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Accelerated receptor shedding inhibits kidney injury molecule-1 (KIM-1)-mediated efferocytosis

传出细胞增多 细胞生物学 细胞凋亡 炎症 急性肾损伤 吞噬作用 化学 医学 免疫学 癌症研究 生物 巨噬细胞 内科学 生物化学 体外
作者
R. Gandhi,James Yi,Jihyen Ha,Hang Shi,Ola Z. Ismail,Sahra Nathoo,Joseph V. Bonventre,Xizhong Zhang,Lakshman Gunaratnam
出处
期刊:American Journal of Physiology-renal Physiology [American Physical Society]
卷期号:307 (2): F205-F221 被引量:35
标识
DOI:10.1152/ajprenal.00638.2013
摘要

Efficient clearance of apoptotic cells (efferocytosis) prevents inflammation and permits repair following tissue injury. Kidney injury molecule-1 (KIM-1) is a receptor for phosphatidylserine, an "eat-me" signal exposed on the surface of apoptotic cells that marks them for phagocytic clearance. KIM-1 is upregulated on proximal tubule epithelial cells (PTECs) during ischemic acute kidney injury (AKI), enabling efferocytosis by surviving PTECs. KIM-1 is spontaneously cleaved at its ectodomain region to generate a soluble fragment that serves a sensitive and specific biomarker for AKI, but the biological relevance of KIM-1 shedding is unknown. Here, we sought to determine how KIM-1 shedding might regulate efferocytosis. Using cells that endogenously and exogenously express KIM-1, we found that hydrogen peroxide-mediated oxidative injury or PMA treatment accelerated KIM-1 shedding in a dose-dependent manner. KIM-1 shedding was also accelerated when apoptotic cells were added. Accelerated shedding or the presence of excess soluble KIM-1 in the extracellular milieu significantly inhibited efferocytosis. We also identified that TNF-α-converting enzyme (TACE or ADAM17) mediates both the spontaneous and PMA-accelerated shedding of KIM-1. While accelerated shedding inhibited efferocytosis, we found that spontaneous KIM-1 cleavage does not affect the phagocytic efficiency of PTECs. Our results suggest that KIM-1 shedding is accelerated by worsening cellular injury, and excess soluble KIM-1 competitively inhibits efferocytosis. These findings may be important in AKI when there is severe cellular injury.
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