Pannexin-1 influences peritoneal cavity cell population but is not involved in NLRP3 inflammasome activation.
10.1007/s13238-013-2114-1
- Author:
Hongbin WANG
1
;
Yue XING
;
Liming MAO
;
Yi LUO
;
Lishan KANG
;
Guangxun MENG
Author Information
1. Unit of Innate Immunity, Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Shanghai 200025, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Carrier Proteins;
metabolism;
Cell Line;
Connexins;
antagonists & inhibitors;
deficiency;
genetics;
metabolism;
HEK293 Cells;
Humans;
Inflammasomes;
metabolism;
Macrophages;
cytology;
metabolism;
Mice;
Mice, Inbred C57BL;
NLR Family, Pyrin Domain-Containing 3 Protein;
Nerve Tissue Proteins;
antagonists & inhibitors;
deficiency;
genetics;
metabolism;
Peritoneal Cavity;
cytology;
Peritonitis;
chemically induced;
metabolism;
pathology;
RNA Interference;
RNA, Small Interfering;
metabolism;
Thioglycolates;
toxicity
- From:
Protein & Cell
2013;4(4):259-265
- CountryChina
- Language:English
-
Abstract:
Pannexin-1 (Panx1) forms nonselective large channel in cell plasma membrane and has been shown to be associated with NLRP3 inflammasome activation, ATP release and phagocytes recruitment. In the current study, by manipulation of Panx1 expression in human myeloid cells and application of Panx1 deficient mice, we failed to find a correlation between Panx1 and NLRP3 inflammasome activation, although an interaction between these two proteins was evident. However, in thioglycollate induced peritonitis, Panx1 deficient mice showed much more phagocytes infiltration. Further analyses showed that mice deficient for Panx1 exhibited enlarged F4/80(low)Gr1(-)Ly6C(-)cell population in the peritonea. Our study thus reveals an important role for Panx1 in regulation of peritoneal cell population and peritonitis development.
