Browsing by Author "Ocaranza, Maria Paz"

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    Enalapril attenuates downregulation of angiotensin-converting enzyme 2 in the late phase of ventricular dysfunction in myocardial infarcted rat
    (LIPPINCOTT WILLIAMS & WILKINS, 2006) Ocaranza, Maria Paz; Godoy, Ivan; Jalil, Jorge E.; Varas, Manuel; Collantes, Patricia; Pinto, Melissa; Roman, Maritza; Ramirez, Cristian; Copaja, Miguel; Diaz Araya, Guillermo; Castro, Pablo; Lavandero, Sergio
    The early and long-term effects of coronary artery ligation on the plasma and left ventricular angiotensin-converting enzyme (ACE and ACE2) activities, ACE and ACE2 mRNA levels, circulating angiotensin (Ang) levels [Ang I, Ang-(1-7), Ang-(1-9), and Ang II], and cardiac function were evaluated 1 and 8 weeks after experimental myocardial infarction in adult Sprague Dawley rats. Sham-operated rats were used as controls. Coronary artery ligation caused myocardial infarction, hypertrophy, and dysfunction 8 weeks after surgery. At week 1, circulating Ang II and Ang-(1-9) levels as well as left ventricular and plasma ACE and ACE2 activities increased in myocardial-infarcted rats as compared with controls. At 8 weeks post-myocardial infarction, circulating ACE activity, ACE mRNA levels, and Ang II levels remained higher, but plasma and left ventricular ACE2 activities and mRNA levels and circulating levels of Ang-(1-9) were lower than in controls. No changes in plasma Ang-(1-7) levels were observed at any time. Enalapril prevented cardiac hypertrophy and dysfunction as well as the changes in left ventricular ACE, left ventricular and plasmatic ACE2, and circulating levels of Ang II and Ang-(1-9) after 8 weeks postinfafction. Thus, the decrease in ACE2 expression and activity and circulating Ang-(1-9) levels in late ventricular dysfunction post-myocardial infarction were prevented with enalapril. These findings suggest that in this second arm of the renin-angiotensin system, ACE2 may act through Ang-(1-9), rather than Ang-(1-7), as a counterregulator of the first arm, where ACE catalyzes the formation of Ang II.
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    Osmotically-induced genes are controlled by the transcription factor TonEBP in cultured cardiomyocytes
    (ACADEMIC PRESS INC ELSEVIER SCIENCE, 2008) Navarro, Paola; Chiong, Mario; Volkwein, Karen; Moraga, Francisco; Ocaranza, Maria Paz; Jalil, Jorge E.; Lim, Sun Woo; Kim, Jeong Ah; Kwon, H. Moo; Lavandero, Sergio
    Changes in cardiac osmolarity occur in myocardial infarction. Osmoregulatory mechanism may, therefore, play a Crucial role in cardiomyocyte survival. Tonicity-responsive enhancer binding protein (TonEBP) is a key transcription factor participating in the adaptation of cells to increases in tonicity. However, it is unknown whether cardiac TonEBP is activated by tonicity. Hypertonicity activated transcriptional activity of TonEBP, increased the amounts of both TonEBP mRNA and protein, and induced both the mRNA and protein of TonEBP target genes (aldose reductase and heat shock protein-70). Hypotonicity decreased the amount of TonEBP protein indicating bidirectional osmoregulation of this transcription factor. Adenoviral expression of a dominant negative TonEBP suppressed the hypertonicity-dependent increase of aldose reductase protein. These results indicated that TonEBP controls osmoregulatory mechanisms in cardiomyocytes. (C) 2008 Elsevier Inc. All rights reserved.