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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
Published on: February 16, 2015
Increased ecto-metallopeptidase activity in cells undergoing apoptosis
T J Piva1, C M Davern, K G Francis
1QCF Cancer Research Unit, Queensland Institute of Medical Research and Joint Experimental Oncology Program, University of Queensland, Brisbane, Queensland 4702, Australia. t.piva@cqu.edu.au
Journal of Cellular Biochemistry
|February 2, 2000
Summary
Cell surface ectoprotease activity increases during apoptosis, facilitating the release of growth factors and cytokines. This controlled release may prevent inflammation during programmed cell death, aiding tissue repair.
Area of Science:
- Cell Biology
- Biochemistry
- Molecular Biology
Background:
- Cell surface proteases regulate the release of bioactive molecules like growth factors and cytokines.
- Stressful agents can induce programmed cell death (apoptosis) or necrosis.
- Ectoprotease activity is implicated in the release of these molecules.
Purpose of the Study:
- To investigate the role of ectoprotease activity in the release of cell surface molecules following cellular stress.
- To determine if ectoprotease activity differs between apoptosis and necrosis.
- To explore the implications of these changes for tissue repair and inflammatory responses.
Main Methods:
- HeLa cells were exposed to various stress agents (UVC, actinomycin D, cycloheximide, cisplatinum).
- Ectoprotease activity was measured on the cell surface.
- The release of specific molecules, including transforming growth factor-alpha (TGFalpha), was monitored.
- Cell viability was assessed to distinguish between apoptosis and necrosis.
Main Results:
- Increased metalloprotease activity was observed on the HeLa cell surface after stress induction.
- Ectoprotease activity significantly increased on apoptotic cells but showed little change on viable cells.
- Necrotic cells exhibited decreased ectoprotease activity, with the exception of TGFalphaase.
- The release of TGFalpha and other bioactive molecules was linked to increased ectoprotease activity.
Conclusions:
- Preferential activation or retention of ectoproteases on apoptotic cells drives the release of bioactive molecules.
- This mechanism may contribute to tissue repair processes.
- The observed changes in ectoprotease activity could explain the lack of inflammation associated with apoptotic cell death.
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