Subacute treatment of carprofen facilitate splenocardiac resolution deficit in cardiac injury.

Journal of Leukocyte Biology
Ganesh V HaladeJeevan Kumar Jadapalli

Abstract

Inflammation-limiting nonsteroidal pain relievers magnify myocardial infarction (MI) incidences and increase re-admission events in heart failure (HF) patients. However, the molecular and cellular mechanism of this provocative adverse effect is unclear. Our goal was to determine whether carprofen (CAP) impedes splenic leukocyte-directed acute inflammation-resolving response in cardiac injury. After subacute CAP treatment, mice were subjected to permanent coronary ligation maintaining MI- and naïve-controls. Spleen and left ventricle (LV) leukocytes were quantitated using flow cytometry pre- and 24 h post-MI. The inflammation resolution mediators were quantified using mass spectrometry while splenocardiac apoptosis and leukocyte phagocytosis were measured by immunofluorescence and ImageStream, respectively. Subacute CAP treatment promoted strain and cardiac dysfunction before MI and coronary occlusion showed signs of acute HF in CAP and MI-controls. Subacute CAP-injected mice had pre-activated splenic neutrophils, an over activated "don't eat me" signal (CD47) with reduced total Mϕs (F4/80+ ) and reparative Mϕs (F4/80/Ly6Clo /CD206) compared with control in LV and spleen. Post-MI, CAP pre-activated neutrophils (Ly6G+ ) were inte...Continue Reading

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Citations

Apr 17, 2020·Journal of the American Heart Association·Amanda B PullenGanesh V Halade
Feb 16, 2019·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Vasundhara KainGanesh V Halade
Oct 20, 2019·Pharmacology & Therapeutics·Vasundhara Kain, Ganesh V Halade
Oct 9, 2021·American Journal of Physiology. Heart and Circulatory Physiology·Merry L LindseyZamaneh Kassiri

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