Format

Send to

Choose Destination
Cell Rep. 2014 Apr 10;7(1):35-44. doi: 10.1016/j.celrep.2014.02.029. Epub 2014 Mar 20.

ROS regulate cardiac function via a distinct paracrine mechanism.

Author information

1
Development, Aging and Regeneration Program, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037, USA; Free Radical Biology and Aging Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA. Electronic address: limh@omrf.org.
2
Immunobiology and Cancer Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.
3
Key Laboratory of Marine Biogenetic Resources, The Third Institute of Oceanography, State Oceanic Administration, Xiamen, Fujian 361005, China.
4
Development, Aging and Regeneration Program, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037, USA.
5
Development, Aging and Regeneration Program, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037, USA. Electronic address: rolf@sanfordburnham.org.

Abstract

Reactive oxygen species (ROS) can act cell autonomously and in a paracrine manner by diffusing into nearby cells. Here, we reveal a ROS-mediated paracrine signaling mechanism that does not require entry of ROS into target cells. We found that under physiological conditions, nonmyocytic pericardial cells (PCs) of the Drosophila heart contain elevated levels of ROS compared to the neighboring cardiomyocytes (CMs). We show that ROS in PCs act in a paracrine manner to regulate normal cardiac function, not by diffusing into the CMs to exert their function, but by eliciting a downstream D-MKK3-D-p38 MAPK signaling cascade in PCs that acts on the CMs to regulate their function. We find that ROS-D-p38 signaling in PCs during development is also important for establishing normal adult cardiac function. Our results provide evidence for a previously unrecognized role of ROS in mediating PC/CM interactions that significantly modulates heart function.

PMID:
24656823
PMCID:
PMC4164050
DOI:
10.1016/j.celrep.2014.02.029
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center