کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8962225 | 1646548 | 2018 | 17 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Autocrine GABA signaling distinctively regulates phenotypic activation of mouse pulmonary macrophages
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
In response to micro-environmental cues such as microbial infections or T-helper 1 and 2 (TH1 and TH2) cytokines, macrophages (MÏs) develop into M1- or M2-like phenotypes. Phenotypic polarization/activation of MÏs are also essentially regulated by autocrine signals. Type-A γ-aminobutyric acid receptor (GABAAR)-mediated autocrine signaling is critical for phenotypic differentiation and transformation of various cell types. The present study explored whether GABAAR signaling regulates lung MÏ (LMÏ) phenotypic activation under M1/TH1 and M2/TH2 environments. Results showed that GABAAR subunits were expressed by primary LMÏ of mice and the mouse MÏ cell line RAW264.7. The expression levels of GABAAR subunits in mouse LMÏs and RAW264.7 cells decreased or increased concurrently with classical (M1) or alternative (M2) activation, respectively. Moreover, activation or blockade of GABAARs distinctively influenced the phenotypic characteristics of MÏ. These results suggested that microenvironments leading to LMÏ phenotypic polarization concurrently modulates autocrine GABA signaling and its role in MÏ activation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Immunology - Volume 332, October 2018, Pages 7-23
Journal: Cellular Immunology - Volume 332, October 2018, Pages 7-23
نویسندگان
Luan Januzi, Jacob W. Poirier, Matthew J.E. Maksoud, Yun-Yan Xiang, Rudolf A.W. Veldhuizen, Sean E. Gill, Sean P. Cregan, Haibo Zhang, Gregory A. Dekaban, Wei-Yang Lu,