Key result
Silencing of JAB1 reduced extracellular matrix deposition and suppressed inflammation in high glucose-induced glomerular mesangial cells through down-regulation of ANGPTL2.
Why the study?
The role of c-Jun activation domain-binding protein 1 (JAB1) in diabetic nephropathy was not established.
Does silencing of JAB1 reduce inflammation and extracellular matrix deposition in high glucose-induced human glomerular mesangial cells?
Does silencing of JAB1 reduce inflammation and extracellular matrix deposition in high glucose-induced human glomerular mesangial cells?
Answers are grounded in this paper and cite their sources.
Silencing JAB1 attenuates high glucose-induced inflammation and extracellular matrix deposition in glomerular mesangial cells via ANGPTL2 down-regulation, highlighting a potential target for diabetic nephropathy.
Diabetic or hyperglycaemic conditions stimulate the inflammatory response, excessive accumulation of extracellular matrix, and result in glomerulosclerosis, a scarring process of diabetic nephropathy. c-Jun activation domain-binding protein 1 (JAB1) functions as a regulator of pathways involved in cellular apoptosis and proliferation. The role of JAB1 in diabetic nephropathy was investigated in this study. Firstly, glomerular mesangial cells (GMCs) were treated with high glucose, and high glucose conditions induced up-regulation of JAB1 in the GMCs. Moreover, IL-6, TNF-α, MCP-1, and IL-1β were also elevated in high glucose-induced GMCs. Secondly, silencing of JAB1 reduced the levels of IL-6, TNF-α, MCP-1, and IL-1β in high glucose-induced GMCs. In addition, silencing of JAB1 attenuated the high glucose-induced decrease of superoxide dismutase (SOD) and the increase of reactive oxygen species (ROS) and malondialdehyde (MDA). The increased TGF-β1, collagen I, collagen IV, and fibronectin levels in high glucose-induced GMCs were restored by knockdown of JAB1. Thirdly, angiopoietin-like protein 2 (ANGPTL2) expression was reduced by JAB1. Over-expression of ANGPTL2 weakened the JAB1 silence-induced decrease of IL-6, TNF-α, MCP-1, IL-1β, TGF-β1, collagen I, collagen IV, and fibronectin. In conclusion, silencing of JAB1 reduced extracellular matrix deposition and suppressed inflammation in high glucose-induced GMCs through down-regulation of ANGPTL2.
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Zhu et al. (2021) studied Diabetic nephropathy (in vitro model). JAB1 silencing (si-JAB1) vs. Negative control siRNA (si-NC) was evaluated on Inflammation and extracellular matrix deposition markers (p=<0.01). Silencing of JAB1 reduced extracellular matrix deposition and suppressed inflammation in high glucose-induced glomerular mesangial cells through down-regulation of ANGPTL2.
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