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Cell proliferation in mesenteric microvascular network remodeling in response to elevated hemodynamic stress
Walter L Murfee1, Eric J Van Gieson, Richard J Price
1Department of Biomedical Engineering, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA. wlm5e@virginia.edu
Annals of Biomedical Engineering
|January 29, 2005
Summary
Increased mechanical stress on rat mesenteric microvessels did not stimulate vascular or perivascular cell proliferation. Smooth muscle cell coverage changes are not due to cell division in response to moderate hemodynamic stress.
Area of Science:
- Cardiovascular Biology
- Vascular Remodeling
- Cellular Proliferation
Background:
- Microvascular remodeling involves changes in vessel structure, including smooth muscle cell (SMC) coverage.
- The role of cell proliferation in SMC coverage increases under mechanical stress is not fully understood.
Purpose of the Study:
- To quantify vascular and perivascular cell proliferation during microvascular remodeling.
- To investigate the impact of increased mechanical stress on SMC coverage and cell division.
Main Methods:
- Induction of hemodynamic stress via coordinated artery/vein ligation in rat mesentery.
- Measurement of 5-bromo-2'-deoxyuridine (BRDU) incorporation in smooth muscle alpha-actin positive vessels at 2, 5, and 10 days post-ligation.
Main Results:
- BRDU incorporation increased at 2 days in both sham and ligated groups, with no significant difference between them.
- Cell proliferation returned to baseline levels by 5 days in both experimental groups.
- Moderate hemodynamic stress did not induce significant perivascular cell proliferation.
Conclusions:
- Increased SMC coverage in response to moderate mechanical stress does not involve proliferation of vascular or perivascular cells.
- The mechanisms behind increased SMC coverage under hemodynamic stress require further investigation beyond cell division.