Document Detail

Induction of mitogen-activated protein kinases is proportional to the amount of pressure overload.
MedLine Citation:
PMID:  19901160     Owner:  NLM     Status:  MEDLINE    
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.
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:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-11-09
Journal Detail:
Title:  Hypertension     Volume:  55     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2010 Jan 
Date Detail:
Created Date:  2009-12-18     Completed Date:  2010-01-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  137-43     Citation Subset:  IM    
Division of Cardiology, Federico II University, Via Pansini 5, 80131 Naples, Italy.
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MeSH Terms
Aorta / physiopathology
Atrial Natriuretic Factor / genetics
Blood Pressure / physiology*
Blotting, Northern
Blotting, Western
Constriction, Pathologic
Enzyme Activation
Gene Expression
Hypertension / enzymology,  genetics,  physiopathology*
Leukocytes / enzymology
MAP Kinase Signaling System / physiology*
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
p38 Mitogen-Activated Protein Kinases / blood,  metabolism
Reg. No./Substance:
85637-73-6/Atrial Natriuretic Factor; EC Protein Kinase 1; EC Protein Kinase 8; EC Protein Kinases; EC Mitogen-Activated Protein Kinases
Comment In:
Hypertension. 2010 Jan;55(1):23-5   [PMID:  19901156 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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