The perturbed membrane of cells undergoing apoptosis is susceptible to type II secretory phospholipase A2 to liberate arachidonic acid

Atsumi, Gen‐ichi; Murakami, Makoto; Tajima, Masae; Shimbara, Satoko; Hara, Naomi; Kudo, Ichiro

doi:10.1016/s0005-2760(97)00082-9

Cited by 101 publications

(78 citation statements)

References 56 publications

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“…Nonetheless, bidirectional interaction between cPLA 2 and sPLA 2 s may represent a general action leading to optimal AA release in mammalian cells, and the role of sPLA 2 s could be to amplify the primary responses initiated by intracellular cPLA 2 . It has been reported that sPLA 2 -IIA effectively hydrolyzes membrane vesicles shed from activated platelets (80) and the membranes of cells undergoing apoptosis (76). These observations imply diverse patterns of actions for sPLA 2 .…”

Section: Discussionmentioning

confidence: 89%

“…It would be of interest to test whether sPLA 2 -IIC has some function in the sperm acrosome reaction and the fusion of sperm and oocyte plasma membranes (74,75), in which PLA 2 is believed to play a key role. Cells undergoing apoptosis in such tissues are an attractive candidate for the sPLA 2 -IIC target, since we have recently shown that hydrolysis of apoptotic cell membranes by sPLA 2 -IIA does not require anchoring to proteoglycans on the plasma membranes (76).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Functions of Five Distinct Mammalian Phospholipase A2s in Regulating Arachidonic Acid Release

Murakami¹,

Shimbara²,

Kambe³

et al. 1998

Journal of Biological Chemistry

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352

267

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

The Functions of Five Distinct Mammalian Phospholipase A2s in Regulating Arachidonic Acid Release

Murakami¹,

Shimbara²,

Kambe³

et al. 1998

Journal of Biological Chemistry

Self Cite

352

267

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“…In fact the recent demonstration that cells undergoing apoptosis are more susceptible to membrane hydrolysis by rodent group IIa PLA 2 (54) and the fact that the anionic lipid phosphatidylserine moves to the extracellular face of the plasma membrane during apoptosis (55) is consistent with a membrane component-dependent augmentation of group IIa PLA 2 catalysis. Interestingly mouse group IIa PLA 2 mutant KE4 was as potent as wild type in eliciting arachidonate released from apoptotic cells, and it was suggested that heparan sulfate binding is not required for PLA 2 activity on apoptotic cells (54). A likely explanation in light of the present results is as follows.…”

Section: Basic Clusters Of the Interfacial Binding Site Are Most Impomentioning

confidence: 81%

Action of Human Group IIa Secreted Phospholipase A2on Cell Membranes

Koduri¹,

Baker²,

Snitko³

et al. 1998

Journal of Biological Chemistry

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Human group IIa phospholipase A 2 (hIIa-PLA2) is a highly basic protein that is secreted from a number of cells during inflammation and may play a role in arachidonate liberation and in destruction of invading bacteria. It has been proposed that rodent group IIa PLA 2 is anchored to cell surfaces via attachment to heparan sulfate proteoglycan and that this interaction facilitates lipolysis. hIIa-PLA2 contains 13 lysines, 2 histidines, and 10 arginines that fall into 10 clusters. A panel of 26 hIIa-PLA2 mutants were prepared in which 1-4 basic residues in each cluster were changed to glutamate or aspartate (charge reversal). A detailed analysis of the affinities of these mutants for anionic vesicles and for heparin and heparan sulfate in vitro and of the specific activities of these proteins for hydrolysis of vesicles in vitro and of living cell membranes reveal the following trends: 1) the affinity of hIIa-PLA2 for heparin and heparan sulfate is modulated not by a highly localized site of basic residues but by diffuse sites that partially overlap with the interfacial binding site. In contrast, only those residues on the interfacial binding site of hIIa-PLA2 are involved in binding to membranes; 2) the relative ability of these mutants to hydrolyze cellular phospholipids when enzymes were added exogenously to CHO-K1, NIH-3T3, and RAW 264.7 cells correlates with their relative in vitro affinity for vesicles and not with their affinity for heparin and heparan sulfate. 3) The rates of exogenous hIIa-PLA2-catalyzed fatty acid release from wild type CHO-K1 cells and two mutant lines, one lacking glycosaminoglycan and one lacking heparan sulfate, were similar. Thus basic residues that modulate interfacial binding are important for plasma membrane fatty acid release by exogenously added hIIa-PLA2. Binding of hIIa-PLA2 to cell surface heparan sulfate does not modulate plasma membrane phospholipid hydrolysis by exogenously added hIIa-PLA2.

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“…However, it is not known whether LPC generation during apoptosis occurs intracellularly, extracellularly, or both, as the perturbed membrane structure is susceptible to secretory phospholipase A2 activity. 25 Later, it was shown that ABCA1 might be important for the release of lysophospholipids during apoptosis, as knockdown of ABCA1 resulted in the reduced migration of macrophages toward apoptotic cell supernatants. However, the authors did not show that this was caused by the specific reduction of LPC in the supernatants.…”

Section: Steps Involved In Clearancementioning

confidence: 99%

Do not let death do us part: ‘find-me’ signals in communication between dying cells and the phagocytes

2016

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The turnover and clearance of cells is an essential process that is part of many physiological and pathological processes. Improper or deficient clearance of apoptotic cells can lead to excessive inflammation and autoimmune disease. The steps involved in cell clearance include: migration of the phagocyte toward the proximity of the dying cells, specific recognition and internalization of the dying cell, and degradation of the corpse. The ability of phagocytes to recognize and react to dying cells to perform efficient and immunologically silent engulfment has been well-characterized in vitro and in vivo. However, how apoptotic cells themselves initiate the corpse removal and also influence the cells within the neighboring environment during clearance was less understood. Recent exciting observations suggest that apoptotic cells can attract phagocytes through the regulated release of 'find-me' signals. More recent studies also suggest that these find-me signals can have additional roles outside of phagocyte attraction to help orchestrate engulfment. This review will discuss our current understanding of the different find-me signals released by apoptotic cells, how they may be relevant in vivo, and their additional roles in facilitating engulfment.

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The perturbed membrane of cells undergoing apoptosis is susceptible to type II secretory phospholipase A2 to liberate arachidonic acid

Cited by 101 publications

References 56 publications

The Functions of Five Distinct Mammalian Phospholipase A2s in Regulating Arachidonic Acid Release

The Functions of Five Distinct Mammalian Phospholipase A2s in Regulating Arachidonic Acid Release

Action of Human Group IIa Secreted Phospholipase A2on Cell Membranes

Do not let death do us part: ‘find-me’ signals in communication between dying cells and the phagocytes

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