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Merck
  • Internalization of apoptotic cells during efferocytosis requires Mertk-mediated calcium influx.

Internalization of apoptotic cells during efferocytosis requires Mertk-mediated calcium influx.

Cell death & disease (2023-07-01)
Susumin Yang, Chanhyuk Min, Hyunji Moon, Byeongjin Moon, Juyeon Lee, Jaeseon Jeon, Hagyeong Kwon, Deokyun Jang, Daeho Park
摘要

Phagocytosis of apoptotic cells, called efferocytosis, requires calcium inside and outside of phagocytes. Due to its necessity, calcium flux is sophisticatedly modulated, and the level of intracellular calcium in phagocytes is ultimately elevated during efferocytosis. However, the role of elevated intracellular calcium in efferocytosis remains elusive. Here, we report that Mertk-mediated intracellular calcium elevation is necessary for internalization of apoptotic cells during efferocytosis. Drastic depletion of intracellular calcium abrogated the internalization step of efferocytosis by delaying phagocytic cup extension and closure. Especially, the defect of phagocytic cup closure for internalization of apoptotic cells was caused by impaired F-actin disassembly and the attenuated interaction of Calmodulin with myosin light chain kinase (MLCK), leading to diminished myosin light chain (MLC) phosphorylation. Genetic and pharmacological impairment of the Calmodulin-MLCK-MLC axis or Mertk-mediated calcium influx also resulted in inefficient efferocytosis due to a defect in internalization of the targets. Taken together, our observations imply that intracellular calcium elevation through Mertk-mediated calcium influx facilitates efferocytosis by inducing myosin II-mediated contraction and F-actin disassembly required for internalization of apoptotic cells.

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Sigma-Aldrich
ML-7, powder
Sigma-Aldrich
单克隆抗肌球蛋白轻链激酶 小鼠抗, clone K36, ascites fluid
Sigma-Aldrich
抗钙调蛋白抗体, Upstate®, from mouse