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Typus
Verschleierung
Bearbeiter
Graf Isolan
Gesichtet
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Untersuchte Arbeit:
Seite: 12, Zeilen: 6-30
Quelle: Periasamy und Huke 2001
Seite(n): 1053, 1054, Zeilen: 0
A number of studies suggest that alterations in SR Ca2+ handling are a critical feature of the hypertrophied or failing myocardium. Alterations in the expression of different SR proteins and associated Ca2+ transport abnormalities in cardiac hypertrophy and heart failure have been reviewed by Houser et al. (2000). The SERCA2a isoform plays a central role in SR Ca2+ handling required for excitation-contraction coupling in the heart. Moreover, it was shown for mouse, rat and rabbit that the expression of SERCA pump gradually increases during development (Luss et al., 1999; Reed et al., 2000; Chen et al., 2000; Fisher et al., 1992; Gombosova et al., 1998). This increase was accompanied by a shortening of relaxation time in neonatal ventricle (Gombosova et al., 1998). In adult heart SERCA levels are not steady but influenced by aging and fluctuations

in thyroid hormone level. A decrease in content and activity of SERCA was described in experimental models of senescence and in senescent human myocardium (Taffet et al., 1993; Cain et al., 1998). This decrease was associated with a prolonged contraction time and depressed myocardial function. Therefore, several naturally occurring variations in SERCA expression level correlate with the contractile status of the heart. The expression level of SERCA pump protein appears to be a critical determinant of cardiac contractility.

Varying degrees of defects in the SR Ca2+ uptake have been identified in animal models of heart disease and have been shown to correlate with altered contractile function (reviewed in Arai et al., 1994). Studies from many laboratories have shown that the expression level of SERCA is significantly decreased in pressure overload-induced hypertrophy/heart failure (Nagai et al., 1989; Feldman et al., 1993; Matsui et al., 1995; Qi et al., 1997; Aoyagi et al., 1999). In these studies decreased SR calcium transport was observed (Arai et [al., 1994; Feldman et al., 1993; 1993; Matsui et al., 1995; Qi et al., 1997; Kiss et al., 1995).]


Arai M, Matsui H and Periasamy M (1994) Sarcoendoplasmic reticulum gene expression in cardiac hypertrophy and heart failure. Circ Res 74: 555–564.

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.

Cain BS, Medlum DR, Joo KS, Wang JF, Meng X, Clefeland JC Jr, Banerjee A and Harken AH (1998) Human SERCA2a levels correlate inversely with age in senescent human myocardium. Am J Coll Cardiol 32: 458–467.

Chen F, Ding S, Lee BS and Wetzel GT (2000) Sarcoplasmic reticulum Ca2+ ATPase and cell contraction in developing rabbit heart. J Mol Cell Cardiol 32: 745–755.

Feldman AM, Weinberg EO, Ray PE and Lorell BH (1993) Selective changes in cardiac gene expression during compensated hypertrophy and the transition to cardiac decompensation in rats with chronic aortic banding. Circ Res 73: 184– 192.

Fisher DJ, Tate CA and Phillips S (1992) Developmental regulation of the sarcoplasmic reticulum pump in the rabbit heart. Pediatr Res 31: 474–479.

Gombosova I, Boknik P, Kirchhefer U, Knapp J, Luss H, Muller FU, Muller T, Vahlensiek U, Schmitz W, Bodor GS and Neumann J (1998) Postnatal changes in contractile time parameters, calcium regulatory proteins, and phosphatases. Am J Physiol 274: H2123–H2132.

Houser SR, Piacentino V and Weisser J (2000) Abnormalities of calcium cycling in the hypertrophied and failing heart. J Mol Cell Cardiol 32: 1595–1607.

Kiss E, Ball NA, Kranias EG and Walsh RA (1995) Differential changes in cardiac phospholamban and sarcoplasmic reticular Ca2+-ATPase protein levels. Effects on Ca2+transport and mechanics in compensated pressure-overload hypertrophy and congestive heart failure. Circ Res 77: 759–764.

Luss I, Boknik P, Jones LR, Kirchhefer U, Knapp J, Linck B, Luss H, Meissner A, Muller FR, Schmitz W, Vahlensieck U and Neumann J (1999) Expression of cardiac calcium regulatory proteins in atrium v ventricle in different species. J Mol Cell Cardiol 31: 1299–1314.

Matsui H, MacLennan DH, Alpert N and Periasamy M (1995) Sarcoplasmic reticulum gene expression in pressure overload-induced cardiac hypertrophy in rabbit. Am J Physiol 268: C252–C258.

Nagai R, Herzberg AZ, Brandl CJ, Fuji J, Tada M, MacLennan DH, Alpert NR and Periasamy M (1989) Regulation of myocardial Ca2+ATPase and phospholamban mRNA expression in response to pressure overload and thyroid hormone. Proc Natl Acad Sci USA 86: 2966–2970.

Qi M, Shannon TR, Euler DE, Bers DM and Samarel AM (1997) Downregulation of sarcoplasmic reticulum Ca2+-ATPase during progression of left ventricular hypertrophy. Am J Physiol 272: H2416–H2424.

Reed TD, Babu GJ, Ji Y, Zilberman A, Ver Heyen M, Wuytack F and Periasamy M (2000) The expression of SR calcium transport ATPase and the Na/Ca exchanger are antithetically regulated during mouse cardiac development and in hypo/hyperthyroidism. J Mol Cell Cardiol 32: 453–464.

Taffet GE, Pham TT, Bick DL, Entman ML, Pownall HJ and Bick RJ (1993) The calcium uptake of the rat heart sarcoplasmic reticulum is altered by dietary lipid. J Membr Biol 131: 963–998.

[Seite 1053]

A number of studies, conducted on animal models of heart failure and human failing hearts, suggest that alterations in SR Ca2+ handling are a critical feature of the hypertrophied or failing myocardium. Alterations in the expression of different SR proteins and its associated Ca2+ transport abnormalities in cardiac hypertrophy and heart failure have been recently reviewed by Houser et al.6

[Seite 1054]

The SERCA2a isoform plays a central role in SR Ca2+ handling required for excitation-contraction coupling in the heart. [...] Moreover, it was shown for mouse, rat and rabbit that the expression of SERCA pump gradually increases during development.16,19–22 This increase was again accompanied by a shortening of relaxation time in adult v neonatal ventricle.22 In addition also in adult hearts SERCA levels are not steady, but are influenced by aging and fluctuations in thyroid hormone levels. A decrease in content and activity of SERCA was described in experimental models of senescence and in senescent human myocardium.23,24 This decrease was associated with a prolonged contraction time and depressed myocardial function. [...]

Therefore, several naturally occurring variations in SERCA expression level correlate with the contractile status of the heart. The expression level of SERCA pump protein appears to be a critical determinant of cardiac contractility. [...]

Varying degrees of defects in the SR Ca2+ uptake function have been identified in animal models of heart disease and have been shown to correlate with altered contractile SERCA2a Pump Expression Level in the function (reviewed in Arai et al.7). Studies from many laboratories have shown that the expression level of SERCA is significantly decreased in pressure overload (PO)-induced hypertrophy/heart failure.30–34 In these studies decreased SR calcium transport and formation of the phosphoenzyme intermediate, E-P, was observed.7,31–33,35


6. HOUSER SR, PIACENTINO V, WEISSER J. Abnormalities of calcium cycling in the hypertrophied and failing heart. J Mol Cell Cardiol 2000; 32: 1595–1607.

7. ARAI M, MATSUI H, PERIASAMY M. Sarcoendoplasmic reticulum gene expression in cardiac hypertrophy and heart failure. Circ Res 1994; 74: 555–564.

16. LUSS I, BOKNIK P, JONES LR, KIRCHHEFER U, KNAPP J, LINK B, LUSS H, MEISSNER A, MULLER FR, SCHMITZ W, VAHLENSIECK U, NEUMANN J. Expression of cardiac calcium regulatory proteins in atrium v ventricle in different species. J Mol Cell Cardiol 1999; 31: 1299–1314.

19. REED TD, BABU GJ, JI Y, ZILBERMAN A, VER HEYEN M, WUYTACK F, PERIASAMY M. The expression of SR calcium transport ATPase and the Na/Ca exchanger are antithetically regulated during mouse cardiac development and in hypo/hyperthyroidism. J Mol Cell Cardiol 2000; 32: 453–464.

20. CHEN F, DING S, LEE BS, WETZEL GT. Sarcoplasmic reticulum Ca(2+)ATPase and cell contraction in developing rabbit heart. J Mol Cell Cardiol 2000; 32: 745–755.

21. FISHER DJ, TATE CA, PHILLIPS S. Developmental regulation of the sarcoplasmic reticulum pump in the rabbit heart. Pediatr Res 1992; 31: 474–479.

22. GOMBOSOVA I, BOKNIK P, KIRCHHEFER U, KNAPP J, LUSS H, MULLER FU, MULLER T, VAHLENSIECK U, SCHMITZ W, BODOR GS, NEUMANN J. Postnatal changes in contractile time parameters, calcium regulatory proteins, and phosphatases. Am J Physiol 1998; 274: H2123–H2132.

23. TAFFET GE, PHAM TT, BICK DL, ENTMAN ML, POWNALL HJ, BICK RJ. The calcium uptake of the rat heart sarcoplasmic reticulum is altered by dietary lipid. J Membr Biol 1993; 131: 963–998.

24. CAIN BS, MEDLUM DR, JOO KS, WANG JF, MENG X, CLEFELAND JC JR, BANERJEE A, HARKEN AH. Human SERCA2a levels correlate inversely with age in senescent human myocardium. J Am Cardiol 1998; 32: 458–467.

30. NAGAI R, HERZBERG AZ, BRANDL CJ, FUJI J, TADA M, MACLENNAN DH, ALPERT NR, PERIASAMY M. Regulation of myocardial Ca2+ ATPase and phospholamban mRNA expression in response to pressure overload and thyroid hormone. Proc Natl Acad Sci USA 1989; 86: 2966–2970.

31. FELDMAN AM, WEINBERG EO, RAY PE, LORELL BH. Selective changes in cardiac gene expression during compensated hypertrophy and the transition to cardiac decompensation in rats with chronic aortic banding. Circ Res 1993; 73: 184–192.

32. MATSUI H, MACLENNAN DH, ALPERT N, PERIASAMY M. Sarcoplasmic reticulum gene expression in pressure overload-induced cardiac hypertrophy in rabbit. Am J Physiol 1995; 268: C252–C258.

33. QI M, SHANNON TR, EULER DE, BERS DM, SAMAREL AM. Downregulation of sarcoplasmic reticulum Ca2+-ATPase during progression of left ventricular hypertrophy. Am J Physiol 1997; 272: H2416–H2424.

34. AOYAGI T, YONEKURA K, ETO Y, MATSUMOTO A, YOKOYAMA I, SUGIURA S, MONOMURA S, HIRATAA Y, BAKER DL, PERIASAMY M. 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: 919–926.

35. KISS E, BALL NA, KRANIAS EG,WALSH RA. Differential changes in cardiac phospholamban and sarcoplasmic reticular Ca(2+)-ATPase protein levels. Effects on Ca2+ transport and mechanics in compensated pressure-overload hypertrophy and congestive heart failure. Circ Res 1995; 77: 759-764.

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