دورية أكاديمية
أعرض في EDS

Nuclear factor of activated T cells is activated in the endothelium of retinal microvessels in diabetic mice.

التفاصيل البيبلوغرافية
العنوان: Nuclear factor of activated T cells is activated in the endothelium of retinal microvessels in diabetic mice.
المؤلفون: Zetterqvist AV; Department of Clinical Sciences in Malmö, Lund University, 20502 Malmö, Sweden., Blanco F; Department of Clinical Sciences in Malmö, Lund University, 20502 Malmö, Sweden ; Departamento de Biofísica, Facultad de Medicina, Universidad de la República, 11800 Montevideo, Uruguay., Öhman J; Department of Clinical Sciences in Malmö, Lund University, 20502 Malmö, Sweden., Kotova O; Department of Clinical Sciences in Malmö, Lund University, 20502 Malmö, Sweden., Berglund LM; Department of Clinical Sciences in Malmö, Lund University, 20502 Malmö, Sweden., de Frutos Garcia S; Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA., Al-Naemi R; Department of Clinical Sciences in Malmö, Lund University, 20502 Malmö, Sweden., Wigren M; Department of Clinical Sciences in Malmö, Lund University, 20502 Malmö, Sweden., McGuire PG; Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA., Gonzalez Bosc LV; Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA., Gomez MF; Department of Clinical Sciences in Malmö, Lund University, 20502 Malmö, Sweden.
المصدر: Journal of diabetes research [J Diabetes Res] 2015; Vol. 2015, pp. 428473. Date of Electronic Publication: 2015 Mar 31.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Hindawi Limited Country of Publication: England NLM ID: 101605237 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2314-6753 (Electronic) NLM ISO Abbreviation: J Diabetes Res Subsets: MEDLINE
أسماء مطبوعة: Publication: <2019>-: London, United Kingdom : Hindawi Limited
Original Publication: Nasr City, Cairo : Hindawi Publishing Corporation, [2013]-
مواضيع طبية MeSH: Diabetes Mellitus, Experimental/*metabolism , Endothelium, Vascular/*metabolism , Microvessels/*metabolism , NFATC Transcription Factors/*metabolism , Retinal Vein/*metabolism, Animals ; Aorta/metabolism ; Calcium/metabolism ; Diabetes Complications ; Glucose Tolerance Test ; Hyperglycemia/metabolism ; Inflammation ; Intercellular Adhesion Molecule-1/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microcirculation ; Osteopontin/metabolism ; Permeability ; Pyrazoles/chemistry ; Retinal Vessels/pathology ; Signal Transduction
مستخلص: The pathogenesis of diabetic retinopathy (DR) remains unclear but hyperglycemia is an established risk factor. Endothelial dysfunction and changes in Ca2+ signaling have been shown to precede the onset of DR. We recently demonstrated that high extracellular glucose activates the Ca(2+)/calcineurin-dependent transcription factor NFAT in cerebral arteries and aorta, promoting the expression of inflammatory markers. Here we show, using confocal immunofluorescence, that NFAT is expressed in the endothelium of retinal microvessels and is readily activated by high glucose. This was inhibited by the NFAT blocker A-285222 as well as by the ectonucleotidase apyrase, suggesting a mechanism involving the release of extracellular nucleotides. Acute hyperglycemia induced by an IP-GTT (intraperitoneal glucose tolerance test) resulted in increased NFATc3 nuclear accumulation and NFAT-dependent transcriptional activity in retinal vessels of NFAT-luciferase reporter mice. In both Akita (Ins2(+/-) ) and streptozotocin- (STZ-) induced diabetic mice, NFAT transcriptional activity was elevated in retinal vessels. In vivo inhibition of NFAT with A-285222 decreased the expression of OPN and ICAM-1 mRNA in retinal vessels, prevented a diabetes driven downregulation of anti-inflammatory IL-10 in retina, and abrogated the increased vascular permeability observed in diabetic mice. Results identify NFAT signaling as a putative target for treatment of microvascular complications in diabetes.
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معلومات مُعتمدة: R01 HL088151 United States HL NHLBI NIH HHS
المشرفين على المادة: 0 (A 285222)
0 (Icam1 protein, mouse)
0 (NFATC Transcription Factors)
0 (Nfatc1 protein, mouse)
0 (Nfatc2 protein, mouse)
0 (Nfatc3 protein, mouse)
0 (Nfatc4 protein, mouse)
0 (Pyrazoles)
106441-73-0 (Osteopontin)
126547-89-5 (Intercellular Adhesion Molecule-1)
SY7Q814VUP (Calcium)
تواريخ الأحداث: Date Created: 20150429 Date Completed: 20151217 Latest Revision: 20190723
رمز التحديث: 20230127
مُعرف محوري في PubMed: PMC4396720
DOI: 10.1155/2015/428473
PMID: 25918731
قاعدة البيانات: MEDLINE
الوصف
تدمد:2314-6753
DOI:10.1155/2015/428473