α7-Nicotinic Acetylcholine Receptor Signaling in Cardiac Regeneration
Heart disease is the leading cause of death in the U.S. Loss of heart regenerative capacity in adult mammals is a principle reason why adults fail to recover from heart diseases. In contrast, neonatal mammals possess extraordinary heart regenerative capacity. Unraveling mechanisms of heart regeneration during the neonatal period is fundamental to understanding why adult hearts fail to regenerate. Previous studies revealed that cholinergic nerves and macrophages are crucial to heart regeneration. However, their interaction during heart inflammation and regeneration is poorly investigated. My study aims to understand how α7-nicotinic acetylcholine receptor (α7-nAChR) signaling between cholinergic nerves and macrophages regulates inflammation and regeneration after heart injury. Immunohistochemistry and trichrome staining showed decreased number of proliferating cardiomyocytes and increased scar formation following myocardial infarction in neonatal α7-nAChR knockout mice. Subsequent experiments will study the activation of different macrophage lineages in neonates by flow cytometry. The study of mechanisms of heart regeneration will bring us closer to the goal of reactivating the adult human heart for cardiac repair.