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Inhibition of high salt‐induced activation of NLRP3 inflammasome by mesenchymal stem cell transplantation in the renal medulla in Dahl S rats (1074.7)
Author(s) -
Li Xiaoxue,
Zhu Qing,
Conley Sabena,
Hu Junping,
Li PinLan,
Li Ningjun
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1074.7
Subject(s) - inflammasome , nalp3 , transplantation , medicine , endocrinology , kidney , mesenchymal stem cell , renal medulla , medullary cavity , chemistry , pathology , inflammation
Activation of NALP3 inflammasome has been shown to be involved in various renal pathological conditions. It remains unknown whether renal NALP3 inflammasome activation participates in the abnormal renal response to high salt diet in Dahl salt sensitive rats. In addition, whether inhibition of NALP3 inflammasome activation contributes to the renal protective actions of stem cells is not clear. The present study detected the response of NALP3 inflammasome to high salt intake and determined the effect of mesenchymal stem cell (MSC) transplantation on inflammasome activation. Immunostaining showed that 3 essential components of the NALP3 inflammasome, NALP3, ASC and caspase‐1, were all mainly present in distal tubules and collecting ducts. Interestingly, the renal medullary mRNA and protein levels of these inflammasome components were remarkably increased by 2‐4 fold in response to high salt intake in Dahl S rats, while remained no change in normal rats. High salt‐induced increases of renal medullar inflammasome were significantly blocked by MSC transplantation into the renal medulla compared with control cell in Dahl S rats. These data suggested that high salt‐induced activation of renal medullary inflammasome may contribute to the renal medullary dysfunction in Dahl S rats and that inhibition of inflammasome activation may be one of the mechanisms for the protective effects of stem cells in the renal medulla. Grant Funding Source : HL089563 and HL106042