Contribution of High Mobility Group Box 1 to NicotineInduced Podocyte Injury
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abstract
High mobility group box 1 protein (HMGB1), a nuclear DNA binding protein is released under pathological conditions and locally act as one of the potent damageassociated molecular patterns (DAMPs) to produce tissue injury and chronic inflammation. However, it remains unknown whether HMGB1 is implicated in nicotineinduced podocyte injury. In the present study, we found that nicotine dosedependently increased the production of HMGB1 in cultured podocytes, and that HMGB1 binder and inhibitor, glycyrrhizin (Gly) completely blocked its release induced by nicotine. Immunofluorescence and western blot analysis showed that nicotine treatment significantly decreased the podocin expression compared to control cells. However, prior treatment with Gly attenuated the nicotineinduced podocin reduction. Furthermore, western blot analysis showed that nicotine treatment significantly increased the TLR4 expression compared to control cells but not in Gly treated cells. In addition, prior treatment with TLR4 siRNA transfection significantly attenuated the nicotineinduced podocin reduction in podocytes. Based on these results, it is concluded that HMGB1 is one of important mediators of nicotineinduced podocyte injury. HMGB1 may be a therapeutic target for treatment or prevention of glomerulosclerosis associated with smoking.Support or Funding InformationNational Institutes of Health (DK104031)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
