Tsc1 controls the development and function of alveolar macrophages

被引：6

作者：

Chen, Song ^{[1
]}

Yang, Qiongmei ^{[2
]}

Liu, Jingru ^{[3
]}

Huang, Huifang ^{[3
]}

Shi, Mingxia ^{[2
]}

Feng, Xiaoming ^{[1
]}

机构：

[1] Chinese Acad Med Sci, Inst Hematol & Hosp Blood Dis, State Key Lab Expt Hematol, Peking Union Med Coll, 288 Nanjing Rd, Tianjin 300020, Peoples R China

[2] Kunming Med Univ, Affiliated Hosp 1, Hematol Res Ctr Yunnan Prov, Dept Hematol, Kunming 650032, Yunnan, Peoples R China

[3] Fujian Med Univ, Union Hosp, Cent Lab, Fuzhou 350001, Fujian, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2018年 / 498卷 / 03期

基金：

中国国家自然科学基金;

关键词：

Alveolar macrophages; Tsc1; Development; Proliferation; Function; TISSUE-RESIDENT MACROPHAGES; FETAL MONOCYTES; GM-CSF; ALLERGIC INFLAMMATION; HOMEOSTASIS; LUNG; DIFFERENTIATION; DISEASE; CELLS; MICE;

D O I：

10.1016/j.bbrc.2018.03.027

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. (C) 2018 Elsevier Inc. All rights reserved.

引用

页码：592 / 596

页数：5

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