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Olivares-Silva F, De Gregorio N, Espitia-Corredor J, et al. Resolvin-D1 attenuation of angiotensin II-induced cardiac inflammation in mice is associated with prevention of cardiac remodeling and hypertension. Biochim Biophys Acta Mol Basis Dis. 2021;1867(12):166241doi: 10.1016/j.bbadis.2021.166241.
Olivares-Silva, F., De Gregorio, N., Espitia-Corredor, J., Espinoza, C., Vivar, R., Silva, D., Osorio, J. M., Lavandero, S., Peiró, C., Sánchez-Ferrer, C., & Díaz-Araya, G. (2021). Resolvin-D1 attenuation of angiotensin II-induced cardiac inflammation in mice is associated with prevention of cardiac remodeling and hypertension. Biochimica et biophysica acta. Molecular basis of disease, 1867(12), 166241. https://doi.org/10.1016/j.bbadis.2021.166241
Olivares-Silva, Francisco, et al. "Resolvin-D1 attenuation of angiotensin II-induced cardiac inflammation in mice is associated with prevention of cardiac remodeling and hypertension." Biochimica et biophysica acta. Molecular basis of disease vol. 1867,12 (2021): 166241. doi: https://doi.org/10.1016/j.bbadis.2021.166241
Olivares-Silva F, De Gregorio N, Espitia-Corredor J, Espinoza C, Vivar R, Silva D, Osorio JM, Lavandero S, Peiró C, Sánchez-Ferrer C, Díaz-Araya G. Resolvin-D1 attenuation of angiotensin II-induced cardiac inflammation in mice is associated with prevention of cardiac remodeling and hypertension. Biochim Biophys Acta Mol Basis Dis. 2021 Dec 01;1867(12):166241. doi: 10.1016/j.bbadis.2021.166241. Epub 2021 Aug 13. PMID: 34400298.
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Biochim Biophys Acta Mol Basis Dis. 2021 Dec 01;1867(12):166241. doi: 10.1016/j.bbadis.2021.166241. Epub 2021 Aug 13.

Resolvin-D1 attenuation of angiotensin II-induced cardiac inflammation in mice is associated with prevention of cardiac remodeling and hypertension.

Biochimica et biophysica acta. Molecular basis of disease

Francisco Olivares-Silva, Nicole De Gregorio, Jenaro Espitia-Corredor, Claudio Espinoza, Raúl Vivar, David Silva, José Miguel Osorio, Sergio Lavandero, Concepción Peiró, Carlos Sánchez-Ferrer, Guillermo Díaz-Araya

Affiliations

  1. Department of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, Universidad de Chile, Santiago, Chile; Advanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine, Universidad de Chile, Santiago, Chile.
  2. Advanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine, Universidad de Chile, Santiago, Chile.
  3. Department of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, Universidad de Chile, Santiago, Chile; Department of Pharmacology, Faculty of Medicine, Universidad Autónoma de Madrid and Instituto de Investigación Sanitaria Hospital Universitario La Paz (IdiPAZ), Spain.
  4. Department of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, Universidad de Chile, Santiago, Chile.
  5. Pharmacology Program, Biomedical Sciences Institute, Faculty of Medicine, Universidad de Chile, Santiago, Chile.
  6. Advanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine, Universidad de Chile, Santiago, Chile; Cardiology Division, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
  7. Department of Pharmacology, Faculty of Medicine, Universidad Autónoma de Madrid and Instituto de Investigación Sanitaria Hospital Universitario La Paz (IdiPAZ), Spain.
  8. Department of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, Universidad de Chile, Santiago, Chile; Advanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine, Universidad de Chile, Santiago, Chile. Electronic address: [email protected].

PMID: 34400298 DOI: 10.1016/j.bbadis.2021.166241

Abstract

AIMS: Despite the broad pharmacological arsenal to treat hypertension, chronic patients may develop irreversible cardiac remodeling and fibrosis. Angiotensin II, the main peptide responsible for the Renin-Angiotensin-Aldosterone-System, has been closely linked to cardiac remodeling, hypertrophy, fibrosis, and hypertension, and some of these effects are induced by inflammatory mediators. Resolvin-D1 (RvD1) elicits potent anti-inflammatory and pro-resolving effects in various pathological models. In this study, we aimed to examine whether RvD1 ameliorates cardiac remodeling and hypertension triggered by angiotensin II.

METHODS AND RESULTS: Alzet® osmotic mini-pumps filled with angiotensin II (1.5 mg/kg/day) were implanted in male C57BL/6 J mice for 7 or 14 days. RvD1 (3 μg/kg/day, i.p) was administered one day after the surgery and during the complete infusion period. Blood pressure and myocardial functional parameters were assessed by echocardiography. At the end of the experimental procedure, blood and heart tissue were harvested, and plasma and histological parameters were studied. After 7 and 14 days, RvD1 reduced the increase of neutrophil and macrophage infiltration triggered by angiotensin II, and also reduced ICAM-1 and VCAM-1 expression levels. RvD1 also reduced cytokine plasma levels (IL-1β, TNF-α, IL-6, KC, MCP-1), cardiac hypertrophy, interstitial and perivascular fibrosis, and hypertension.

CONCLUSIONS: This study unveils novel cardioprotective effects of RvD1 in angiotensin II-induced hypertension and cardiac remodeling by attenuating inflammation and provides insights into a potential clinical application.

Copyright © 2021 Elsevier B.V. All rights reserved.

Keywords: Angiotensin II; Cardiac remodeling; Hypertension; Inflammation; Resolvin-D1

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