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Association of EGF Receptor and NLRs signaling with Cardiac Inflammation and Fibrosis in Mice Exposed to Fine Particulate Matter
Author(s) -
Jin Yuefei,
Wu Zhaoke,
Wang Na,
Duan Shuyin,
Wu Yongjun,
Wang Jing,
Wu Weidong,
Feng Feifei
Publication year - 2016
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21806
Subject(s) - inflammation , fibrosis , cardiac fibrosis , epidermal growth factor receptor , neuroinflammation , receptor , endocrinology , medicine , immunology , chemistry
ЄAmbient fine particulate matter (PM 2.5 ) could induce cardiovascular diseases (CVD), but the mechanism remains unknown. To investigate the roles of epidermal growth factor receptor (EGFR) and NOD‐like receptors (NLRs) in PM 2.5 ‐induced cardiac injury, we set up a BALB/c mice model of PM 2.5 ‐induced cardiac inflammation and fibrosis with intratracheal instillation of PM 2.5 suspension (4.0 mg/kg b.w.) for 5 consecutive days (once per day). After exposure, we found that mRNA levels of CXCL1, interleukin (IL)‐6, and IL‐18 were elevated, but interestingly, mRNA level of NLRP12 was significant decreased in heart tissue from PM 2.5 ‐induced mice compared with those of saline‐treated mice using real‐time PCR. Protein levels of phospho‐EGFR (Tyr1068), phospho‐Akt (Thr308), NLRP3, NF‐κB‐p52/p100, and NF‐κB‐p65 in heart tissue of PM 2.5 ‐exposed mice were all significantly increased using immunohistochemistry or Western blotting. Therefore, PM 2.5 exposure could induce cardiac inflammatory injury in mice, which may be involved with EGFR/Akt signaling, NLRP3, and NLRP12.