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Effects of estrogen on the vascular injury response in estrogen receptor alpha, beta (double) knockout mice.

Karas, R H (författare)
Schulten, H (författare)
Pare, G (författare)
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Aronovitz, M J (författare)
Ohlsson, Claes, 1965 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för internmedicin,Institute of Internal Medicine, Dept of Medicine
Gustafsson, J A (författare)
Karolinska Institutet
Mendelsohn, M E (författare)
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 (creator_code:org_t)
Ovid Technologies (Wolters Kluwer Health), 2001
2001
Engelska.
Ingår i: Circulation research. - : Ovid Technologies (Wolters Kluwer Health). - 1524-4571 .- 0009-7330. ; 89:6, s. 534-9
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • The two known estrogen receptors, ERalpha and ERbeta, mediate the effects of estrogen in all target tissues, including blood vessels. We have shown previously that estrogen inhibits vascular injury response to the same extent in female wild-type (WT), ERalpha knockout (ERalphaKO(CH)), and ERbeta knockout (ERbetaKO(CH)) mice. We generated mice harboring disruptions of both ERalpha and ERbeta genes (ERalpha,betaKO(CH)) by breeding and studied the effect of 17beta-estradiol (E2) on vascular injury responses in ovariectomized female ERalpha,betaKO(CH) mice and WT littermates. E2 inhibited increases in vascular medial area following injury in the WT mice but not in the ERalpha,betaKO(CH) mice, demonstrating for the first time that the two known estrogen receptors are necessary and sufficient to mediate estrogen inhibition of a component of the vascular injury response. Surprisingly, as in WT littermates, E2 still significantly increased uterine weight and inhibited vascular smooth muscle cell (VSMC) proliferation following injury in the ERalpha,betaKO(CH) mice. These data support that the role of estrogen receptors differs for specific components of the vascular injury response in the ERalpha,betaKO(CH) mice. The results leave unresolved whether E2 inhibition of VSMC proliferation in ERalpha,betaKO(CH) mice is caused by a receptor-independent mechanism, an unidentified receptor responsive to estrogen, or residual activity of the ERalpha splice variant reported previously in the parental ERalphaKO(CH) mice. These possibilities may be resolved by studies of mice in which ERalpha has been fully disrupted (ERalphaKO(St)), which are in progress.

Nyckelord

Animals
Bromodeoxyuridine
metabolism
Carotid Arteries
drug effects
pathology
Carotid Artery Injuries
drug therapy
genetics
Cell Division
drug effects
Estradiol
therapeutic use
Estrogen Receptor alpha
Estrogen Receptor beta
Estrogens
therapeutic use
Female
Genotype
Mice
Mice
Knockout
Muscle
Smooth
Vascular
cytology
drug effects
metabolism
Ovariectomy
Receptors
Estrogen
genetics

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