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Effect of estrogen on vascular smooth muscle cells is dependent upon cellular phenotype
1Centre for Research in Vascular Biology, Department of Anatomical Sciences, University of Queensland, Brisbane, Australia.
Abstract:
To investigate the growth-regulating action of estrogen on vascular smooth muscle cells (SMC), effects of beta-17-estradiol (beta-E2) on phenotypic modulation and proliferation of rabbit aortic SMC were observed in vitro. At 10(-8)M, beta-E2 significantly slowed the decrease in volume fraction of myofilaments (Vv myo) of freshly dispersed SMCs in primary culture, indicating an inhibitory effect of beta-E2 on spontaneous phenotypic modulation of SMC from a contractile to a synthetic phenotype. Freshly dispersed SMCs treated with beta-E2 also had a relatively longer quiescent phase than control cells before intense proliferation occurred. This was in contrast to SMCs in passage 2 3 (synthetic state), where beta-E2-treated cells replicated significantly faster than untreated cells. beta-E2 also markedly enhanced the serum-induced DNA synthesis of synthetic SMCs in a concentration-dependent manner within physiological range (10(-10)to 10(-8)M). These findings indicate that the growth-regulating effect of estrogen on vascular SMC is dependent on the cell's phenotypic state. It delays the cell cycle re-entry of the contractile SMCs by retarding their phenotypic modulation: however, once cells have modulated to the synthetic phenotype, it promotes their replication.
Insights
Estrogen (beta-estradiol) affects vascular smooth muscle cell (SMC) growth differently based on cell type. It slows the transition of contractile SMCs to synthetic cells but promotes proliferation of already synthetic SMCs.
Area of Science:
- Vascular Biology
- Endocrinology
- Cell Biology
Background:
- Estrogen's role in vascular health is complex and may involve direct effects on vascular smooth muscle cells (SMCs).
- Vascular SMCs can exist in different phenotypic states, influencing their proliferative capacity and response to stimuli.
- Understanding how hormones like estrogen modulate SMC behavior is crucial for cardiovascular disease research.
Purpose of the Study:
- To investigate the in vitro effects of beta-17-estradiol (beta-E2) on the phenotypic modulation and proliferation of rabbit aortic SMCs.
- To determine if estrogen's growth-regulating action on SMCs is dependent on the cell's phenotypic state.
Main Methods:
- Primary cultures of rabbit aortic SMCs were established and treated with beta-E2 at various concentrations.
- Phenotypic modulation was assessed by measuring the volume fraction of myofilaments (Vv myo).
- Cell proliferation was evaluated by observing the quiescent phase duration and DNA synthesis (e.g., serum-induced DNA synthesis).
Main Results:
- Beta-E2 (10(-8)M) significantly inhibited the phenotypic modulation of freshly dispersed contractile SMCs, preserving myofilament content.
- Beta-E2 treatment led to a longer quiescent phase in freshly dispersed SMCs before proliferation.
- In contrast, beta-E2 significantly enhanced the proliferation and DNA synthesis of synthetic SMCs (passage 2-3) in a concentration-dependent manner.
Conclusions:
- Estrogen's effect on vascular SMC growth is state-dependent.
- Beta-E2 delays cell cycle re-entry in contractile SMCs by retarding phenotypic modulation.
- Once modulated to a synthetic phenotype, beta-E2 promotes SMC replication, suggesting a dual role in vascular remodeling.