Search: WFRF:(Karas M)
> (2000-2004) >
Effects of estrogen...
Effects of estrogen on the vascular injury response in estrogen receptor alpha, beta (double) knockout mice.
-
Karas, R H (author)
-
Schulten, H (author)
-
Pare, G (author)
-
show more...
-
Aronovitz, M J (author)
-
- Ohlsson, Claes, 1965 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för internmedicin,Institute of Internal Medicine, Dept of Medicine
-
- Gustafsson, J A (author)
- Karolinska Institutet
-
Mendelsohn, M E (author)
-
show less...
-
(creator_code:org_t)
- Ovid Technologies (Wolters Kluwer Health), 2001
- 2001
- English.
-
In: Circulation research. - : Ovid Technologies (Wolters Kluwer Health). - 1524-4571 .- 0009-7330. ; 89:6, s. 534-9
- Related links:
-
https://www.ahajourn...
-
show more...
-
https://gup.ub.gu.se...
-
http://kipublication...
-
https://doi.org/10.1...
-
show less...
Abstract
Subject headings
Close
- 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.
Keyword
- 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
Publication and Content Type
- ref (subject category)
- art (subject category)
Find in a library
To the university's database