Uric acid‐induced endoplasmic reticulum stress triggers phenotypic change in rat glomerular mesangial cells. Issue 10 (19th September 2013)

• Record Type: Journal Article
• Authors: Li, Shasha; Zhao, Fei; Cheng, Shaoli; Wang, Xinyang; Hao, Yaning
• Is Part Of: Nephrology. Volume 18:Issue 10(2013)
• Page Start: 682
• Page End: 689
• Publication Date: 2013-09-19
• Subjects: Nephrology -- Periodicals; Kidneys -- Diseases -- Periodicals; Nephrologists -- Periodicals; 616.61; 616.61
• DOI: 10.1111/nep.12127
• Languages: English
• ISSNs: 1320-5358

Abstract

<abstract abstract-type="main"> <title>Abstract</title> <sec id="nep12127-sec-0001" sec-type="section"> <title>Aim</title> <p>The aim of this study was to explore the contribution and the mechanism of uric acid (UA) to phenotypic change in rat glomerular mesangial cells.</p> </sec> <sec id="nep12127-sec-0002" sec-type="section"> <title>Methods</title> <p>Rat glomerular mesangial cells (HBZY‐1) were exposed to UA (0.05 mmol/L to 0.4 mmol/L) for 24 h to 48 h. Subsequently, 4‐phenyl butyric acid (4‐PBA) (5 mg/dL) was added and 48 h incubation was performed. HBZY‐1 cells exposed to UA (0.4 mmol/L) were incubated for 48 h. After incubation, the cells were examined under an inverted microscope and transmission electron microscope to observe their morphologies and the expressions of α‐smooth muscle actin (α‐SMA), transforming growth factor‐β1 (TGF‐β1), fibronectin (FN), glucose regulated protein 78 (GRP78), and the protein disulfide isomerase (PDI) proteins and mRNA in the HBZY‐1 cells were measured by Western blot and reversed transcription‐polymerase chain reaction.</p> </sec> <sec id="nep12127-sec-0003" sec-type="section"> <title>Results</title> <p>HBZY‐1 cultured in UA showed evident morphological changes under transmission electron microscopy. The soluble UA stimulated the upregulation of the α‐SMA, TGF‐β1 and FN mRNA and proteins in a concentration‐ and time‐dependent manner. UA‐induced endoplasmic reticulum (ER) stress, as evidenced by the upregulation of the mRNA and protein expressions of GRP78 and PDI. However, the upregulation was reverted by 4‐PBA, an inhibitor of ER stress.</p> </sec> <sec id="nep12127-sec-0004" sec-type="section"> <title>Conclusions</title> <p>Uric acid induces phenotypic change in HBZY‐1 cells. ER stress plays a central role in UA‐induced phenotypic transformation <italic>in vitro</italic>. 4‐PBA may be beneficial in attenuating UA‐induced glomerular injury.</p> </sec> </abstract>