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The MEKK1-JNK pathway plays a protective role in pressure overload but does not mediate cardiac hypertrophy
Junichi Sadoshima, … , Dorothy E. Vatner, Stephen F. Vatner
Junichi Sadoshima, … , Dorothy E. Vatner, Stephen F. Vatner
Published July 15, 2002
Citation Information: J Clin Invest. 2002;110(2):271-279. https://doi.org/10.1172/JCI14938.
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Article Genetics

The MEKK1-JNK pathway plays a protective role in pressure overload but does not mediate cardiac hypertrophy

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Abstract

Research Article

Authors

Junichi Sadoshima, Olivier Montagne, Qian Wang, Guiping Yang, Jill Warden, Jing Liu, Gen Takagi, Vijaya Karoor, Chull Hong, Gary L. Johnson, Dorothy E. Vatner, Stephen F. Vatner

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Figure 5

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Pressure overload causes more inflammatory lesions, predominantly consis...
Pressure overload causes more inflammatory lesions, predominantly consisting of macrophages, as well as apoptosis of the inflammatory cells in the left ventricle in MEKK1–/– mice. Hematoxylin-and-eosin staining reveals an increased number of inflammatory lesions in MEKK1–/– mice (b) compared with control mice (a). Bar = 150 μm.(c) The inflammatory lesions in LV myocardium were measured by image analysis software. There was an increase in inflammatory lesions in MEKK1–/– mice compared with control mice after 7 days of pressure overload. *P < 0.05; n = 5. (d) Macrophages, lymphocytes, and neutrophils in the LV myocardium from MEKK1–/– mice subjected to pressure overload were stained as described in Methods. The inflammatory cells primarily consisted of macrophages.

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