| Induction of mitogen-activated protein kinases is proportional to the amount of pressure overload. | |
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MedLine Citation:
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PMID: 19901160 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Pressure overload has been shown to induce mitogen activated protein kinases (MAPKs) and reactivate the atrial natriuretic factor in the heart. To test the sensitivity of these signals to pressure overload, we assayed the activity of MAPKs extracellular signal-regulated kinase, c-Jun N-terminal kinase 1, and p38 in protein lysates from the left ventricle (LV) or white blood cells (WBC) isolated from aortic banded mice with varying levels of pressure overload. In separated mice we measured atrial natriuretic factor mRNA levels by Northern blotting. As expected, a significant induction of atrial natriuretic factor mRNA levels was observed after aortic banding, and it significantly correlated with the trans-stenotic systolic pressure gradient but not with the LV weight:body weight ratio. In contrast, a significant correlation with systolic pressure gradient or LV weight:body weight ratio was observed for all of the MAPK activity detected in LV samples or WBCs. Importantly, LV activation of MAPKs significantly correlated with their activation in WBCs from the same animal. To test whether MAPK activation in WBCs might reflect uncontrolled blood pressure levels in humans, we assayed extracellular signal-regulated kinase, c-Jun N-terminal kinase 1, and p38 activation in WBCs isolated from normotensive volunteers, hypertensive patients with controlled blood pressure values, or hypertensive patients with uncontrolled blood pressure values. Interestingly, in hypertensive patients with controlled blood pressure values, LV mass and extracellular signal-regulated kinase phosphorylation were significantly reduced compared with those in hypertensive patients with uncontrolled blood pressure values. These results suggest that MAPKs are sensors of pressure overload and that extracellular signal-regulated kinase activation in WBCs might be used as a novel surrogate biomarker of uncontrolled human hypertension. |
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Authors:
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Giovanni Esposito; Cinzia Perrino; Gabriele Giacomo Schiattarella; Lorena Belardo; Elisa di Pietro; Anna Franzone; Giuliana Capretti; Giuseppe Gargiulo; Gianluigi Pironti; Alessandro Cannavo; Anna Sannino; Raffaele Izzo; Massimo Chiariello |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-11-09 |
Journal Detail:
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Title: Hypertension Volume: 55 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2010 Jan |
Date Detail:
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Created Date: 2009-12-18 Completed Date: 2010-01-21 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 137-43 Citation Subset: IM |
Affiliation:
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Division of Cardiology, Federico II University, Via Pansini 5, 80131 Naples, Italy. espogiov@unina.it |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Aorta / physiopathology Atrial Natriuretic Factor / genetics Blood Pressure / physiology* Blotting, Northern Blotting, Western Constriction, Pathologic Enzyme Activation Female Gene Expression Humans Hypertension / enzymology, genetics, physiopathology* Hypertrophy Leukocytes / enzymology MAP Kinase Signaling System / physiology* Male Mice Middle Aged Mitogen-Activated Protein Kinase 1 / blood, metabolism Mitogen-Activated Protein Kinase 8 / blood, metabolism Mitogen-Activated Protein Kinases / blood, metabolism* Myocardium / metabolism, pathology Phosphorylation Pressure p38 Mitogen-Activated Protein Kinases / blood, metabolism |
| Chemical | |
Reg. No./Substance:
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85637-73-6/Atrial Natriuretic Factor; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 8; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases |
| Comments/Corrections | |
Comment In:
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Hypertension. 2010 Jan;55(1):23-5
[PMID:
19901156
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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