DEL-1 is an Endogenous Senolytic Protein that Inhibits Senescence-Associated Bone Loss.

Jong-Hyung Lim, Kridtapat Sirisereephap, Hui Wang, Giulia Trimaglio, Kyoung-Jin Chung, Jonathan Korostoff, Tetsuhiro Kajikawa, Xiaofei Li, Meircurius D C Surboyo, Tomoki Maekawa, Triantafyllos Chavakis, George Hajishengallis

Department of Basic and Translational Sciences, Laboratory of Innate Immunity and Inflammation, Penn Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.Department of Basic and Translational Sciences, Laboratory of Innate Immunity and Inflammation, Penn Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. · pubmed

Paper

Abstract

Accumulation of senescent cells in the bone microenvironment, including bone marrow mesenchymal stromal cells (BM-MSCs), contributes to aging-related bone degeneration. Developmental endothelial locus-1 (DEL-1), the expression of which declines with old age is herein described as an endogenous secreted senolytic protein. DEL-1 promotes apoptosis of senescent BM-MSCs via a β3 integrin/CD73/adenosine/p38 mitogen-activated protein kinase (p38 MAPK)/B-cell lymphoma-2 (BCL-2) pathway, thereby leading to their clearance by macrophages. DEL-1-deficiency displays increased abundance of β3 integrin-rich CD73

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Research summary

DEL-1 is identified as a senolytic protein that promotes the clearance of senescent bone marrow mesenchymal stromal cells, potentially addressing a root cause of age-related bone degeneration. The paper is relevant as it explores a mechanism that could mitigate the effects of cellular senescence, a key factor in the aging process.

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