Endothelial Cells, Estrogen and Angiogenesis
Increasing clinical evidence supports a role for estrogen in modulating vascular cell function. Premenopausal women enjoy relative protection from heart attacks and strokes compared with men. After menopause, the incidence of atherosclerotic cardiovascular disease rapidly approximates that of men (Stampfer et al. 1990). Moreover, several studies have indicated that postmenopausal estrogen replacement therapy may decrease the incidence of subsequent cardiovascular events in women (Grady et al. 1992; Psaty et al. 1994; Folsom et al. 1995; Writing Group for the PEPI Trial 1995). A role for estrogen in vascular biology is further suggested by the observation that women have higher rates of certain inflammatory diseases than do men, including several diseases that are associated with local angiogenesis (Beeson 1994). Third, spider angiomas are common occurrences in pregnant women or in men with chronic liver disease. After pregnancy ends, or when the cause of the high-estrogen status of the men with hepatic dysfunction is addressed, the angiomas usually resolve (Pirovino et al. 1988). Together, these findings support the concept that estrogen has clinically significant effects on endothelial cell activity related to both atherosclerosis and angiogenesis.
KeywordsMigration Phenol Estrogen Testosterone Polyacrylamide
Unable to display preview. Download preview PDF.
- Beeson PB (1994) Age and sex associations of 40 autoimmune diseases. J Am Med Assoc 96: 457–462Google Scholar
- Cid MC, Kleinman HK, Grant DS, Schnaper HW, Fauci AS, Hoffman GS (1994a) Estradiol enhances leukocyte binding to tumor necrosis factor ( TNF)-stimulated endothelial cells via an increase in TNF-induced adhesion molecules E-selectin, intercellular adhesion molecule typel and vascular cell adhesion molecule typel. J Clin Invest 93: 17–25Google Scholar
- Cid MC, Esparza J, Grant DG, Morales DE, McGowan KA, Urbano-Marquez A, Schnaper HW, Kleinman HK (1994b) Estradiol increases endothelial cell attachment to extracellular matrix proteins through an increase in integrin expression. Clin Res 42: 131AGoogle Scholar
- Kim-Schulze S, McGowan KA, Hubchak SC, Cid MC, Martin MB, Kleinman HK, Greene GL, Schnaper HW (1996) Expression of an estrogen receptorGoogle Scholar
- by human coronary artery and umbilical vein endothelial cells. Circulation 94:1402–1407Google Scholar
- Raines EW, Ross R (1991) Mechanisms of plaque formation. Cellular changes and the possible role of growth-regulatory molecules. Atheroscler Rev 23: 143–152Google Scholar