Abstract
Objectives: Cardiovascular disease is rare in premenopausal women, but increases after the menopause when hormone replacement therapy reduces coronary events. Vascular smooth muscle cell (SMC) proliferation and migration occur in atherosclerosis, restenosis and venous graft disease. We studied the effects of 17β-estradiol on SMC proliferation and migration. Methods: SMC were cultured from saphenous veins of postmenopausal women and age-matched men. Cell growth was determined by 3H-thymidine incorporation and cell counting. Migration of SMC was assessed in 4-well chambers. SMC were seeded in one corner and PDGF-BB in filter paper glued onto the opposite wall. Results: PDGF-BB (5 ng/ml for 24 h) similarly stimulated 3H-thymidine incorporation in female (511 ± 57%; n = 8) and male (528 ± 62%; n = 12) SMC. This was reduced by 17β-estradiol (10-8-10-6 M; female 313 ± 52%; male 337 ± 54%; P <0.05). PDGF-BB increased the number of SMC (P <0.0001 at 10 days) obtained from females (153 ± 3%; n = 5) and males (150 ± 4%; n = 5), which was inhibited by 17β-estradiol (10-6 M; female 134 ± 7%; male 128 ± 5%; P <0.05). Similar results were obtained with basic fibroblast growth factor. In contrast to 17β-estradiol, another steroid (dexamethasone) had no effects on 3H-thymidine incorporation in these cells stimulated with PDGF-BB. PDGF-BB (0.01-1 ng) stimulated SMC migration (P <0.05) which was inhibited by 17β-estradiol (10-10-10-6 M; n = 5; P <0.005). Conclusion: 17β-Estradiol inhibits growth-factor-induced SMC proliferation and migration regardless of gender. These effects of 17β-estradiol may contribute to its cardiovascular protective properties in postmenopausal women during replacement therapy.
| Original language | English |
|---|---|
| Pages (from-to) | 980-985 |
| Number of pages | 6 |
| Journal | Cardiovascular Research |
| Volume | 32 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - Nov 1996 |
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Keywords
- estrogen
- FGF
- human, saphenous vein
- PDGF
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
17β-Estradiol inhibits proliferation and migration of human vascular smooth muscle cells : Similar effects in cells from postmenopausal females and in males. / Dai-Do, Do; Espinosa, Emma; Liu, Guizhen; Rabelink, Ton J.; Julmy, Friedgard; Yang, Zhihong; Mahler, Felix; Lüscher, Thomas F.
In: Cardiovascular Research, Vol. 32, No. 5, 11.1996, p. 980-985.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - 17β-Estradiol inhibits proliferation and migration of human vascular smooth muscle cells
T2 - Similar effects in cells from postmenopausal females and in males
AU - Dai-Do, Do
AU - Espinosa, Emma
AU - Liu, Guizhen
AU - Rabelink, Ton J.
AU - Julmy, Friedgard
AU - Yang, Zhihong
AU - Mahler, Felix
AU - Lüscher, Thomas F.
PY - 1996/11
Y1 - 1996/11
N2 - Objectives: Cardiovascular disease is rare in premenopausal women, but increases after the menopause when hormone replacement therapy reduces coronary events. Vascular smooth muscle cell (SMC) proliferation and migration occur in atherosclerosis, restenosis and venous graft disease. We studied the effects of 17β-estradiol on SMC proliferation and migration. Methods: SMC were cultured from saphenous veins of postmenopausal women and age-matched men. Cell growth was determined by 3H-thymidine incorporation and cell counting. Migration of SMC was assessed in 4-well chambers. SMC were seeded in one corner and PDGF-BB in filter paper glued onto the opposite wall. Results: PDGF-BB (5 ng/ml for 24 h) similarly stimulated 3H-thymidine incorporation in female (511 ± 57%; n = 8) and male (528 ± 62%; n = 12) SMC. This was reduced by 17β-estradiol (10-8-10-6 M; female 313 ± 52%; male 337 ± 54%; P <0.05). PDGF-BB increased the number of SMC (P <0.0001 at 10 days) obtained from females (153 ± 3%; n = 5) and males (150 ± 4%; n = 5), which was inhibited by 17β-estradiol (10-6 M; female 134 ± 7%; male 128 ± 5%; P <0.05). Similar results were obtained with basic fibroblast growth factor. In contrast to 17β-estradiol, another steroid (dexamethasone) had no effects on 3H-thymidine incorporation in these cells stimulated with PDGF-BB. PDGF-BB (0.01-1 ng) stimulated SMC migration (P <0.05) which was inhibited by 17β-estradiol (10-10-10-6 M; n = 5; P <0.005). Conclusion: 17β-Estradiol inhibits growth-factor-induced SMC proliferation and migration regardless of gender. These effects of 17β-estradiol may contribute to its cardiovascular protective properties in postmenopausal women during replacement therapy.
AB - Objectives: Cardiovascular disease is rare in premenopausal women, but increases after the menopause when hormone replacement therapy reduces coronary events. Vascular smooth muscle cell (SMC) proliferation and migration occur in atherosclerosis, restenosis and venous graft disease. We studied the effects of 17β-estradiol on SMC proliferation and migration. Methods: SMC were cultured from saphenous veins of postmenopausal women and age-matched men. Cell growth was determined by 3H-thymidine incorporation and cell counting. Migration of SMC was assessed in 4-well chambers. SMC were seeded in one corner and PDGF-BB in filter paper glued onto the opposite wall. Results: PDGF-BB (5 ng/ml for 24 h) similarly stimulated 3H-thymidine incorporation in female (511 ± 57%; n = 8) and male (528 ± 62%; n = 12) SMC. This was reduced by 17β-estradiol (10-8-10-6 M; female 313 ± 52%; male 337 ± 54%; P <0.05). PDGF-BB increased the number of SMC (P <0.0001 at 10 days) obtained from females (153 ± 3%; n = 5) and males (150 ± 4%; n = 5), which was inhibited by 17β-estradiol (10-6 M; female 134 ± 7%; male 128 ± 5%; P <0.05). Similar results were obtained with basic fibroblast growth factor. In contrast to 17β-estradiol, another steroid (dexamethasone) had no effects on 3H-thymidine incorporation in these cells stimulated with PDGF-BB. PDGF-BB (0.01-1 ng) stimulated SMC migration (P <0.05) which was inhibited by 17β-estradiol (10-10-10-6 M; n = 5; P <0.005). Conclusion: 17β-Estradiol inhibits growth-factor-induced SMC proliferation and migration regardless of gender. These effects of 17β-estradiol may contribute to its cardiovascular protective properties in postmenopausal women during replacement therapy.
KW - estrogen
KW - FGF
KW - human, saphenous vein
KW - PDGF
UR - http://www.scopus.com/inward/record.url?scp=0009769490&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0009769490&partnerID=8YFLogxK
U2 - 10.1016/0008-6363(96)00149-6
DO - 10.1016/0008-6363(96)00149-6
M3 - Article
C2 - 8944830
AN - SCOPUS:0009769490
VL - 32
SP - 980
EP - 985
JO - Cardiovascular Research
JF - Cardiovascular Research
SN - 0008-6363
IS - 5
ER -