|
|
|
|
|
| Vizotto,V.A.; Carvalho,R.F.; Sugizaki,M.M.; Lima,A.P.; Aragon,F.F.; Padovani,C.R.; Castro,A.V.B.; Dal Pai-Silva,M.; Nogueira,C.R.; Cicogna,A.C.. |
| We have shown that myocardial dysfunction induced by food restriction is related to calcium handling. Although cardiac function is depressed in food-restricted animals, there is limited information about the molecular mechanisms that lead to this abnormality. The present study evaluated the effects of food restriction on calcium cycling, focusing on sarcoplasmic Ca2+-ATPase (SERCA2), phospholamban (PLB), and ryanodine channel (RYR2) mRNA expressions in rat myocardium. Male Wistar-Kyoto rats, 60 days old, were submitted to ad libitum feeding (control rats) or 50% diet restriction for 90 days. The levels of left ventricle SERCA2, PLB, and RYR2 were measured using semi-quantitative RT-PCR. Body and ventricular weights were reduced in 50% food-restricted... |
| Tipo: Info:eu-repo/semantics/other |
Palavras-chave: Food restriction; SERCA2; Ryanodine channel; Phospholamban; MRNA. |
| Ano: 2007 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2007000100004 |
| |
|
|
| Mattiazzi,A.; Mundiña-Weilenmann,C.; Vittone,L.; Said,M.; Kranias,E.G.. |
| The sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a) is under the control of an SR protein named phospholamban (PLN). Dephosphorylated PLN inhibits SERCA2a, whereas phosphorylation of PLN at either the Ser16 site by PKA or the Thr17 site by CaMKII reverses this inhibition, thus increasing SERCA2a activity and the rate of Ca2+ uptake by the SR. This leads to an increase in the velocity of relaxation, SR Ca2+ load and myocardial contractility. In the intact heart, ß-adrenoceptor stimulation results in phosphorylation of PLN at both Ser16 and Thr17 residues. Phosphorylation of the Thr17 residue requires both stimulation of the CaMKII signaling pathways and inhibition of PP1, the major phosphatase that dephosphorylates PLN. These two prerequisites appear to... |
| Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Phospholamban; Thr17 site phosphorylation; SS-adrenergic stimulation; Acidosis; Ischemia. |
| Ano: 2006 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2006000500001 |
| |
|
|
|
