The family of 14‐3‐3 proteins and specifically 14‐3‐3σ are up‐regulated during the development of renal pathologies

Abstract

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.

Functional damage of endothelial progenitor cells is attenuated by 14‐3‐3‐n through inhibition of mitochondrial injury and oxidative stress

“…14‐3‐3 proteins belong to the family members of acidic intracellular proteins (Stevers et al, 2018). It was reported that 14‐3‐3 proteins could regulate the process of cell apoptosis (Rizou et al, 2018). For example, 14‐3‐3‐η could suppress apoptosis caused by ischemia and diabetes (Chen et al, 2007; Gurusamy et al, 2004).…”

Expression profile and prognostic value of SFN in human ovarian cancer

“…Stratifin (SFN) is a cell cycle checkpoint protein and a regulator of mitotic translation. To response the DNA damage, SFN often plays a role in inhibiting DNA errors during mitosis [4,5]. Generally, SFN is expressed at low levels on the nervous and reproductive systems, including in the cortex, retina, placenta, and ovary [6].…”

Identification of molecular biomarkers and pathways of NSCLC: insights from a systems biomedicine perspective

“…Stratifin (SFN) is a member of the 14-3-3 protein family, a highly preserved group of proteins participating by 7 isoforms. SFN is engaged with many significant biological functions like cell cycle apoptosis, regulation of signal transduction pathways, and cell proliferation [ 24 , 25 ].. SFN often plays a role in inhibiting DNA errors during mitosis to respond to DNA damage [ 26 ]. SFN had a high expression of malignant progression in early-stage lung adenocarcinoma [ 24 , 27 ].…”