17β-Estradiol inhibits proliferation and migration of human vascular smooth muscle cells: Similar effects in cells from postmenopausal females and in males

Do Dai-Do, Emma Espinosa, Guizhen Liu, Ton J. Rabelink, Friedgard Julmy, Zhihong Yang, Felix Mahler, Thomas F. Lüscher

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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 languageEnglish
Pages (from-to)980-985
Number of pages6
JournalCardiovascular Research
Volume32
Issue number5
DOIs
Publication statusPublished - Nov 1996

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Vascular Smooth Muscle
Smooth Muscle Myocytes
Estradiol
Cell Movement
Thymidine
Cell Proliferation
Hormone Replacement Therapy
Saphenous Vein
Fibroblast Growth Factor 2
Menopause
Dexamethasone
Atherosclerosis
Intercellular Signaling Peptides and Proteins
Cardiovascular Diseases
Steroids
platelet-derived growth factor BB
Transplants
Growth

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 journalArticle

Dai-Do, Do ; Espinosa, Emma ; Liu, Guizhen ; Rabelink, Ton J. ; Julmy, Friedgard ; Yang, Zhihong ; Mahler, Felix ; Lüscher, Thomas F. / 17β-Estradiol inhibits proliferation and migration of human vascular smooth muscle cells : Similar effects in cells from postmenopausal females and in males. In: Cardiovascular Research. 1996 ; Vol. 32, No. 5. pp. 980-985.
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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.",
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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.

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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.

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