Transplantation of young ovaries restored cardioprotective influence in postreproductive-aged mice

Jeffrey B. Mason, Shelley L. Cargill, Stephen M Griffey, J. Rachel Reader, Gary B. Anderson, James R. Carey

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The female cardioprotective advantage, present in mammals of a reproductively competent age, is lost during the transition to a postreproductive state. The role of reproductive hormones in this transition is most evident in women with premature ovarian failure, where reduced estrogen production has been associated with an increased incidence of early death from cardiovascular disease. Previously, we reported that postreproductive-aged mice that received young ovaries displayed an increased life span. Subsequent histopathological analysis suggested the presence of a cardioprotective effect associated with the restoration of ovarian influence. This restoration in postreproductive-aged mice produced a sharp decrease in evidence of significant cardiomyopathy at death, compared with sham-transplanted mice (36.0% vs. 73.3%, respectively). Within the intact transplant group, evidence of cardiomyopathy at death was decreased in mice that were reproductively cycling at the time of transplant, compared with acyclic mice (26.7% vs. 50.0%, respectively). This observation reflects the importance of timing in restoration of ovarian influence in this study. Transplantation of young ovaries to intact, postreproductive-aged female mice provided significant, long-term restoration of a cardioprotective benefit, similar to that previously present during a reproductively competent age. In these mice, restoration of ovarian influence through ovarian transplantation may, in effect, have postponed the advance of age-associated cardiomyopathy to a point where the disease did not reach a clinically relevant threshold during the lifetime of the recipients. These results offer support for previous clinical observations suggesting that hormone replacement therapy can produce divergent results if initiated during the perimenopausal period, compared with the postmenopausal ages.

Original languageEnglish (US)
Pages (from-to)448-456
Number of pages9
JournalAging Cell
Volume10
Issue number3
DOIs
StatePublished - Jun 2011

Fingerprint

Ovary
Transplantation
Cardiomyopathies
Primary Ovarian Insufficiency
Transplants
Hormone Replacement Therapy
Mammals
Estrogens
Cardiovascular Diseases
Hormones
Incidence

Keywords

  • Endocrinology
  • Estradiol
  • Mouse models
  • Senescence
  • Sex hormones

ASJC Scopus subject areas

  • Aging
  • Cell Biology

Cite this

Transplantation of young ovaries restored cardioprotective influence in postreproductive-aged mice. / Mason, Jeffrey B.; Cargill, Shelley L.; Griffey, Stephen M; Reader, J. Rachel; Anderson, Gary B.; Carey, James R.

In: Aging Cell, Vol. 10, No. 3, 06.2011, p. 448-456.

Research output: Contribution to journalArticle

Mason, Jeffrey B. ; Cargill, Shelley L. ; Griffey, Stephen M ; Reader, J. Rachel ; Anderson, Gary B. ; Carey, James R. / Transplantation of young ovaries restored cardioprotective influence in postreproductive-aged mice. In: Aging Cell. 2011 ; Vol. 10, No. 3. pp. 448-456.
@article{4d60ad021f364caab771aefba97053e9,
title = "Transplantation of young ovaries restored cardioprotective influence in postreproductive-aged mice",
abstract = "The female cardioprotective advantage, present in mammals of a reproductively competent age, is lost during the transition to a postreproductive state. The role of reproductive hormones in this transition is most evident in women with premature ovarian failure, where reduced estrogen production has been associated with an increased incidence of early death from cardiovascular disease. Previously, we reported that postreproductive-aged mice that received young ovaries displayed an increased life span. Subsequent histopathological analysis suggested the presence of a cardioprotective effect associated with the restoration of ovarian influence. This restoration in postreproductive-aged mice produced a sharp decrease in evidence of significant cardiomyopathy at death, compared with sham-transplanted mice (36.0{\%} vs. 73.3{\%}, respectively). Within the intact transplant group, evidence of cardiomyopathy at death was decreased in mice that were reproductively cycling at the time of transplant, compared with acyclic mice (26.7{\%} vs. 50.0{\%}, respectively). This observation reflects the importance of timing in restoration of ovarian influence in this study. Transplantation of young ovaries to intact, postreproductive-aged female mice provided significant, long-term restoration of a cardioprotective benefit, similar to that previously present during a reproductively competent age. In these mice, restoration of ovarian influence through ovarian transplantation may, in effect, have postponed the advance of age-associated cardiomyopathy to a point where the disease did not reach a clinically relevant threshold during the lifetime of the recipients. These results offer support for previous clinical observations suggesting that hormone replacement therapy can produce divergent results if initiated during the perimenopausal period, compared with the postmenopausal ages.",
keywords = "Endocrinology, Estradiol, Mouse models, Senescence, Sex hormones",
author = "Mason, {Jeffrey B.} and Cargill, {Shelley L.} and Griffey, {Stephen M} and Reader, {J. Rachel} and Anderson, {Gary B.} and Carey, {James R.}",
year = "2011",
month = "6",
doi = "10.1111/j.1474-9726.2011.00691.x",
language = "English (US)",
volume = "10",
pages = "448--456",
journal = "Aging Cell",
issn = "1474-9718",
publisher = "Wiley-Blackwell",
number = "3",

}

TY - JOUR

T1 - Transplantation of young ovaries restored cardioprotective influence in postreproductive-aged mice

AU - Mason, Jeffrey B.

AU - Cargill, Shelley L.

AU - Griffey, Stephen M

AU - Reader, J. Rachel

AU - Anderson, Gary B.

AU - Carey, James R.

PY - 2011/6

Y1 - 2011/6

N2 - The female cardioprotective advantage, present in mammals of a reproductively competent age, is lost during the transition to a postreproductive state. The role of reproductive hormones in this transition is most evident in women with premature ovarian failure, where reduced estrogen production has been associated with an increased incidence of early death from cardiovascular disease. Previously, we reported that postreproductive-aged mice that received young ovaries displayed an increased life span. Subsequent histopathological analysis suggested the presence of a cardioprotective effect associated with the restoration of ovarian influence. This restoration in postreproductive-aged mice produced a sharp decrease in evidence of significant cardiomyopathy at death, compared with sham-transplanted mice (36.0% vs. 73.3%, respectively). Within the intact transplant group, evidence of cardiomyopathy at death was decreased in mice that were reproductively cycling at the time of transplant, compared with acyclic mice (26.7% vs. 50.0%, respectively). This observation reflects the importance of timing in restoration of ovarian influence in this study. Transplantation of young ovaries to intact, postreproductive-aged female mice provided significant, long-term restoration of a cardioprotective benefit, similar to that previously present during a reproductively competent age. In these mice, restoration of ovarian influence through ovarian transplantation may, in effect, have postponed the advance of age-associated cardiomyopathy to a point where the disease did not reach a clinically relevant threshold during the lifetime of the recipients. These results offer support for previous clinical observations suggesting that hormone replacement therapy can produce divergent results if initiated during the perimenopausal period, compared with the postmenopausal ages.

AB - The female cardioprotective advantage, present in mammals of a reproductively competent age, is lost during the transition to a postreproductive state. The role of reproductive hormones in this transition is most evident in women with premature ovarian failure, where reduced estrogen production has been associated with an increased incidence of early death from cardiovascular disease. Previously, we reported that postreproductive-aged mice that received young ovaries displayed an increased life span. Subsequent histopathological analysis suggested the presence of a cardioprotective effect associated with the restoration of ovarian influence. This restoration in postreproductive-aged mice produced a sharp decrease in evidence of significant cardiomyopathy at death, compared with sham-transplanted mice (36.0% vs. 73.3%, respectively). Within the intact transplant group, evidence of cardiomyopathy at death was decreased in mice that were reproductively cycling at the time of transplant, compared with acyclic mice (26.7% vs. 50.0%, respectively). This observation reflects the importance of timing in restoration of ovarian influence in this study. Transplantation of young ovaries to intact, postreproductive-aged female mice provided significant, long-term restoration of a cardioprotective benefit, similar to that previously present during a reproductively competent age. In these mice, restoration of ovarian influence through ovarian transplantation may, in effect, have postponed the advance of age-associated cardiomyopathy to a point where the disease did not reach a clinically relevant threshold during the lifetime of the recipients. These results offer support for previous clinical observations suggesting that hormone replacement therapy can produce divergent results if initiated during the perimenopausal period, compared with the postmenopausal ages.

KW - Endocrinology

KW - Estradiol

KW - Mouse models

KW - Senescence

KW - Sex hormones

UR - http://www.scopus.com/inward/record.url?scp=79955955250&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79955955250&partnerID=8YFLogxK

U2 - 10.1111/j.1474-9726.2011.00691.x

DO - 10.1111/j.1474-9726.2011.00691.x

M3 - Article

C2 - 21385306

AN - SCOPUS:79955955250

VL - 10

SP - 448

EP - 456

JO - Aging Cell

JF - Aging Cell

SN - 1474-9718

IS - 3

ER -