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      Cardiac Hypertrophy in the Prague- Hypertensive Rat Is Associated with Enhanced JNK2 but not ERK Tissue Activity

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          Mitogen-activated protein (MAP) kinases are important intracellular mediators for proliferation and hypertrophy and therefore may also regulate cardiomyoblast growth in hypertensive heart disease. Thus, the aim of the present study was to examine the activities of MAP kinases, namely extracellular signal-regulated kinase (ERK)1,2, c-Jun NH<sub>2</sub>-terminal kinases (JNK)1,2 and p38 MAP kinase, in myocardial tissue of 12-week-old Prague normotensive (PNR) and hypertensive rats (PHR), a model of genetic hypertension with marked cardiac hypertrophy. Systolic blood pressure was 121 ± 5 in PNR and 208 ± 15 mm Hg in PHR (p < 0.01). Total heart weight was 247 ± 4 in PNR vs. 316 ± 4 mg/100 g body weight in PHR (p < 0.01). Left and right ventricular weights were 121 ± 5 and 53 ± 3 in PNR vs. 168 ± 4 (p < 0.01) and 57 ± 2 mg/100 g body weight (n.s.) in PHR. Using anti-ERK2 Western blot analysis as well as immunocomplex ERK activity assay, we found no activation of ERK2 in left or right ventricular tissue of PHR and PNR. Similary, p38 MAP kinase phosphorylation and activity were not detectable. In contrast, Western blot analysis using antiphospho-JNK antibodies revealed in myocardial tissue of right and left ventricles significantly greater phosphorylation of JNK2 in PHR than in PNR. This finding was confirmed by immunocomplex JNK activity assay using ATF-2 as substrate, which demonstrated a significant increase in JNK activity in the left ventricle of PHR as compared to PNR (6.4 ± 1.5 vs. 2.5 ± 0.5 OD; each n = 5; p < 0.05). In conclusion, cardiac JNK2 seems to be regulated differently from ERK2 in this rat model. In PHR, as compared to PNR, we found enhanced activity of JNK2 in the left and right ventricles suggesting that JNK2 is involved in hypertensive cardiac disease. The rise in JNK in both ventricles may result indirectly from humoral stimuli, e.g., endothelin-1 and/or angiotensin II, and may contribute to ventricular hypertrophy in this model of spontaneous hypertension.

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          Most cited references 6

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          Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitro.

          Hypertrophy is a fundamental adaptive process employed by postmitotic cardiac and skeletal muscle in response to mechanical load. How muscle cells convert mechanical stimuli into growth signals has been a long-standing question. Using an in vitro model of load (stretch)-induced cardiac hypertrophy, we demonstrate that mechanical stretch causes release of angiotensin II (Ang II) from cardiac myocytes and that Ang II acts as an initial mediator of the stretch-induced hypertrophic response. The results not only provide direct evidence for the autocrine mechanism in load-induced growth of cardiac muscle cells, but also define the pathophysiological role of the local (cardiac) renin-angiotensin system.
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            The MAP kinase cascade is essential for diverse signal transduction pathways.

            Mitogen-activated protein (MAP) kinases are activated by combined tyrosine and threonine phosphorylation catalysed by MAP kinase kinase, a novel class of protein kinases with dual specificity for both tyrosine and serine/threonine. MAP kinase kinase is turned on by serine/threonine phosphorylation catalysed by an immediate upstream kinase. The MAP kinase cascade appears to be conserved during evolution and thus might play an essential role in diverse intracellular signaling processes from yeasts to vertebrates.
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              Sounding the Alarm: Protein Kinase Cascades Activated by Stress and Inflammation


                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                24 January 2001
                : 24
                : 1
                : 52-56
                aRenal Section, Medical Policlinic, University of Bonn, Germany, and bDepartment of Experimental Medicine, Institute of Clinical and Experimental Medicine, Prague, Czech Republic
                54206 Kidney Blood Press Res 2001;24:52–56
                © 2001 S. Karger AG, Basel

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                Figures: 4, References: 20, Pages: 5
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