Signal transduction pathways involved in macrophage migration induced by peritoneal fluid chemotactic factors in stages I and II endometriosis

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This study investigated the signal transduction pathways activated by peritoneal fluid chemotactic factors, which mediate macrophage migration in patients with early-stage endometriosis.

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Abstract

ObjectiveTo explore the role of G-protein coupled signaling pathways in activation of macrophage migration in endometriosis stages I and II.DesignCase controlled study.SettingUniversity hospital.Patient(s)Fifteen patients undergoing laparoscopy for elective sterilization (n = 5) or for diagnosis of endometriosis stages I and II associated with infertility (n = 10).Intervention(s)Peritoneal fluid samples were collected during laparoscopy.Main outcome measure(s)Macrophage migration induced by peritoneal fluid from patients with endometriosis stages I and II (PF SI-II) and potential G-protein coupled receptors and second messengers involved in macrophage activation.Result(s)Potential G-protein coupled receptors and second messengers involved in macrophage activation were evaluated after incubation of U-937 cells differentiated into macrophages with inhibitors of phospholipase A and C, adenylate cyclase, and protein kinase A and C. Macrophage chemotactic activity induced by PF SI-II was inhibited in the presence of a phospholipase C and A2 inhibitor (IC50= 30 microM) and after treatment with myristoylated protein kinase C peptide inhibitor (50 nM). An increase in inositol phosphate (IP3) was also observed in macrophages exposed to PF SI-II. Activation of multiple G-proteins in macrophages was examined after exposure of cells to PF SI-II in the presence and absence of Bordettela pertussis and cholera toxins. No effect on macrophage migration was observed.Conclusion(s)Macrophage chemotaxis induced by PF SI-II appears to involve activation of pertussis toxin-insensitive G-protein coupled receptors in macrophages. Our data suggest that these events lead to subsequent activation of phospholipases followed by generation of IP3 and potential mobilization of intracellular Ca2+. Subsequent phosphorylation of target proteins by protein kinase C may regulate the chemotactic responses. The adenylate cyclase pathway does not appear to play a role in this process.

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Condition tags

endometriosis

MeSH descriptors

Ascitic Fluid Chemotactic Factors Endometriosis Macrophages Signal Transduction Ascitic Fluid Case-Control Studies Cell Line Cell Movement Cell Movement Chemotactic Factors Endometriosis Endometriosis Enzyme Inhibitors Enzyme Inhibitors Female GTP-Binding Proteins GTP-Binding Proteins Humans Macrophages

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (37)

Cited by (3)

SciLite annotations

chemicals 3
peptide inositol phosphate hexose + c4h5n3o2
organisms 2
strain 18323 tholera

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