Skip to main content
Erschienen in: Pediatric Cardiology 5/2009

01.07.2009 | Riley Symposium

Insights into the Characteristics of Mammalian Cardiomyocyte Terminal Differentiation Shown Through the Study of Mice with a Dysfunctional c-Kit

verfasst von: Nawazish Naqvi, Ming Li, Eiji Yahiro, Robert M. Graham, Ahsan Husain

Erschienen in: Pediatric Cardiology | Ausgabe 5/2009

Einloggen, um Zugang zu erhalten

Abstract

Mammalian cardiomyocytes withdraw from the cell cycle soon after birth. This process is called terminal differentiation. The c-kit, a receptor tyrosine kinase, is expressed on cardiomyocytes immediately after birth but for only a few days. In mice with genetic c-kit dysfunction, adult cardiomyocytes are phenotypically indistinguishable from those of wild type mice, except that they are capable of proliferation in vivo after acute pressure overload. This review explores the idea that postnatal cardiomyocyte differentiation and cell cycle withdrawal are distinct processes and that terminal differentiation may not simply be due to altered expression of genes that regulate the cell cycle but could involve c-kit induced epigenetic change.
Literatur
1.
Zurück zum Zitat Ahuja P, Sdek P, MacLellan WR (2007) Cardiac myocyte cell cycle control in development, disease, and regeneration. Physiol Rev 87:521–544PubMedCrossRef Ahuja P, Sdek P, MacLellan WR (2007) Cardiac myocyte cell cycle control in development, disease, and regeneration. Physiol Rev 87:521–544PubMedCrossRef
2.
Zurück zum Zitat Ausma J, Schaart G, Thoné F et al (1995) Chronic ischemic viable myocardium in man: aspects of dedifferentiation. Cardiovasc Pathol 4:29–37CrossRef Ausma J, Schaart G, Thoné F et al (1995) Chronic ischemic viable myocardium in man: aspects of dedifferentiation. Cardiovasc Pathol 4:29–37CrossRef
3.
Zurück zum Zitat Chaudhry HW, Dashoush NH, Tang H et al (2004) Cyclin A2 mediates cardiomyocyte mitosis in the postmitotic myocardium. J Biol Chem 279:35858–35866PubMedCrossRef Chaudhry HW, Dashoush NH, Tang H et al (2004) Cyclin A2 mediates cardiomyocyte mitosis in the postmitotic myocardium. J Biol Chem 279:35858–35866PubMedCrossRef
4.
Zurück zum Zitat Ehler E, Rothen BM, Hämmerle SP et al (1999) Myofibrillogenesis in the developing chicken heart: assembly of Z-disk, M-line, and the thick filaments. J Cell Sci 112:1529–1539PubMed Ehler E, Rothen BM, Hämmerle SP et al (1999) Myofibrillogenesis in the developing chicken heart: assembly of Z-disk, M-line, and the thick filaments. J Cell Sci 112:1529–1539PubMed
5.
Zurück zum Zitat Engel FB, Schebesta M, Duong MT et al (2005) p38 MAP kinase inhibition enables proliferation of adult mammalian cardiomyocytes. Genes Dev 19:1175–1187PubMedCrossRef Engel FB, Schebesta M, Duong MT et al (2005) p38 MAP kinase inhibition enables proliferation of adult mammalian cardiomyocytes. Genes Dev 19:1175–1187PubMedCrossRef
6.
Zurück zum Zitat Esposito G, Rapacciuolo A, Naga Prasad SV et al (2002) Genetic alterations that inhibit in vivo pressure-overload hypertrophy prevent cardiac dysfunction despite increased wall stress. Circulation 105:85–92PubMedCrossRef Esposito G, Rapacciuolo A, Naga Prasad SV et al (2002) Genetic alterations that inhibit in vivo pressure-overload hypertrophy prevent cardiac dysfunction despite increased wall stress. Circulation 105:85–92PubMedCrossRef
7.
Zurück zum Zitat Gulick J, Subramaniam A, Neumann J, Robbins J (1991) Isolation and characterization of the mouse cardiac myosin heavy chain genes. J Biol Chem 266:9180–9185PubMed Gulick J, Subramaniam A, Neumann J, Robbins J (1991) Isolation and characterization of the mouse cardiac myosin heavy chain genes. J Biol Chem 266:9180–9185PubMed
8.
Zurück zum Zitat Herget GW, Neuburger M, Plagwitz R, Adler CP (1997) DNA content, ploidy level, and number of nuclei in the human heart after myocardial infarction. Cardiovasc Res 36:45–51PubMedCrossRef Herget GW, Neuburger M, Plagwitz R, Adler CP (1997) DNA content, ploidy level, and number of nuclei in the human heart after myocardial infarction. Cardiovasc Res 36:45–51PubMedCrossRef
9.
Zurück zum Zitat Hirschy A, Schatzmann F, Ehler E, Perriard JC (2006) Establishment of cardiac cytoarchitecture in the developing mouse heart. Dev Biol 289:430–441PubMedCrossRef Hirschy A, Schatzmann F, Ehler E, Perriard JC (2006) Establishment of cardiac cytoarchitecture in the developing mouse heart. Dev Biol 289:430–441PubMedCrossRef
10.
Zurück zum Zitat Hubbard SR (2004) Juxtamembrane autoinhibition in receptor tyrosine kinases. Nat Rev Mol Cell Biol 5:464–471PubMedCrossRef Hubbard SR (2004) Juxtamembrane autoinhibition in receptor tyrosine kinases. Nat Rev Mol Cell Biol 5:464–471PubMedCrossRef
11.
Zurück zum Zitat Li M, Naqvi N, Yahiro E, Liu K et al (2008) C-kit is required for cardiomyocyte terminal differentiation. Circ Res 102:677–685PubMedCrossRef Li M, Naqvi N, Yahiro E, Liu K et al (2008) C-kit is required for cardiomyocyte terminal differentiation. Circ Res 102:677–685PubMedCrossRef
12.
Zurück zum Zitat Mol CD, Lim KB, Sridhar V et al (2003) Structure of a c-kit product complex reveals the basis for kinase transactivation. J Biol Chem 278:31461–31464PubMedCrossRef Mol CD, Lim KB, Sridhar V et al (2003) Structure of a c-kit product complex reveals the basis for kinase transactivation. J Biol Chem 278:31461–31464PubMedCrossRef
13.
Zurück zum Zitat Mol CD, Dougan DR, Schneider TR et al (2004) Structural basis for the autoinhibition and STI-571 inhibition of c-kit tyrosine kinase. J Biol Chem 279:31655–31663PubMedCrossRef Mol CD, Dougan DR, Schneider TR et al (2004) Structural basis for the autoinhibition and STI-571 inhibition of c-kit tyrosine kinase. J Biol Chem 279:31655–31663PubMedCrossRef
14.
Zurück zum Zitat Ng WA, Grupp IL, Subramaniam A, Robbins J (1991) Cardiac myosin heavy chain mRNA expression and myocardial function in the mouse heart. Circ Res 68:1742–1750PubMed Ng WA, Grupp IL, Subramaniam A, Robbins J (1991) Cardiac myosin heavy chain mRNA expression and myocardial function in the mouse heart. Circ Res 68:1742–1750PubMed
15.
Zurück zum Zitat Nocka K, Majumder S, Chabot B, Ray P et al (1989) Expression of c-kit gene products in known cellular targets of W mutations in normal and W mutant mice: evidence for an impaired c-kit kinase in mutant mice. Genes Dev 3:816–826PubMedCrossRef Nocka K, Majumder S, Chabot B, Ray P et al (1989) Expression of c-kit gene products in known cellular targets of W mutations in normal and W mutant mice: evidence for an impaired c-kit kinase in mutant mice. Genes Dev 3:816–826PubMedCrossRef
16.
Zurück zum Zitat Nocka K, Tan JC, Chiu E et al (1990) Molecular bases of dominant negative and loss of function mutations at the murine c-kit/white spotting lOCUS: W37, W′, W41, and W. EMBO J 9:1805–1813PubMed Nocka K, Tan JC, Chiu E et al (1990) Molecular bases of dominant negative and loss of function mutations at the murine c-kit/white spotting lOCUS: W37, W′, W41, and W. EMBO J 9:1805–1813PubMed
17.
Zurück zum Zitat Oberpriller JO, Oberpriller JC (1974) Response of the adult newt ventricle to injury. J Exp Zool 187:249–253PubMedCrossRef Oberpriller JO, Oberpriller JC (1974) Response of the adult newt ventricle to injury. J Exp Zool 187:249–253PubMedCrossRef
18.
Zurück zum Zitat Pasumarthi KB, Nakajima H, Nakajima HO et al (2005) Targeted expression of cyclin D2 results in cardiomyocyte DNA synthesis and infarct regression in transgenic mice. Circ Res 96:110–118PubMedCrossRef Pasumarthi KB, Nakajima H, Nakajima HO et al (2005) Targeted expression of cyclin D2 results in cardiomyocyte DNA synthesis and infarct regression in transgenic mice. Circ Res 96:110–118PubMedCrossRef
19.
Zurück zum Zitat Poolman RA, Brooks G (1998) Expressions and activities of cell cycle regulatory molecules during the transition from myocyte hyperplasia to hypertrophy. J Mol Cell Cardiol 10:2121–2135CrossRef Poolman RA, Brooks G (1998) Expressions and activities of cell cycle regulatory molecules during the transition from myocyte hyperplasia to hypertrophy. J Mol Cell Cardiol 10:2121–2135CrossRef
20.
Zurück zum Zitat Poolman RA, Gilchrist R, Brooks G (1998) Cell cycle profiles and expressions of p21CIP1 AND P27KIP1 during myocyte development. Int J Cardiol 67:133–142PubMedCrossRef Poolman RA, Gilchrist R, Brooks G (1998) Cell cycle profiles and expressions of p21CIP1 AND P27KIP1 during myocyte development. Int J Cardiol 67:133–142PubMedCrossRef
21.
Zurück zum Zitat Poolman RA, Li JM, Durand B, Brooks G (1999) Altered expression of cell cycle proteins and prolonged duration of cardiac myocyte hyperplasia in p27KIP1 knockout mice. Circ Res 85:117–127PubMed Poolman RA, Li JM, Durand B, Brooks G (1999) Altered expression of cell cycle proteins and prolonged duration of cardiac myocyte hyperplasia in p27KIP1 knockout mice. Circ Res 85:117–127PubMed
22.
Zurück zum Zitat Poss KD, Wilson LG, Keating MT (2002) Heart regeneration in zebrafish. Science 298:2188–2190PubMedCrossRef Poss KD, Wilson LG, Keating MT (2002) Heart regeneration in zebrafish. Science 298:2188–2190PubMedCrossRef
23.
Zurück zum Zitat Rumyantsev PP (1977) Interrelations of the proliferation and differentiation processes during cardiact myogenesis and regeneration. Int Rev Cytol 51:186–273PubMed Rumyantsev PP (1977) Interrelations of the proliferation and differentiation processes during cardiact myogenesis and regeneration. Int Rev Cytol 51:186–273PubMed
24.
Zurück zum Zitat Soonpaa MH, Field LJ (1997) Assessment of cardiomyocyte DNA synthesis in normal and injured adult mouse hearts. Am J Physiol 272:H220–H226PubMed Soonpaa MH, Field LJ (1997) Assessment of cardiomyocyte DNA synthesis in normal and injured adult mouse hearts. Am J Physiol 272:H220–H226PubMed
25.
Zurück zum Zitat Soonpaa MH, Kim KK, Pjak L et al (1996) Cardiomyocyte DNA synthesis and binucleation during murine development. Am J Physiol 271:2183–2189 Soonpaa MH, Kim KK, Pjak L et al (1996) Cardiomyocyte DNA synthesis and binucleation during murine development. Am J Physiol 271:2183–2189
26.
Zurück zum Zitat Soonpaa MH, Koh GY, Pajak L et al (1997) Cyclin D1 overexpression promotes cardiomyocyte DNA synthesis and multinucleation in transgenic mice. J Clin Invest 99:2644–2654PubMedCrossRef Soonpaa MH, Koh GY, Pajak L et al (1997) Cyclin D1 overexpression promotes cardiomyocyte DNA synthesis and multinucleation in transgenic mice. J Clin Invest 99:2644–2654PubMedCrossRef
27.
Zurück zum Zitat Zeller R, Bloch KD, Williams BS et al (1987) Localized expression of the atrial natriuretic factor gene during cardiac embryogenesis. Genes Dev 1:693–698PubMedCrossRef Zeller R, Bloch KD, Williams BS et al (1987) Localized expression of the atrial natriuretic factor gene during cardiac embryogenesis. Genes Dev 1:693–698PubMedCrossRef
Metadaten
Titel
Insights into the Characteristics of Mammalian Cardiomyocyte Terminal Differentiation Shown Through the Study of Mice with a Dysfunctional c-Kit
verfasst von
Nawazish Naqvi
Ming Li
Eiji Yahiro
Robert M. Graham
Ahsan Husain
Publikationsdatum
01.07.2009
Verlag
Springer-Verlag
Erschienen in
Pediatric Cardiology / Ausgabe 5/2009
Print ISSN: 0172-0643
Elektronische ISSN: 1432-1971
DOI
https://doi.org/10.1007/s00246-008-9366-1

Weitere Artikel der Ausgabe 5/2009

Pediatric Cardiology 5/2009 Zur Ausgabe

Ein Drittel der jungen Ärztinnen und Ärzte erwägt abzuwandern

07.05.2024 Medizinstudium Nachrichten

Extreme Arbeitsverdichtung und kaum Supervision: Dr. Andrea Martini, Sprecherin des Bündnisses Junge Ärztinnen und Ärzte (BJÄ) über den Frust des ärztlichen Nachwuchses und die Vorteile des Rucksack-Modells.

Vorhofflimmern bei Jüngeren gefährlicher als gedacht

06.05.2024 Vorhofflimmern Nachrichten

Immer mehr jüngere Menschen leiden unter Vorhofflimmern. Betroffene unter 65 Jahren haben viele Risikofaktoren und ein signifikant erhöhtes Sterberisiko verglichen mit Gleichaltrigen ohne die Erkrankung.

Chronisches Koronarsyndrom: Gefahr von Hospitalisierung wegen Herzinsuffizienz

06.05.2024 Herzinsuffizienz Nachrichten

Obwohl ein rezidivierender Herzinfarkt bei chronischem Koronarsyndrom wahrscheinlich die Hauptsorge sowohl der Patienten als auch der Ärzte ist, sind andere Ereignisse womöglich gefährlicher. Laut einer französischen Studie stellt eine Hospitalisation wegen Herzinsuffizienz eine größere Gefahr dar.

Das Risiko für Vorhofflimmern in der Bevölkerung steigt

02.05.2024 Vorhofflimmern Nachrichten

Das Risiko, im Lauf des Lebens an Vorhofflimmern zu erkranken, ist in den vergangenen 20 Jahren gestiegen: Laut dänischen Zahlen wird es drei von zehn Personen treffen. Das hat Folgen weit über die Schlaganfallgefährdung hinaus.

Update Kardiologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.