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Effect of estrogen and AT1 receptor blocker on neointima formation.
Hypertension. 2002 Oct; 40(4):451-7; discussion 448-50.H

Abstract

The present study explored the possibility that estrogen may enhance the inhibitory effect of an angiotensin (Ang) II type 1 (AT1) receptor blocker on neointima formation in vascular injury, and investigated the signaling mechanism involved in their actions. Polyethylene cuff placement around the femoral artery of mice induced neointima formation and increased bromodeoxyuridine (BrdU) incorporation into vascular smooth muscle cells. These changes were significantly smaller in female mice than in male mice. Ovariectomy enhanced neointima formation and BrdU incorporation in the injured artery, which were reversed by 17beta-estradiol (80 microg/kg per day) replacement. Treatment with a selective AT1 receptor blocker, olmesartan (3 mg/kg per day), significantly inhibited neointima formation and BrdU incorporation, whereas the inhibitory effects of olmesartan were more marked in intact female mice than in male or ovariectomized mice. Phosphorylation of extracellular signal-regulated kinase (ERK), signal transducer and activator of transcription (STAT) 1, and STAT3 was increased in the injured artery. These increases were significantly smaller in intact female mice than in male or ovariectomized mice. Olmesartan or estrogen attenuated the phosphorylation of ERK and STAT in the injured artery, whereas these inhibitory effects were greater in intact female mice. Lower doses of olmesartan (0.5 mg/kg per day) or 17beta-estradiol (20 microg/kg per day) did not influence neointima formation, BrdU incorporation, and ERK and STAT phosphorylation in ovariectomized mice, whereas coadministration of olmesartan and 17beta-estradiol at these doses attenuated these parameters. These results indicate that estrogen and an AT1 receptor blocker synergistically attenuate vascular remodeling, which is at least partly via inhibition of ERK and STAT activity.

Authors+Show Affiliations

Department of Medical Biochemistry, Ehime University School of Medicine, Ehime, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12364346

Citation

Liu, Hong-Wei, et al. "Effect of Estrogen and AT1 Receptor Blocker On Neointima Formation." Hypertension (Dallas, Tex. : 1979), vol. 40, no. 4, 2002, pp. 451-7; discussion 448-50.
Liu HW, Iwai M, Takeda-Matsubara Y, et al. Effect of estrogen and AT1 receptor blocker on neointima formation. Hypertension. 2002;40(4):451-7; discussion 448-50.
Liu, H. W., Iwai, M., Takeda-Matsubara, Y., Wu, L., Li, J. M., Okumura, M., Cui, T. X., & Horiuchi, M. (2002). Effect of estrogen and AT1 receptor blocker on neointima formation. Hypertension (Dallas, Tex. : 1979), 40(4), 451-7; discussion 448-50.
Liu HW, et al. Effect of Estrogen and AT1 Receptor Blocker On Neointima Formation. Hypertension. 2002;40(4):451-7; discussion 448-50. PubMed PMID: 12364346.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of estrogen and AT1 receptor blocker on neointima formation. AU - Liu,Hong-Wei, AU - Iwai,Masaru, AU - Takeda-Matsubara,Yuko, AU - Wu,Lan, AU - Li,Jian-Mei, AU - Okumura,Midori, AU - Cui,Tai-Xing, AU - Horiuchi,Masatsugu, PY - 2002/10/5/pubmed PY - 2002/10/17/medline PY - 2002/10/5/entrez SP - 451-7; discussion 448-50 JF - Hypertension (Dallas, Tex. : 1979) JO - Hypertension VL - 40 IS - 4 N2 - The present study explored the possibility that estrogen may enhance the inhibitory effect of an angiotensin (Ang) II type 1 (AT1) receptor blocker on neointima formation in vascular injury, and investigated the signaling mechanism involved in their actions. Polyethylene cuff placement around the femoral artery of mice induced neointima formation and increased bromodeoxyuridine (BrdU) incorporation into vascular smooth muscle cells. These changes were significantly smaller in female mice than in male mice. Ovariectomy enhanced neointima formation and BrdU incorporation in the injured artery, which were reversed by 17beta-estradiol (80 microg/kg per day) replacement. Treatment with a selective AT1 receptor blocker, olmesartan (3 mg/kg per day), significantly inhibited neointima formation and BrdU incorporation, whereas the inhibitory effects of olmesartan were more marked in intact female mice than in male or ovariectomized mice. Phosphorylation of extracellular signal-regulated kinase (ERK), signal transducer and activator of transcription (STAT) 1, and STAT3 was increased in the injured artery. These increases were significantly smaller in intact female mice than in male or ovariectomized mice. Olmesartan or estrogen attenuated the phosphorylation of ERK and STAT in the injured artery, whereas these inhibitory effects were greater in intact female mice. Lower doses of olmesartan (0.5 mg/kg per day) or 17beta-estradiol (20 microg/kg per day) did not influence neointima formation, BrdU incorporation, and ERK and STAT phosphorylation in ovariectomized mice, whereas coadministration of olmesartan and 17beta-estradiol at these doses attenuated these parameters. These results indicate that estrogen and an AT1 receptor blocker synergistically attenuate vascular remodeling, which is at least partly via inhibition of ERK and STAT activity. SN - 1524-4563 UR - https://www.unboundmedicine.com/medline/citation/12364346/Effect_of_estrogen_and_AT1_receptor_blocker_on_neointima_formation_ L2 - https://www.ahajournals.org/doi/10.1161/01.hyp.0000033466.05496.89?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -