal tubular epithelial cell line HK-2 cells. The mRNA levels of AT1R were determined. The expression of AT1R was silenced by small interf...
Source: Biochemical and Biophysical Research communications - November 25, 2015 Category: Biochemistry Authors: Gong Q, Hou F Tags: Biochem Biophys Res Commun Source Type: research

TRAF2 mediates JNK and STAT3 activation in response to IL-1β and IFNγ and facilitates apoptotic death of insulin-producing β-cells
Publication date: Available online 22 November 2015 Source:Molecular and Cellular Endocrinology Author(s): Michala Cecilie Prause, Lukas Adrian Berchtold, Adriana Ibarra Urizar, Anne Mette Hyldgaard Trauelsen, Nils Billestrup, Thomas Mandrup-Poulsen, Joachim Størling Interleukin-1β (IL-1β) and interferon-γ (IFNγ) contribute to type 1 diabetes (T1D) by inducing β-cell death. Tumor necrosis factor (TNF) receptor-associated factor (TRAF) proteins are adaptors that transduce signaling from a variety of membrane receptors including cytokine receptors. We show here that IL-1β and IFNγ upregulate the expression o...
Source: Molecular and Cellular Endocrinology - November 23, 2015 Category: Endocrinology Source Type: research

Differential expression of endoplasmic reticulum stress-response proteins in different renal tubule subtypes of OVE26 diabetic mice.
Abstract Regulation of the endoplasmic reticulum (ER) stress-response pathway during the course of diabetes specifically in renal tubules is unclear. Since tubule cell dysfunction is critical to progression of diabetic nephropathy, this study analyzed markers of ER stress response and ER chaperones at different stages of diabetes and in different renal tubule subtypes of OVE26 type-1 diabetic mice. ER stress-response-induced chaperones GRP78, GRP94, and protein disulfide isomerase (PDI) were increased in isolated cortical tubules of older diabetic mice, while PDI was decreased in tubules of young diabetic mice. Im...
Source: Cell Stress and Chaperones - October 20, 2015 Category: Cytology Authors: Barati MT, Powell DW, Kechavarzi BD, Isaacs SM, Zheng S, Epstein PN, Cai L, Coventry S, Rane MJ, Klein JB Tags: Cell Stress Chaperones Source Type: research

Identification of transcripts regulated by CUG-BP, Elav-like family member 1 (CELF1) in primary embryonic cardiomyocytes by RNA-seq
Publication date: December 2015 Source:Genomics Data, Volume 6 Author(s): Yotam Blech-Hermoni, Andrea N. Ladd CUG-BP, Elav-like family member 1 (CELF1) is a multi-functional RNA binding protein that regulates pre-mRNA alternative splicing in the nucleus, as well as polyadenylation status, mRNA stability, and translation in the cytoplasm [1]. Dysregulation of CELF1 has been implicated in cardiomyopathies in myotonic dystrophy type 1 and diabetes [2–5], but the targets of CELF1 regulation in the heart have not been systematically investigated. We previously demonstrated that in the developing heart CELF1 expression is ...
Source: Genomics Data - August 25, 2015 Category: Genetics & Stem Cells Source Type: research

Pharmacological strategies for protection of extrahepatic islet transplantation.
This article gathers courses and conditions that lead to islet loss, from organ procurement through islet transplantation, with special emphasis on hypoxia, oxidative stress, and antigen non-specific inflammation, and reviews strategies using pharmacological agents that have shown effectiveness in protecting islets, including a new treatment approach utilizing siRNA. Pharmacological agents that support islet survival and promote β-cell proliferation are also included. Treatment of donor pancreata and/or islets with these agents should increase the effectiveness of islets transplanted into extrahepatic sites. Furthermore, ...
Source: Minerva Endocrinologica - June 4, 2015 Category: Endocrinology Tags: Minerva Endocrinol Source Type: research

Fibroblast growth factor 21 protects the heart from apoptosis in a diabetic mouse model via extracellular signal-regulated kinase 1/2-dependent signalling pathway
Conclusions/interpretation These results demonstrate that FGF21 prevents lipid- or diabetes-induced cardiac apoptosis by activating the ERK1/2–p38 MAPK–AMPK pathway. FGF21 may be a therapeutic target for the treatment of diabetes-related cardiac damage.
Source: Diabetologia - June 4, 2015 Category: Endocrinology Source Type: research

Diabetic neuropathy and the sensory neuron: new molecular targets (P2.010)
CONCLUSIONS: In this study, the increase of CWC22 and CBs expression might reflect an aberrant mRNA splicing demand in experimental diabetic neuropathy whereas loss of SMN may lead to sensory neuron degeneration. Taken together, our findings identify novel degenerative mechanisms that include two new molecular targets relevant to diabetic neuropathy. Supported by: CDA, CIHR, Denyse Lajoie-Lake fellowship.Disclosure: Dr. Kobayashi has nothing to disclose. Dr. Cheng has nothing to disclose. Dr. Cristiane has nothing to disclose. Dr. Zochodne has nothing to disclose.
Source: Neurology - April 8, 2015 Category: Neurology Authors: Kobayashi, M., Cheng, C., de la Hoz, C., Zochodne, D. Tags: Neuromuscular and Clinical Neurophysiology (EMG): Genetics Poster Discussion Session Source Type: research

Featured Article: Selective blockade of the OGF-OGFr pathway by naltrexone accelerates fibroblast proliferation and wound healing
Naltrexone (NTX) is an opioid receptor antagonist that acts at classical and non-classical opioid receptors including the opioid growth factor receptor (OGFr). Animal models of type 1 and type 2 diabetes, as well as normal rodents, have shown that topical NTX enhances the healing rates of corneal epithelium and full-thickness cutaneous wounds. The mechanism of this general opioid antagonist on growth, and in particular the specific receptor pathway involved, is not understood. Tissue culture studies using NIH 3T3 fibroblasts and primary rat auricular fibroblasts were established to evaluate growth following opioid receptor...
Source: Experimental Biology and Medicine - September 29, 2014 Category: Research Authors: Immonen, J. A., Zagon, I. S., McLaughlin, P. J. Tags: Anatomy & amp;amp; Pathology Source Type: research

Regulation of Inflammatory Phenotype in Macrophages by a Diabetes-Induced Long Non-coding RNA.
Abstract The mechanisms by which macrophages mediate the enhanced inflammation associated with diabetes complications are not completely understood. We used RNA-seq to profile the transcriptome of bone marrow macrophages isolated from diabetic db/db mice and identified 1648 differentially expressed genes compared to control db/+ mice. Data analyses revealed that diabetes promoted a pro-inflammatory, pro-fibrotic and dysfunctional alternatively activated macrophage phenotype possibly via transcription factors involved in macrophage function. Notably, diabetes altered levels of several long non-coding RNAs (lncRNAs)...
Source: Diabetes - July 9, 2014 Category: Endocrinology Authors: Reddy MA, Chen Z, Park JT, Wang M, Lanting L, Zhang Q, Bhatt K, Leung A, Wu X, Putta S, Sætrom P, Devaraj S, Natarajan R Tags: Diabetes Source Type: research

Cystathionine-{gamma}-lyase Activity in Type 1 Diabetes Molecular Bases of Disease
This study investigated the activities of cystathionine-γ-lyase (CSE, the enzyme that catalyzes H2S formation) in livers of type 1 diabetic (T1D) animals and in peripheral blood mononuclear cells (PBMC) isolated from T1D patients. T1D is associated with both hyperketonemia (acetoacetate and β-hydroxybutyrate) and hyperglycemia. This study also examined the role of hyperglycemia and hyperketonemia per se in decreased CSE activity using U937 monocytes and PBMC isolated from healthy subjects. Livers from streptozotocin-treated T1D rats demonstrated a significantly higher reactive oxygen species production, lower CSE protein...
Source: Journal of Biological Chemistry - April 25, 2014 Category: Chemistry Authors: Manna, P., Gungor, N., McVie, R., Jain, S. K. Tags: Metabolism Source Type: research

Epigallocatechin-3-Gallate Prevents Autoimmune-Associated Down-Regulation of p21 in Salivary Gland Cells Through a p53-Independent Pathway.
In conclusion, PCNA and p21 levels are altered inversely in the NOD model for SS and in HSG cells, and warrant further study as candidate new markers for salivary dysfunction associated with xerostomia. Induction of p21 by EGCG could provide clinically useful normalization of salivary glands by promoting differentiation and reducing PCNA levels. PMID: 24329914 [PubMed - as supplied by publisher]
Source: Inflammation and Allergy Drug Targets - December 10, 2013 Category: Allergy & Immunology Authors: Dickinson D, Yu H, Ohno S, Thomas C, Derossi S, Yat-Ho M, Yates N, Hahn E, Bisch F, Yamamoto T, Hsu S Tags: Inflamm Allergy Drug Targets Source Type: research

Tcf19 is a novel islet factor necessary for proliferation and survival in the INS-1 {beta}-cell line
Recently, a novel type 1 diabetes association locus was identified at human chromosome 6p31.3, and transcription factor 19 (TCF19) is a likely causal gene. Little is known about Tcf19, and we now show that it plays a role in both proliferation and apoptosis in insulinoma cells. Tcf19 is expressed in mouse and human islets, with increasing mRNA expression in nondiabetic obesity. The expression of Tcf19 is correlated with β-cell mass expansion, suggesting that it may be a transcriptional regulator of β-cell mass. Increasing proliferation and decreasing apoptotic cell death are two strategies to increase pancreatic ...
Source: AJP: Endocrinology and Metabolism - September 1, 2013 Category: Endocrinology Authors: Krautkramer, K. A., Linnemann, A. K., Fontaine, D. A., Whillock, A. L., Harris, T. W., Schleis, G. J., Truchan, N. A., Marty-Santos, L., Lavine, J. A., Cleaver, O., Kimple, M. E., Davis, D. B. Tags: Articles Source Type: research