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Induction of Microstreaming by Nonspherical Bubble Oscillations in an Acoustic Levitation System

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Exploding the necroptotic bubble.

Liat Edry-Botzer¹, Motti Gerlic¹

¹Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel.

|June 22, 2019

Summary

Cell death signals, like phosphatidylserine (PS), usually prevent inflammation. However, similar signals are found in necroptosis, a regulated lytic cell death, challenging previous assumptions.

Keywords:

MLKL RIPK1 RIPK3 annexin V apoptosis cell death extracellular vesicles necroptosis necroptotic bodies phagocytosis phosphatidylserine

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Area of Science:

Cellular biology
Immunology
Pathology

Background:

Apoptotic cell death involves "eat-me" signals, such as phosphatidylserine (PS), to prevent inflammation and promote tissue repair.
These signals are exposed on the cell surface and apoptotic bodies during programmed cell death.

Purpose of the Study:

To investigate the presence and role of "eat-me" and "find-me" signals during necroptosis.
To challenge existing assumptions about regulated lytic cell death pathways.

Main Methods:

Analysis of cell surface markers during necroptosis.
Identification of "eat-me" and "find-me" signals in regulated lytic cell death.

Main Results:

Similar "eat-me" and "find-me" signals, akin to those in apoptosis, were identified during necroptosis.
The findings suggest a more complex role for these signals in different forms of regulated cell death.

Conclusions:

Necroptosis, a form of regulated lytic cell death, shares signaling mechanisms with apoptosis.
This discovery necessitates a re-evaluation of the distinct roles and regulation of cell death pathways.