Cardiac melanocytes influence atrial reactive @entity26 species involved with electrical and structural remodeling in XXXX .

@entity11933 @entity82 @entity7599 @entity19 @entity26 @entity27828 @entity273 @entity519 @entity224 @entity943
Cardiac melanocyte-like cells (CMLCs) contribute to @entity943 when missing the melanin synthesis enzyme @entity27828 (Dct). While scavenging reactive @entity26 species (ROS) in Dct-null @entity19 partially suppressed @entity943 , it remains unclear if CMLCs influence atrial ROS and structure or if the electrical response of CMLCs to ROS differs from that of atrial myocytes. This study is designed to determine if CMLCs contribute to overall atrial oxidative stress or structural remodeling, and if ROS affects the electrophysiology of CMLCs differently than atrial myocytes. Immunohistochemical analysis showed higher expression of the oxidative marker @entity7599 in Dct-null atria versus Dct-heterozygous (Dct-het) atria. Exposing isolated CMLCs from Dct-het and Dct-null @entity19 to @entity273 increased @entity224 anion more in Dct-null CMLCs. Trichrome staining showed increased @entity82 in Dct-null atria, and treating Dct-null @entity19 with the ROS scavenger @entity11933 reduced atrial @entity82 . Action potential recordings from atrial myocytes and isolated Dct-het and Dct-null CMLCs in response to @entity273 showed that the EC50 for action potential duration (APD) prolongation of Dct-null CMLCs was 8.2      1.7   mol/L versus 16.8      2.0   mol/L for Dct-het CMLCs, 19.9      2.1   mol/L for Dct-null atrial myocytes, and 20.5      1.9   mol/L for Dct-het atrial myocytes. However, APD90 was longer in CMLCs versus atrial myocytes in response to @entity273 . @entity273 also induced more afterdepolarizations in CMLCs compared to atrial myocytes. These studies suggest that Dct within CMLCs contributes to @entity519 and remodeling. ROS prolongs APD to a greater extent and induces afterdepolarizations more frequently in CMLCs than in atrial myocytes.
