Adiponectin Inhibits Toll-Like Receptor 4 Mediated Cardiac Inflammation and Injury

Jenke, Alexander; Wilk, Sabrina; Löbel, Madlen; Stehr, Jenny; Poller, Wolfgang; Eriksson, Urs; Schultheiss, Heinz‐Peter; Scheibenbogen, Carmen; Skurk, Carsten

doi:10.1016/s0735-1097(12)61551-4

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“…These effects include the mitigation of macrophage infiltration in the remnant kidney following partial nephrectomy ( 18 ), reduced endothelin-1 and plasminogen-1 production in the renal cortex of STZ-induced diabetic rats ( 55 ) and the reduction of NF-κB activity in angiotensin II-stimulated human renal tubular cells ( 15 ) and high-glucose-treated mesangial cells ( 50 ). The upstream mediators of the inflammatory response were further identified through the use of experimental autoimmune myocarditis models in mice, which indicated that TLR4 may have a critical role in mediating the anti-cardiac inflammation effect of adenovirus-mediated overexpression of APN ( 56 ). The results of the current study, in addition to those of previous studies ( 32 , 57 ), indicates potential cross-talk between the NLRP3-IL-1β pathway and APN signaling, in a TLR4-dependent manner.…”

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confidence: 99%

Uric acid upregulates the adiponectin‑adiponectin receptorï¿½1 pathway in renal proximal tubule epithelial cells

Yang

Xiao

et al. 2017

Mol Med Report

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Adiponectin (APN) is a protein hormone that is primarily derived from adipocytes. It can also be secreted by renal cells. Hypoadiponectinemia has been documented in patients with hyperuricemia, however, whether soluble uric acid (SUA) regulates the expression of APN and APN receptor 1 (AdipoR1) in renal proximal tubule epithelial cells (PTECs) remains to be elucidated. The present study investigated the expression of APN and AdipoR1 in cultured PTECs that were exposed to SUA through immunofluorescence and western blot analysis. In addition, Sprague-Dawley rats with oxonic acid-induced hyperuricemia (HUA) with or without febuxostat treatment were employed as an animal model to measure 24 h urine protein, serum creatinine, urea nitrogen, uric acid and homeostasis model assessment of insulin resistance. Renal pathology was evaluated using hematoxylin and eosin and immunohistochemical staining. APN and AdipoR1 expression in the renal cortex were evaluated by western blotting. The results demonstrated that, in PTECs, the expression of APN and AdipoR1 was constant and increased upon SUA exposure. Similar observations were made within the proximal renal tubules of rats, and the oxonic acid-induced increases in APN and AdipoR1 were offset by febuxostat treatment. Furthermore, SUA-treated PTECs exhibited an increase in the expression of NLR family pyrin domain-containing (NLRP) 3, which was dose-dependent. NLRP3 expression was also significantly increased in the renal cortex of HUA rats compared with control and febuxostat-treated rats. In conclusion, SUA enhanced the expression of APN and AdipoR1 in PTECs, which was associated with an increase in NLRP3 expression. The APN-AdipoR1 pathway was demonstrated to have an important role in in vitro and in vivo models of renal proximal tubule inflammatory injury. Therefore, this pathway may be a potential therapy target in urate nephropathy.

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