Divergent effects of hormone therapy on serum markers of inflammation in postmenopausal women with coronary artery disease on appropriate medical management
Diane Zanger, MDa,
Benjamin K. Yanga,
Jeanette Ardans, BSc,
Myron A. Waclawiw, PhDb,
Gyorgy Csako, MDd,
Larry M. Wahl, PhDc and
Richard O. Cannon, III, MD, FACCa
a Cardiology Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland, USA
b Office of Biostatistics Research, National Heart, Lung and Blood Institute, Bethesda, Maryland, USA
c Immunopathology Section, National Institute of Dental and Craniofacial Research, Bethesda, Maryland, USA
d Clinical Pathology Department, Clinical Center, National Institutes of Health, Bethesda, Maryland, USA

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Figure 1 Serum levels of the cell adhesion molecules E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are shown for the 10 study participants during placebo and hormone therapy (HT) treatment periods of the study. CEE = conjugated equine estrogens; MPA = medroxyprogesterone acetate.
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Figure 2 Matrix metalloproteinase-9 (MMP-9) serum levels by ELISA are shown for the 10 study participants identified by letters A through J (the order of entry into the study) and during placebo and hormone therapy treatment phases of the study. CEE = conjugated equine estrogens; MPA = medroxyprogesterone acetate.
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Figure 3 Panel A: Zymography of paired serum samples from the 10 study participants with coronary artery disease shows digestion of gelatin at the 92 kDa band, indicative of the proenzyme form of MMP-9, during placebo () and hormone therapy (+) treatment periods of the study. Individual patients are identified by letters A through J and correspond with the identification letters in Figure 2. Panel B: Optical scanning of the zymograms from panel A, with values reported as densitometric units. Solid bars = placebo; open bars = estrogen. MMP = matrix metalloproteinase.
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