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| Autor | Ronald Vlasblom, Alice Muller, René J.P. Musters, Marian J. Zuidwijk, Cornelis van Hardeveld, Walter J. Paulus, Warner S. Simonides |
| Titel | Contractile arrest reveals calcium-dependent stimulation of SERCA2a mRNA expression in cultured ventricular cardiomyocytes |
| Zeitschrift | Cardiovascular Research |
| Ausgabe | 18 |
| Datum | 10. Mai 2004 |
| Seiten | 537–544 |
| DOI | 10.1016/j.cardiores.2004.04.005 |
| URL | http://cardiovascres.oxfordjournals.org/content/63/3/537.full.pdf |
Literaturverz. |
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| Fußnoten | nein |
| Fragmente | 2 |
| [1.] Analyse:Aa/Fragment 013 02 - Diskussion Zuletzt bearbeitet: 2013-04-08 23:30:41 Graf Isolan | Aa, Fragment, SMWFragment, Schutzlevel, Verschleierung, Vlasblom et al 2004, ZuSichten |
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| This down-regulation of SERCA2a may affect calcium handling and contribute to contractile dysfunction, as suggested by the improved contractility of hypertrophied myocardium following SERCA2a protein over expression using transgenic approaches (Muller et al., 2003; Meyer and Dillmann, 1998). [...]
The reduction of myocardial SERCA2a mRNA and protein expression in pathological hypertrophy was attributed to reduced SERCA2a promoter activity (Dumas et al., 1997). This finding was further corroborated by lower activity of a - 1800 bp SERCA2a promoter fragment when transfected in vivo in pressure-overloaded, hypertrophic hearts (Aoyagi et al., 1999; Takizawa et al., 1999). Aoyagi T, Yonekura K, Eto Y, Matsumoto A, Yokoyama I, Sugiura S, Momomura S, Hirata Y, Baker DL and Periasamy M (1999) The sarcoplasmic reticulum Ca2+-ATPase (SERCA2) gene promoter activity is decreased in response to severe left ventricular pressure-overload hypertrophy in rat hearts. J Mol Cell Cardiol 31:919–926. Dumas AR, Wisnewsky C, Boheler KR, Keurs HT, Fiszman MY and Schwartz K (1997) The sarco(endo)plasmic reticulum Ca2+-ATPase gene is regulated at the transcriptional level during compensated left ventricular hypertrophy in the rat. Comptes Rendus de l'Academie des Sciences-Series III-Sciences de la Vie. 320:963–969. Meyer M, and Dillmann WH (1998) Sarcoplasmic reticulum Ca2+-ATPase over expression by adenovirus mediated gene transfer and in transgenic mice. Cardiovasc Res 37: 360–366. Muller OJ, Lange M, Rattunde H, Lorenzen HP, Muller M, Frey N, et al. (2003) Transgenic rat hearts overexpressing SERCA2a show improved contractility under baseline conditions and pressure overload. Cardiovasc Res 59: 380–389 Takizawa T, Arai M, Yoguchi A, Tomaru K, Kurabayashi M and Nagai R (1999) Transcription of the SERCA2 gene is decreased in pressure-overloaded hearts: a study using in vivo direct gene transfer into living myocardium. J Mol Cell Cardiol 31: 2167–2174. |
This downregulation may affect calcium handling and contribute to contractile dysfunction, as suggested by the improved contractility of hypertrophied myocardium following SERCA2a protein overexpression using transgenic approaches [3,4]. The reduction of myocardial SERCA2a mRNA and protein expression in pathological hypertrophy was attributed to reduced SERCA2a promoter activity [5]. This finding was further corroborated by lower activity of a 1800 bp SERCA2a promoter fragment when transfected in vivo in pressure-overloaded, hypertrophic hearts [6,7].
[3] Muller OJ, Lange M, Rattunde H, Lorenzen HP, Muller M, Frey N, et al. Transgenic rat hearts overexpressing SERCA2a show improved contractility under baseline conditions and pressure overload. Cardiovasc Res 2003;59:380–9. [4] Meyer M, Dillmann WH. Sarcoplasmic reticulum Ca2+-ATPase overexpression by adenovirus mediated gene transfer and in transgenic mice. Cardiovasc Res 1998;37:360–6. [5] Dumas AR, Wisnewsky C, Boheler KR, Keurs HT, Fiszman MY, Schwartz K. The sarco(endo)plasmic reticulum Ca2+-ATPase gene is regulated at the transcriptional level during compensated left ventricular hypertrophy in the rat. Comptes Rendus de l’Academie des Sciences-Series III-Sciences de la Vie 1997;320:963–9. [6] Aoyagi T, Yonekura K, Eto Y, Matsumoto A, Yokoyama I, Sugiura S, et al. The sarcoplasmic reticulum Ca2+-ATPase (SERCA2) gene promoter activity is decreased in response to severe left ventricular pressure-overload hypertrophy in rat hearts. J Mol Cell Cardiol 1999;31:919– 26. [7] Takizawa T, Arai M, Yoguchi A, Tomaru K, Kurabayashi M, Nagai R. Transcription of the SERCA2 gene is decreased in pressure-overloaded hearts: a study using in vivo direct gene transfer into living myocardium. J Mol Cell Cardiol 1999;31:2167–74. |
Identisch bis hin zu den Literaturverweisen. Übernahmen bleiben ungekennzeichnet. Fragment komplementiert Aa/Fragment_013_05. |
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| [2.] Analyse:Aa/Fragment 013 17 - Diskussion Zuletzt bearbeitet: 2013-02-06 23:11:57 Graf Isolan | Aa, Fragment, SMWFragment, Schutzlevel, Verschleierung, Vlasblom et al 2004, ZuSichten |
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| In myocardial hypertrophy induced by calcineurin over expression, both a fall in SERCA2a mRNA (Molkentin et al 1998) and a rise in SERCA2a protein (Chu et al., 2002) have been observed. In neonatal cardiomyocytes an up-regulation of SERCA2a mRNA expression was found in absence of contractile activity. This is likely due to calcineurin signaling and synergistic stimulation of the SERCA2a promoter by NFATc4 and MEF2c.
Chu G, Carr AN, Young KB, Lester JW, Yatani A, Sanbe A, et al. (2002) Enhanced myocyte contractility and Ca2+ handling in a calcineurin transgenic model of heart failure. Cardiovasc. Res 54: 105–116. Molkentin JD, Lu JR, Antos CL, Markham B, Richardson J, Robbins J, Grant SR and Olson EN (1998) A calcineurin-dependent transcriptional pathway for cardiac hypertrophy. Cell 93: 215-228. |
[Seite 537]
Conclusion: Following contractile arrest with BDM, upregulation of SERCA2a mRNA expression by CN/CAMK-II signaling becomes evident. [Seite 538] In myocardial hypertrophy induced by CN overexpression, both a fall in SERCA2a mRNA [12] and a rise in SERCA2a protein [16] have been observed. [Seite 543] 5. Conclusions [...] Both CN and CAMK-II pathways are involved in the calcium-dependent upregulation, most likely due to synergistic stimulation of the SERCA2a promoter by NFATc4 and MEF2c. [12] Molkentin JD, Lu JR, Antos CL, Markham B, Richardson J, Robbins J, et al. A calcineurin-dependent transcriptional pathway for cardiac hypertrophy. Cell 1998;93:215–28. [16] Chu G, Carr AN, Young KB, Lester JW, Yatani A, Sanbe A, et al. Enhanced myocyte contractility and Ca2+ handling in a calcineurin transgenic model of heart failure. Cardiovasc Res 2002;54:105– 16. |
Patchwork: vielfach identisch bis hin zu den Literaturverweisen. Übernahmen bleiben ungekennzeichnet. |
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