Open AccessGlobal Deletion of TSPO Does Not Affect the Viability and Gene Expression Profile
Author(s) -
Huaishan Wang,
Kangle Zhai,
Yingchao Xue,
Jia Yang,
Qi Yang,
Yi Fu,
Yu Hu,
Fang Liu,
Weiqing Wang,
Liyuan Cui,
Hui Chen,
Jianmin Zhang,
Wei He
Publication year - 2016
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0167307
Subject(s) - translocator protein , knockout mouse , biology , heterozygote advantage , viability assay , phenotype , gene expression , inflammation , immune system , population , wild type , microbiology and biotechnology , gene , cell , immunology , genetics , microglia , medicine , allele , environmental health , mutant
Translocator Protein (18kDa, TSPO) is a mitochondrial outer membrane transmembrane protein. Its expression is elevated during inflammation and injury. However, the function of TSPO in vivo is still controversial. Here, we constructed a TSPO global knockout (KO) mouse with a Cre-LoxP system that abolished TSPO protein expression in all tissues and showed normal phenotypes in the physiological condition. The birth rates of TSPO heterozygote (Het) x Het or KO x KO breeding were consistent with Mendel’s Law, suggesting a normal viability of TSPO KO mice at birth. RNA-seq analysis showed no significant difference in the gene expression profile of lung tissues from TSPO KO mice compared with wild type mice, including the genes associated with bronchial alveoli immune homeostasis. The alveolar macrophage population was not affected by TSPO deletion in the physiological condition. Our findings contradict the results of Papadopoulos , but confirmed Selvaraj ’s findings. This study confirms TSPO deficiency does not affect viability and bronchial alveolar immune homeostasis.