Τίτλος:
The family of 14-3-3 proteins and specifically 14-3-3σ are up-regulated during the development of renal pathologies
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Chronic kidney disease, the end result of most renal and some systemic diseases, is a common condition where renal function is compromised due to fibrosis. During renal fibrosis, calreticulin, a multifunctional chaperone of the endoplasmic reticulum (ER) is up-regulated in tubular epithelial cells (TECs) both in vitro and in vivo. Proteomic analysis of cultured TECs overexpressing calreticulin led to the identification of the family of 14-3-3 proteins as key proteins overexpressed as well. Furthermore, an increased expression in the majority of 14-3-3 family members was observed in 3 different animal models of renal pathologies: the unilateral ureteric obstruction, the nephrotoxic serum administration and the ischaemia-reperfusion. In all these models, the 14-3-3σ isoform (also known as stratifin) was predominantly overexpressed. As in all these models ischaemia is a common denominator, we showed that the ischaemia-induced transcription factor HIF1α is specifically associated with the promoter region of the 14-3-3σ gene. Finally, we evaluated the expression of the family of 14-3-3 proteins and specifically 14-3-3σ in biopsies from IgA nephropathy and membranous nephropathy patients. These results propose an involvement of 14-3-3σ in renal pathology and provide evidence for the first time that hypoxia may be responsible for its altered expression. © 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
Συγγραφείς:
Rizou, M.
Frangou, E.A.
Marineli, F.
Prakoura, N.
Zoidakis, J.
Gakiopoulou, H.
Liapis, G.
Kavvadas, P.
Chatziantoniou, C.
Makridakis, M.
Vlahou, A.
Boletis, J.
Vlahakos, D.
Goumenos, D.
Daphnis, E.
Iatrou, C.
Charonis, A.S.
Περιοδικό:
Journal of Cellular and Molecular Medicine
Εκδότης:
Blackwell Publishing Inc.
Λέξεις-κλειδιά:
calreticulin; complementary DNA; immunoglobulin A; messenger RNA; peptides and proteins; protein 14 3 3; stratifin; transcription factor HIF1 alpha; unclassified drug; calreticulin; calreticulin, human; exoribonuclease; HIF1A protein, human; hypoxia inducible factor 1alpha; isoenzyme; protein 14 3 3; SFN protein, human; tumor marker, animal experiment; animal model; animal tissue; Article; cell culture; chromatin immunoprecipitation; controlled study; densitometry; experimental glomerulonephritis; gene overexpression; homeostasis; housekeeping gene; human; human cell; hypoxia; immunoglobulin A nephropathy; immunohistochemistry; kidney fibrosis; kidney tubule epithelium; male; matrix assisted laser desorption ionization time of flight mass spectrometry; mouse; nephrectomy; nephrotoxicity; nonhuman; priority journal; protein expression; proteomics; real time polymerase chain reaction; reperfusion injury; upregulation; ureter obstruction; Western blotting; animal; C57BL mouse; cell line; chronic kidney failure; disease model; epithelium cell; fibrosis; gene expression regulation; genetics; kidney tubule; membranous glomerulonephritis; metabolism; pathology; procedures; promoter region; signal transduction, 14-3-3 Proteins; Animals; Biomarkers, Tumor; Calreticulin; Cell Line; Disease Models, Animal; Epithelial Cells; Exoribonucleases; Fibrosis; Gene Expression Regulation; Glomerulonephritis, IGA; Glomerulonephritis, Membranous; Humans; Hypoxia-Inducible Factor 1, alpha Subunit; Isoenzymes; Kidney Tubules; Male; Mice; Mice, Inbred C57BL; Promoter Regions, Genetic; Proteomics; Renal Insufficiency, Chronic; Reperfusion Injury; Signal Transduction; Ureteral Obstruction
