Regulation of Mesenchymal Cell Fate by Transfer of Active Gasdermin-D via Monocyte-Derived Extracellular Vesicles

被引:4
|
作者
Sarkar, Anasuya [1 ,2 ,3 ,4 ]
Das, Srabani [1 ,2 ]
Bone, Hannah [1 ,2 ]
DeVengencie, Ivana [1 ,2 ]
Prasad, Jayendra [1 ,2 ]
Farkas, Daniela [1 ,2 ]
Londino, James D. [1 ,2 ]
Nho, Richard S. [1 ,2 ]
Rojas, Mauricio [1 ,2 ]
Horowitz, Jeffrey C. [1 ,2 ,3 ,4 ]
机构
[1] Ohio State Univ, Dept Internal Med cine, Div Pulm Crit Care & Sleep Med, Columbus, OH USA
[2] Ohio State Univ, Davis Heart & Lung Res Inst, Columbus, OH USA
[3] Ohio State Univ, 473 West 12th Ave, DHLRI 515, Columbus 43210, OH USA
[4] Ohio State Univ, 241 West 11th Ave, Suite 5085, Columbus, OH 43201 USA
来源
JOURNAL OF IMMUNOLOGY | 2023年 / 210卷 / 06期
基金
美国国家卫生研究院;
关键词
Top Reads; IDIOPATHIC PULMONARY-FIBROSIS; MEMBRANE MICROPARTICLES; LUNG FIBROSIS; APOPTOSIS; ACTIVATION; MECHANISMS; MYOFIBROBLASTS; PYROPTOSIS; INTERLEUKIN-1-BETA; INHIBITION;
D O I
10.4049/jimmunol.2200511
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Fibrosis is characterized by inappropriately persistent myofibroblast accumulation and excessive extracellular matrix deposition with the disruption of tissue architecture and organ dysfunction. Regulated death of reparative mesenchymal cells is critical for normal wound repair, but profibrotic signaling promotes myofibroblast resistance to apoptotic stimuli. A complex interplay between immune cells and structural cells underlies lung fibrogenesis. However, there is a paucity of knowledge on how these cell populations interact to orchestrate physiologic and pathologic repair of the injured lung. In this context, gasdermin-D (GsdmD) is a cytoplasmic protein that is activated following cleavage by inflammatory caspases and induces regulated cell death by forming pores in cell membranes. This study was undertaken to evaluate the impact of human (Thp-1) monocyte-derived extracellular vesicles and GsdmD on human lung fibroblast death. Our data show that active GsdmD delivered by monocyte-derived extracellular vesicles induces caspase-independent fibroblast and myofibroblast death. This cell death was partly mediated by GsdmD-independent induction of cellular inhibitor of apoptosis 2 (cIAP-2) in the recipient fibroblast population. Our findings, to our knowledge, define a novel paradigm by which inflammatory monocytes may orchestrate the death of mesenchymal cells in physiologic wound healing, illustrating the potential to leverage this mechanism to eliminate mesenchymal cells and facilitate the resolution of fibrotic repair. The Journal of Immunology, 2023, 210: 832-841.
引用
收藏
页码:832 / 841
页数:11
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