Premium
Role of Myeloid Cell‐Specific Beta2‐Adrenergic Receptor in Regulating Leukocyte Immune Response during Myocardial Infarction
Author(s) -
Nayak Tapas,
Bajpai Anamika,
Strong Joshua,
Carter Rhonda,
Tilley Douglas
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.05352
Subject(s) - myeloid , immune system , chemokine , medicine , ejection fraction , immunology , integrin alpha m , inflammation , myocardial infarction , heart failure
Myocardial infarction (MI) remain one of the leading global causes of socioeconomic burden and mortality which often leads to heart failure (HF). MI triggers release of various cytokines/chemokines and promotes robust inflammatory signaling cascades by regulating activation and spatio‐temporal leukocyte migration (neutrophils and monocytes/macrophages) to the infarct area, which are very much essential for post‐infarct tissue modification and cardiac repair. Additionally, pro‐inflammatory and reparative macrophages are also thought to orchestrate post‐infarct immune responses. However, myeloid specific β2‐AR signaling mediated regulation of various phenotypic leukocyte sub‐population migration and responsiveness after MI is not fully understood yet. In the current study, we used Cre‐Lox system to generate myeloid specific β2‐AR KO (knock out) mice to determine the impact of β2‐AR deletion on post‐MI cardiac function. Preliminary echocardiography data suggest a significant improvement in terms of %EF (ejection fraction) and %FS (fraction shortening) after 72h of MI induction in β2‐AR KO mice heart as compared to control groups, demonstrating a cardioprotective role of myeloid specific β2‐AR KO. Immune cell profiling by FACS analysis showed a reduced CD45+CD11b+Ly6C+ monocytes, CD45+CD11b+Ly6G+ neutrophils infiltration in β2‐AR KO mice heart as compared to control groups following 4d post‐MI. Thus, we hypothesize that myeloid cell specific β2‐AR may be a crucial regulator of leukocyte immune response which in turn may orchestrate cardiac (patho)physiology following MI. The conclusion drawn from this project may help us understanding the myeloid cell behavior towards acute cardiac injury and repair, which might be further translated for therapeutic use.