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I型肌醇多磷酸-4-磷酸酶通过去磷酸化吞噬体磷脂酰肌醇（3,4）二磷酸负向调节吞噬作用。

Inositol Polyphosphate-4-Phosphatase Type I Negatively Regulates Phagocytosis via Dephosphorylation of Phagosomal PtdIns(3,4)P2.

作者信息

Nigorikawa Kiyomi, Hazeki Kaoru, Sasaki Junko, Omori Yumio, Miyake Mikiko, Morioka Shin, Guo Ying, Sasaki Takehiko, Hazeki Osamu

机构信息

Graduate School of Biomedical & Health Sciences, Hiroshima University, Hiroshima 734-8553, Japan.

Department of Pathology and Immunology, Akita University School of Medicine, Akita 010-8543, Japan.

出版信息

PLoS One. 2015 Nov 4;10(11):e0142091. doi: 10.1371/journal.pone.0142091. eCollection 2015.

DOI:10.1371/journal.pone.0142091
PMID:26535897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4633150/
Abstract

Phagocytosis is a highly conserved process whereby phagocytic cells engulf pathogens and apoptotic bodies. The present study focused on the role of inositol polyphosphate-4-phosphatase type I (Inpp4a) in phagocytosis. Raw264.7 cells that express shRNA against Inpp4a (shInpp4a cells) showed significantly increased phagocytic activity. The introduction of shRNA-resistant human Inpp4a abolished this increase. Macrophages from Inpp4a knockout mice showed similar increases in the phagocytic activity. Inpp4a was recruited to the phagosome membrane by a mechanism other than the direct interaction with Rab5. PtdIns(3,4)P2 increased on the phagosome of shInpp4a cells, while PtdIns(3)P significantly decreased. The results indicate that Inpp4a negatively regulates the phagocytic activity of macrophages as a member of the sequential dephosphorylation system that metabolizes phagosomal PtdIns(3,4,5)P3 to PtdIns(3)P.

摘要

吞噬作用是一个高度保守的过程，通过该过程吞噬细胞吞噬病原体和凋亡小体。本研究聚焦于I型肌醇多磷酸-4-磷酸酶（Inpp4a）在吞噬作用中的作用。表达针对Inpp4a的短发夹RNA的Raw264.7细胞（shInpp4a细胞）显示出吞噬活性显著增加。引入对短发夹RNA具有抗性的人Inpp4a可消除这种增加。来自Inpp4a基因敲除小鼠的巨噬细胞显示出类似的吞噬活性增加。Inpp4a通过一种不同于与Rab5直接相互作用的机制被募集到吞噬体膜上。在shInpp4a细胞的吞噬体上，磷脂酰肌醇-3,4-二磷酸（PtdIns(3,4)P2）增加，而磷脂酰肌醇-3-磷酸（PtdIns(3)P）显著减少。结果表明，Inpp4a作为将吞噬体磷脂酰肌醇-3,4,5-三磷酸（PtdIns(3,4,5)P3）代谢为PtdIns(3)P的顺序去磷酸化系统的一员，对巨噬细胞的吞噬活性起负调节作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/f6cd1726cba6/pone.0142091.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/ca5a1b29a632/pone.0142091.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/2d4aadcd5b86/pone.0142091.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/58062d9826fb/pone.0142091.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/1cfb32cf9a33/pone.0142091.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/c08faedd7906/pone.0142091.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/23a843a24af9/pone.0142091.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/1b3dfe0b9b3e/pone.0142091.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/f6cd1726cba6/pone.0142091.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/ca5a1b29a632/pone.0142091.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/2d4aadcd5b86/pone.0142091.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/58062d9826fb/pone.0142091.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/1cfb32cf9a33/pone.0142091.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/c08faedd7906/pone.0142091.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/23a843a24af9/pone.0142091.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/1b3dfe0b9b3e/pone.0142091.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d5/4633150/f6cd1726cba6/pone.0142091.g008.jpg

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