Estrogen receptor-α prevents right ventricular diastolic dysfunction and fibrosis in female rats-Reference-Cited by-同舟云学术

Estrogen receptor-α prevents right ventricular diastolic dysfunction and fibrosis in female rats

Published:2020-12-01 Issue:6 Volume:319 Page:H1459-H1473
ISSN:0363-6135
Container-title:American Journal of Physiology-Heart and Circulatory Physiology
language:en
Short-container-title:American Journal of Physiology-Heart and Circulatory Physiology

Author:

Cheng Tik-Chee¹,Philip Jennifer L.²,Tabima Diana M.¹,Kumari Santosh³⁴,Yakubov Bakhtiyor⁵,Frump Andrea L.⁵^ORCID,Hacker Timothy A.⁶,Bellofiore Alessandro⁷^ORCID,Li Rongbo⁸,Sun Xin⁸,Goss Kara N.³⁴^ORCID,Lahm Tim⁵⁹¹⁰,Chesler Naomi C.¹⁴^ORCID

Affiliation:

1. Department of Biomedical Engineering, University of Wisconsin-Madison, Madison, Wisconsin

2. Department of Surgery, University of Wisconsin-Madison, Madison, Wisconsin

3. Division of Allergy, Pulmonary and Critical Care Medicine, University of Wisconsin-Madison, Madison, Wisconsin

4. Department of Medicine, University of Wisconsin-Madison, Madison, Wisconsin

5. Division of Pulmonary, Critical Care, Sleep and Occupational Medicine, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana

6. Cardiovascular Research Center, University of Wisconsin-Madison, Madison, Wisconsin

7. Department of Biomedical, Chemical and Materials Engineering, San Jose State University, San Jose, California

8. Department of Pediatrics, University of California San Diego, La Jolla, California

9. Department of Cellular and Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Indianapolis, Indiana

10. Richard L. Roudebush Veterans Affairs Medical Center, Indianapolis, Indiana

Abstract

Using a novel loss-of-function mutation in estrogen receptor-α (ERα), we demonstrate that female, but not male, ERα mutant rats display right ventricular (RV)-vascular uncoupling, diastolic dysfunction, and fibrosis following pressure overload, indicating a sex-dependent role of ERα in protecting against adverse RV remodeling. TIMP metallopeptidase inhibitor 1 (Timp1), matrix metalloproteinase 9 (Mmp9), kallikrein-related peptidase 10 ( Klk10), and Jun Proto-Oncogene ( Jun) were identified as potential mediators in ERα-regulated pathways in RV pressure overload.

Funder

VA Merit Review Award

HHS | NIH | National Heart, Lung, and Blood Institute

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

Link

https://journals.physiology.org/doi/pdf/10.1152/ajpheart.00247.2020

Reference67 articles.

1. Kallikrein Gene Delivery Improves Cardiac Reserve and Attenuates Remodeling After Myocardial Infarction

2. Estrogen Receptor β Protects the Murine Heart Against Left Ventricular Hypertrophy