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آنژیوژنز | رگزایی، رگزایی | آنژیوژنز، انژیوژنز، رگ زایی
M1-like macrophages and pro-inflammatory cytokines have been shown to stimulate angiogenesis [7,25,26], while M2-like macrophages have been shown to stabilize angiogenesis, promote fibroblast proliferation and orchestrate extracellular matrix assembly [26-29].
Finally, the mechanisms of action behind the therapeutic efficacy of ixmyelocel-T remain to be identified, although results from a rat hindlimb ischemia model and in vitro studies suggest that the cells in ixmyelocel-T promote angiogenesis [59].
These two reports further support the theory that both M1 and M2 macrophages contrib- ute to angiogenesis in different ways, so that strategies that promote transient increases in either phenotype may be tailored to enhance angiogenesis.
For example, at least two different pheno- types of macrophages are commonly referred to as M2, including those stimulated in vitro with IL-4 and those stimulated with IL-10, even though these macrophages display distinct phenotypes with dif- ferent effects on angiogenesis, fibrosis, and tissue repair [7,114-117].
, CCR2 re- cruits an inflammatory macrophage subpopulation critical for angiogenesis in tis- sue repair, Blood 120 (3) (2012) 613-625.،CXCL12, also knowm as stromal cell-derived factor I (SDFI), is a che- mokine involved in regulating cell migration.0* Increased expression of CXCL12 in endomelriotic implants attracts stem cells preferentially to endometriotic lesions, preventing their normal migration to the endometrium.0*-07 CXCR4, a chcmokine receptor, and its ligand CXCL12 not only are important in stem cell recruitment but can also induce angiogenesis and tissue growth.0" CXCR7, another receptor for CXCL12, is increased in inflammation and tumor growth.0' Recently, CXCR7 was found to have increased expression in endomelriotic lesions, where it enhances BMDSC recruitment to lesions and perpetuates their growth.07 Lastly, estrogens enhance recruitment of BMDSCs, through increasing CXCL12; as endometriotic lesions have an increased local estrogenic environment, this provides yet another mechanism by which lesions can further ensure their growth and survival.08
Cytokines and growth factors are a large family of soluble proteins and glycoproteins secreted by leukocytes and other cells into the extracellular environment where they act on the same (autocrine) or nearby cells (paracrine), serving as messengers both within and outside the immune system in regulation of cheniotaxis, mitosis, angiogenesis, and differentiation.
As mentioned above, while an impaired cellular immune response may result in ineffective clearance of refluxed endometrial cells from the peritoneal cavity', cytokines and growth factors appear to promote implantation and growth of ectopic endometrium by facilitating its attachment to the peritoneal surface and by stimulating proliferation and angiogenesis.
VEGF is an important mediator oflocal angiogenesis produced by monocytes and macrophages.148 The growth factor stimulates proliferation of vascular endothelial cells and also acts as a chemoattractant for monocytes; it plays an important role in vascularization of endometriotic lesions.148,11,11 VEGF is produced primarily in endometrial glands and is up-regulated by a variety of factors including estrogen and lL-l.'48 Peritoneal fluid VEGF concentrations are increased in women with endometriosis and are usually highest in advanced stages of the disease.
Immune cells in the peritoneal fluid of women with endometriosis also secrete a wide variety of humoral factors (cytokines and growth factors) that stimulate attachment and proliferation of ectopic endometrium and local angiogenesis.،
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