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Growth factors are released by mechanically wounded endothelial cells
P L McNeil1, L Muthukrishnan, E Warder
1Department of Anatomy and Cellular Biology, Harvard Medical School, Boston, Massachusetts 02115.
The Journal of Cell Biology
|August 1, 1989
Summary
Mechanical forces on cells can release growth factors. Scraping endothelial cells caused rapid release of growth-promoting activity, suggesting mechanically induced membrane disruption is key for basic fibroblast growth factor release.
Area of Science:
- Cell Biology
- Biochemistry
- Tissue Engineering
Background:
- Mechanical forces in vivo can trigger growth factor release.
- Cellular responses to mechanical stress are crucial for tissue repair and homeostasis.
- Understanding growth factor release mechanisms is vital for regenerative medicine.
Purpose of the Study:
- To investigate if mechanical forces directly cause growth factor release from cells.
- To identify the mechanism and nature of growth factors released by mechanical stress.
- To explore the role of plasma membrane integrity in growth factor release.
Main Methods:
- Scraping endothelial cells from culture substratum at 37°C to simulate mechanical injury.
- Measuring growth-promoting activity in the culture medium using Swiss 3T3 fibroblasts.
- Assessing the correlation between cell death, temperature, and growth factor release.
- Identifying the specific growth factor responsible for the observed activity.
Main Results:
- Scraping induced rapid release of potent growth-promoting activity into the medium.
- Release was primarily due to mechanical disruption of the plasma membrane, not cell death or extracellular matrix damage.
- Basic fibroblast growth factor (bFGF)-like molecule was identified as a key contributor to the activity.
- Release was more pronounced in newly plated cells compared to older cultures.
Conclusions:
- Mechanical disruption of the plasma membrane is a significant pathway for growth factor release.
- Basic fibroblast growth factor can be released via mechanically induced membrane breaches, bypassing traditional secretion pathways.
- This mechanism provides a direct link between mechanical stimuli and cellular repair processes in vivo.