Role of allograft inflammatory factor‐1 in the regulation of inflammation and oxidative stress in primary peritoneal mesothelial cells

Abstract

Peritoneal dialysis (PD) is often used to treat patients with end stage renal disease, and its long-term complications include excessive inflammation and oxidative stress. Allograft inflammatory factor 1 (AIF-1), as a cytoplasmic protein, is originally identified from infiltrating macrophages, and it was associated with inflammation in the cells other than macrophages, such as endothelial cells and vascular smooth muscle cells. To clarify the molecular mechanisms of AIF-1-modulated pathological changes in the peritoneum during PD, we first detected the AIF-1 expression in peritoneal tissues from PD mice. Results revealed that the pro-fibrotic stimulation caused AIF-1 upregulation and triggered inflammation in peritoneal tissues, and that AIF-1 co-expressed with pancytokeratin (a marker of peritoneal mesothelial cells). We next treated primary mouse peritoneal mesothelial cells (pan-cytokeratin and intercellular adhesion molecule 1 positive cells) with 50 or 100 ng/mL recombinant AIF-1, and evaluated the direct effects of AIF-1 on these cells in vitro. We found that exogenous AIF-1 treatment induced inflammation and oxidative stress in mesothelial cells. Apart from the augmented IL-6 and TNF-a secretion, the level of ROS was upregulated and the activity of anti-oxidative SOD was reduced in cells exposed to AIF-1. Moreover, AIF-1 simulation triggered the activation of NF-kB pathway-enhanced the conversion of IkB to phosphorylated IkB and promoted the translocation of NF-kB p65 from cytoplasm into nucleus. Additionally, AIF-1-evoked inflammation in peritoneal mesothelial cells was attenuated by the addition of NF-kB inhibitor . In brief, this study provides us novel information to understand the molecular regulation mechanisms of AIF-1 in peritoneal fibrosis.

Integration of Transcriptomics and Proteomics Improves the Characterization of the Role of Mussel Gills in a Bacterial Waterborne Infection

“…Several pathogen recognition proteins that could recognize the bacteria and initiate this response were modulated in the transcriptome (Saco et al, 2020) and were identified but not modulated in the proteome: fibrinogen-like proteins or FREPs, different types of lectins, C1-q containing proteins, and allograft inflammatory factor-1 (AIF-1). AIF-1 is a pro-inflammatory cytokine implicated in immune activation in molluscs (De Zoysa et al, 2010;Zhang et al, 2013) and can activate the NF-kB response (Egaña-Gorroño et al, 2019;Zhou et al, 2019). Immune recognition and signaling terms dominated the modulated response in the transcriptomic study of the same infection model, but they were not modulated in the current proteomic approach.…”

The Effect of Allograft Inflammatory Factor-1 on Inflammation, Oxidative Stress, and Autophagy via miR-34a/ATG4B Pathway in Diabetic Kidney Disease

“…AIF-1 is an allograft inflammatory factor and plays an important role in regulating the inflammatory response. Our previous studies have confirmed that it is involved in the regulation of inflammatory reactions in various tissues and organs, including peritoneum [58], kidney [59], and blood vessels [37]. Although increasing evidence has confirmed that AIF-1 contributes to the pathogenesis of DKD [38,60], the exact mechanism is still unclear.…”

The Role of AIF-1 in the Aldosterone-Induced Vascular Calcification Related to Chronic Kidney Disease: Evidence From Mice Model and Cell Co-Culture Model

“…As the spatial conformation of AIF-1 is changed, which could activate several pathological processes, such as inflammation, apoptosis, and oxidative stress ( 25 , 26 ). It was reported that overexpression of AIF-1 in HUVEC could lead to endothelial cell inflammation and oxidative stress through the NF-κB signaling pathway ( 27 ). And the increased level of AIF-1 in VSMCs, induced by external stimulation, could also enhance the expression of cyclin and skeleton protein, thus leading to cell migration and phenotypic transformation, atherosclerosis, and vascular inflammation ( 16 ).…”