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J Am Coll Cardiol, 1999; 34:264-273
© 1999 by the American College of Cardiology Foundation
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EXPERIMENTAL STUDIES

Gender differences in molecular remodeling in pressure overload hypertrophy

Ellen O. Weinberg, PhDa, Christiane D. Thienelt, MDa, Sarah E. Katz, BAa, Jozef Bartunek, MDa, Minori Tajima, MD, PhDa, Susanne Rohrbacha, Pamela S. Douglas, MD, FACCa and Beverly H. Lorell, MD, FACCa

a Charles A. Dana Research Institute and the Harvard-Thorndike Laboratory and the Department of Medicine (Cardiovascular Division) of Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA

Manuscript received June 4, 1998; revised manuscript received February 23, 1999, accepted March 24, 1999.

Reprint requests and correspondence: Dr. Ellen O. Weinberg, Cardiovascular Division, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, Massachusetts 02215
eweinber{at}caregroup.harvard.edu

OBJECTIVES

The objective of this study was to examine gender differences in left ventricular (LV) function and expression of cardiac genes in response to LV pressure overload due to ascending aortic stenosis in rats.

BACKGROUND

Clinical studies have documented gender differences in the pattern of adaptive LV hypertrophy. Whether these differences result from intrinsic differences in molecular adaptation to pressure overload between men and women, or are related to other factors is not known.

METHODS

Male (n = 8) and female (n = 8) Wistar rats underwent ascending aortic stenosis and were studied 6 weeks after banding with gender-matched control rats (male n = 7; female n = 7). The LV contractile reserve was examined in isolated hearts from each group. We compared LV messenger ribonucleic acid (mRNA) levels of atrial natriuretic factor (ANF), beta-myosin heavy chain, sarcoplasmic reticulum Ca2+–adenosine triphosphatase (ATPase) and Na+–Ca2+ exchanger. Reverse transcriptase polymerase chain reaction was used to identify estrogen receptor transcript in cardiac myocytes and LV tissue.

RESULTS

The magnitude of LV hypertrophy (LVH) and systolic wall stress were similar in male and female animals with LVH. Male LVH hearts demonstrated a depressed contractile reserve; in contrast, contractile reserve was preserved in female LVH hearts. The expression of beta-myosin heavy chain and ANF mRNA was greater in male versus female LVH hearts. Sarcoplasmic reticulum Ca2+-ATPase mRNA levels were depressed in male LVH but not in female LVH compared with control rats, and Na+–Ca2+ exchanger mRNA levels were increased similarly in both male and female LVH hearts. Estrogen receptor transcript was detected in both adult male and female cardiac myocytes and LV tissue.

CONCLUSIONS

There are significant gender differences in the LV adaptation to pressure overload despite a similar degree of LVH and systolic wall stress in male and female rats. There is the potential for estrogen signaling through the adult myocyte estrogen receptor in both male and female rats to contribute to gender differences in gene expression in pathologic hypertrophy.

Abbreviations and Acronyms
  ANF = atrial natriuretic factor
  cDNA = complementary deoxyribonucleic acid
  LV = left ventricular
  LVH = left ventricular hypertrophy
  mRNA = messenger ribonucleic acid
  PCR = polymerase chain reaction
  RT = reverse transcriptase
  SERCA-2 = sarcoplasmic reticulum Ca2+–adenosine triphosphatase




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