Is this what DR BP is learning about the relationship between COVID and solid tumors?
Atherosclerosis is a complex inflammatory disease. The progression of atherosclerotic plaques involves many different factors. In the last step, angiogenesis destabilizes and contributes to the plaque rupture. The complex array of anti-angiogenic and pro-angiogenic factors which interact with multiple cells and tissues has to be tightly regulated. Therapeutic strategies may target anti-angiogenic factors in order to prevent tumorigenesis or pro-angiogenic factors, thus preventing ischaemic diseases [2].
Chemokines may exert their regulatory activity on angiogenesis directly or as a consequence of leucocyte infiltration and/or the induction of growth factor expression [31]. The chemokine–receptor interaction is crucial for both arrest and transmigration of inflammatory cells through the endothelium [21]. Binding of RANTES/CCL5 to GAGs and to GPCRs are crucial for its pro-inflammatory activity [42–44]. Mutating the main GAG-binding domain in RANTES has been shown to switch the [A44ANA47]-RANTES/CCL5 chemokine to a potent anti-inflammatory molecule in murine models of inflammatory diseases [42]. The anti-inflammatory properties of a RANTES/CCL5 mutant may be associated with a cardioprotective effect of RANTES/CCL5 inhibition during early myocardial reperfusion. These results indicate that blocking chemokine receptor–ligand interactions might become a novel therapeutic strategy to reduce reperfusion injuries in patients during acute coronary syndromes.
The present review indicates the involvement of chemokines in angiogenesis, notably RANTES/CCL5, mostly known for its inflammatory properties. The pro- or anti-angiogenic effect of RANTES/CCL5 is still controversial. It has been demonstrated that RANTES/CCL5 displayed an anti-angiogenic activity in a sponge-induced angiogenesis model [40]. In contrast, several studies suggest that RANTES/CCL5 may be considered as a pro-angiogenic factor. Inflammatory cells recruited by the binding of RANTES/CCL5 on CCR5 may secrete growth factors involved in vessel formation or in endothelial progenitor cell recruitment [42,45]. Chemokines may induce the migration and the proliferation of endothelial cells [31], thus promoting the angiogenesis. In a mouse model of surgically induced hind limb ischaemia, RANTES/CCL5 exerts a pro-angiogenic effect [46].
Finally, innovative gene technologies as miRNA (microRNA) and advances in animal modelling may be useful to make a major advance in our understanding of the relevance of chemokines in angiogenesis.
Advances in the Cellular and Molecular Biology of Angiogenesis: A Biochemical Society/Wellcome Trust Focused Meeting held at the University of Birmingham, U.K., 27–29 June 2011. Organized and Edited by Stuart Egginton and Roy Bicknell (Birmingham, U.K.).
https://portlandpress.com/biochemsoctrans/art...ANTES-CCL5
Atherosclerosis is a complex inflammatory disease. The progression of atherosclerotic plaques involves many different factors. In the last step, angiogenesis destabilizes and contributes to the plaque rupture. The complex array of anti-angiogenic and pro-angiogenic factors which interact with multiple cells and tissues has to be tightly regulated. Therapeutic strategies may target anti-angiogenic factors in order to prevent tumorigenesis or pro-angiogenic factors, thus preventing ischaemic diseases [2].
Chemokines may exert their regulatory activity on angiogenesis directly or as a consequence of leucocyte infiltration and/or the induction of growth factor expression [31]. The chemokine–receptor interaction is crucial for both arrest and transmigration of inflammatory cells through the endothelium [21]. Binding of RANTES/CCL5 to GAGs and to GPCRs are crucial for its pro-inflammatory activity [42–44]. Mutating the main GAG-binding domain in RANTES has been shown to switch the [A44ANA47]-RANTES/CCL5 chemokine to a potent anti-inflammatory molecule in murine models of inflammatory diseases [42]. The anti-inflammatory properties of a RANTES/CCL5 mutant may be associated with a cardioprotective effect of RANTES/CCL5 inhibition during early myocardial reperfusion. These results indicate that blocking chemokine receptor–ligand interactions might become a novel therapeutic strategy to reduce reperfusion injuries in patients during acute coronary syndromes.
The present review indicates the involvement of chemokines in angiogenesis, notably RANTES/CCL5, mostly known for its inflammatory properties. The pro- or anti-angiogenic effect of RANTES/CCL5 is still controversial. It has been demonstrated that RANTES/CCL5 displayed an anti-angiogenic activity in a sponge-induced angiogenesis model [40]. In contrast, several studies suggest that RANTES/CCL5 may be considered as a pro-angiogenic factor. Inflammatory cells recruited by the binding of RANTES/CCL5 on CCR5 may secrete growth factors involved in vessel formation or in endothelial progenitor cell recruitment [42,45]. Chemokines may induce the migration and the proliferation of endothelial cells [31], thus promoting the angiogenesis. In a mouse model of surgically induced hind limb ischaemia, RANTES/CCL5 exerts a pro-angiogenic effect [46].
Finally, innovative gene technologies as miRNA (microRNA) and advances in animal modelling may be useful to make a major advance in our understanding of the relevance of chemokines in angiogenesis.
Advances in the Cellular and Molecular Biology of Angiogenesis: A Biochemical Society/Wellcome Trust Focused Meeting held at the University of Birmingham, U.K., 27–29 June 2011. Organized and Edited by Stuart Egginton and Roy Bicknell (Birmingham, U.K.).
https://portlandpress.com/biochemsoctrans/art...ANTES-CCL5
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