Journal of cellular and molecular medicine, 2018-09, Vol.22 (9), p.4139-4149
2018
Details
- Autor(en) / Beteiligte
- Titel
- The family of 14‐3‐3 proteins and specifically 14‐3‐3σ are up‐regulated during the development of renal pathologies
- Ist Teil von
- Journal of cellular and molecular medicine, 2018-09, Vol.22 (9), p.4139-4149
- Ort / Verlag
- England: John Wiley & Sons, Inc
- Erscheinungsjahr
- 2018
- Link zum Volltext
- Quelle
- Free E-Journal (出版社公開部分のみ）
- Beschreibungen/Notizen
- 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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1582-1838eISSN: 1582-4934DOI: 10.1111/jcmm.13691Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6111864
- Format
- –
- Schlagworte
- 14-3-3 Proteins - genetics, 14-3-3 Proteins - metabolism, 14‐3‐3 proteins, 14‐3‐3σ, Animal models, Animals, Biomarkers, Tumor - genetics, Biomarkers, Tumor - metabolism, Calreticulin, Calreticulin - genetics, Calreticulin - metabolism, Cell Line, Disease Models, Animal, Endoplasmic reticulum, Epithelial cells, Epithelial Cells - metabolism, Epithelial Cells - pathology, Exoribonucleases - genetics, Exoribonucleases - metabolism, Fibrosis, Gene Expression Regulation, Glomerulonephritis, IGA - genetics, Glomerulonephritis, IGA - metabolism, Glomerulonephritis, IGA - pathology, Glomerulonephritis, Membranous - genetics, Glomerulonephritis, Membranous - metabolism, Glomerulonephritis, Membranous - pathology, HIF1α, Humans, Hypoxia, Hypoxia-Inducible Factor 1, alpha Subunit - genetics, Hypoxia-Inducible Factor 1, alpha Subunit - metabolism, IgA nephropathy, Immunoglobulin A, Ischemia, Isoenzymes - genetics, Isoenzymes - metabolism, Kidney Tubules - metabolism, Kidney Tubules - pathology, Male, Membranous nephropathy, Mice, Mice, Inbred C57BL, Original, Promoter Regions, Genetic, Proteins, Proteomics, Proteomics - methods, Renal function, Renal Insufficiency, Chronic - genetics, Renal Insufficiency, Chronic - metabolism, Renal Insufficiency, Chronic - pathology, renal pathologies, Reperfusion, Reperfusion Injury - genetics, Reperfusion Injury - metabolism, Reperfusion Injury - pathology, Signal Transduction, Stratifin, Ureter, Ureteral Obstruction - genetics, Ureteral Obstruction - metabolism, Ureteral Obstruction - pathology