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May 10, 2023Communications BiologyOpen Access

It takes two to tango: cardiac fibroblast-derived NO-induced cGMP enters cardiac myocytes and increases cAMP by inhibiting PDE3

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Why the study?

The occurrence of NO/cGMP signalling in cardiac cells remains a matter of debate.

Population

Living cardiac slices of mice with cardiomyocyte-specific expression of a FRET-based cGMP indicator (αMHC/cGi-500)

Design

Preclinical laboratory study in living cardiac tissue slices

Authors

LMLukas MengesJGJan GiesenKYKerem Can Yılmaz

Discussion

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Overview

Animal data suggest no immediate clinical implications; leaves open relevance of fibroblast-cardiomyocyte cGMP transfer in human disease.

Structured PICO

P
Population
Living cardiac slices of mice with cardiomyocyte-specific expression of a FRET-based cGMP indicator (αMHC/cGi-500) and mice with genetic inactivation of NO-GC in Tcf21-expressing cardiac fibroblasts
I
Intervention
Stimulation of NO-sensitive guanylyl cyclase (with Forskolin and Isoproterenol)
C
Comparator
Genetic inactivation of NO-GC in Tcf21-expressing cardiac fibroblasts
O
Outcome
cGMP transfer to myocytes, cAMP levels, and phospholamban phosphorylationsurrogate

This study provides evidence in intact tissue that NO-stimulated cGMP transfers from cardiac fibroblasts to cardiomyocytes via gap junctions, enhancing beta-receptor-induced contractile responses by inhibiting PDE3.

Cite This Study

Menges et al. (2023) studied this question.

synapsesocial.com/papers/6a7d5bd4fd19755b5e27874fhttps://doi.org/10.1038/s42003-023-04880-5
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