HSP60 Regulates Monosodium Urate Crystal-Induced Inflammation by Activating the TLR4-NF-κB-MyD88 Signaling Pathway and Disrupting Mitochondrial Function

Figure 1

HSP60 expression was upregulated in gout and MSU crystal-stimulated THP-1-derived macrophages. (a) HSP60 protein level in the plasma from patients with AGA (), IGA (), and HC () was detected by ELISA. (b) HSP60 protein level in PBMCs of patients with AGA, IGA, and HCs was measured by western blot (8 cases in each group). (c) Densitometry analysis of HSP60 protein level in PBMCs. (d–f) THP-1-derived macrophages were primed with LPS (100 ng/ml) for 1 h and then treated with different concentrations of MSU suspension for 12 h. (d) HSP60 secretion was analyzed by ELISA in THP-1-derived macrophages. (e) The relative mRNA expression of HSP60 in MSU crystal-stimulated THP-1-derived macrophages. (f) Representative images of double-labeling HSP60 and mitochondrial marker (MitoTracker) in MSU crystal-stimulated THP-1-derived macrophages. Scale bar: 20 μm. Blue shows nuclei staining with DAPI, quantification of immunofluorescence staining of HSP60 using Image J software. In comparison with absence of MSU crystal treatment and ^# in comparison with 25 μg/ml MSU crystal treatment.

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