Serum profiles of granulocyte-macrophage colony-stimulating factor and C-Cchemokines in hypertensive patients with or without significant hyperlipidemia
Jt. Parissis et al., Serum profiles of granulocyte-macrophage colony-stimulating factor and C-Cchemokines in hypertensive patients with or without significant hyperlipidemia, AM J CARD, 85(6), 2000, pp. 777
Citations number
18
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a glycoprotein
that regulates the proliferation and differentiation of myeloid progenitor
cells.' This factor, in addition to its growth-promoting effects, stimulat
es range of functional activities of mature neutrophils, monocytes, and eos
inophils, including regulation of leukocyte adhesion, superoxide anion gene
ration, and enhancement or induction of cytokine production.(2) Thus, GM-CS
F may contribute to the pathophysiologic events involved in atherosclerosis
and inflammation.(2,3) On the other hand, C-C chemokines or chemotactic cy
tokines are essential factors in the recruitment and activation of leukocyt
es from the circulation into inflammed tissue, and participate in the patho
genesis and progression of human atherosclerosis.(4-6) Recently, some inves
tigators(7,8) have shown that circulating levels of C-C chemokines, such as
macrophage chemoattractant protein-1 (MCP-1) and macrophage inflammatory p
rotein-1 alpha (MIP-1 alpha), are elevated in patients with ischemic heart
disease and congestive heart failure. Furthermore, it is known that conditi
ons such as hyperlipidemia, smoking, and arterial hypertension negatively a
ffect endothelial function and predispose to atherogenesis of human arterie
s.(9,10) However, to the best of our knowledge, no in vivo data exist on GM
-CSF and C-C chemokine levels in arterial hypertension and its combination
with other cardiovascular risk factors. The present study investigates the
differences in serum activity of GM-CSF, MCP-I, and MIP-1 alpha as markers
of an atherosclerotic inflammatory process between hypertensive patients wi
th and without significant hyperlipidemia and before receiving any medical
treatment.