Natriuretic Peptide Receptor B modulates the proliferation of the cardiac cells expressing the Stem Cell Antigen-1.
Brain Natriuretic Peptide (BNP) injections in adult "healthy" or infarcted mice led to increased number of non-myocyte cells (NMCs) expressing the nuclear transcription factor Nkx2.5. The aim of this study was to identify the nature of the cells able to respond to BNP as well as the signaling pathway involved. BNP treatment of neonatal mouse NMCs stimulated Sca-1+cell proliferation. The Sca-1+cells were characterized as being a mixed cell population involving fibroblasts and multipotent precursor cells. Thus, BNP treatment led also to increased number of Sca-1+cells expressing Nkx2.5, in Sca-1+cell cultures in vitro and in vivo, in the hearts of neonatal and adult infarcted mice. Whereas BNP induced Sca-1+cell proliferation via NPR-B receptor and protein kinase G activation, CNP stimulated Sca-1+cell proliferation via NPR-B and a PKG-independent mechanism. We highlighted here a new role for the natriuretic peptide receptor B which was identified as a target able to modulate the proliferation of the Sca-1+cells. The involvement of NPR-B signaling in heart regeneration has, however, to be further investigated.
Unité de Physiopathologie Clinique Centre Hospitalier Universitaire Vaudois and University of Lausanne, Bugnon 7a, 1005 Lausanne, Switzerland.
Stéphanie
S
Rignault-Clerc
Unité de Physiopathologie Clinique Centre Hospitalier Universitaire Vaudois and University of Lausanne, Bugnon 7a, 1005 Lausanne, Switzerland.
Christelle
C
Bielmann
Service de Médecine Intensive Adulte, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Switzerland.
Lucas
L
Liaudet
Unité de Physiopathologie Clinique Centre Hospitalier Universitaire Vaudois and University of Lausanne, Bugnon 7a, 1005 Lausanne, Switzerland.
Bernard
B
Waeber
Unité de Physiopathologie Clinique Centre Hospitalier Universitaire Vaudois and University of Lausanne, Bugnon 7a, 1005 Lausanne, Switzerland.
François
F
Feihl
Unité de Physiopathologie Clinique Centre Hospitalier Universitaire Vaudois and University of Lausanne, Bugnon 7a, 1005 Lausanne, Switzerland.
Nathalie
N
Rosenblatt-Velin
D000818:Animals; D000067696:Ataxin-1 / Q000235:genetics / Q000378:metabolism; D049109:Cell Proliferation; D002478:Cells, Cultured; D017869:Cyclic GMP-Dependent Protein Kinases / Q000378:metabolism; D000072576:Homeobox Protein Nkx-2.5 / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000166:cytology*; D020097:Natriuretic Peptide, Brain / Q000187:drug effects*; D017461:Receptors, Atrial Natriuretic Factor / Q000378:metabolism; D015398:Signal Transduction; D013234:Stem Cells / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D000099242:Atrial Natriuretic Factor Receptor B
D000067696:Ataxin-1; D017869:Cyclic GMP-Dependent Protein Kinases; D000072576:Homeobox Protein Nkx-2.5; D020097:Natriuretic Peptide, Brain; D017461:Receptors, Atrial Natriuretic Factor; D000099242:Atrial Natriuretic Factor Receptor B; C000593750:Atxn1 protein, mouse; C484469:Nkx2-5 protein, mouse