Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P80098 (monocyte chemoattractant protein)
 1,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The recruitment of immunocompetent cells to the site of inflammation represents an essential part of the host defense during continuous ambulatory peritoneal dialysis (CAPD)-related peritonitis. Recently, it was shown that intraperitoneal application of granulocyte macrophage-colony stimulating factor (GM-CSF) leads to a marked transient recruitment of macrophages, paralleled by an increase in monocyte chemoattractant protein (MCP)-1. We, therefore, tested the in vitro effect of GM-CSF on the release of the chemotaxins interleukin (IL)-8 and MCP-1 by human peritoneal macrophages. Cells were stimulated with recombinant GM-CSF for 4, 12, and 20 hours in concentrations ranging from 0.1 to 100 pg/mL. Cells stimulated with lipopolysaccharide (LPS) or unstimulated cells served as control. Recombinant GM-CSF at concentrations found during CAPD peritonitis in vivo significantly increased the release of IL-8 and MCP-1 in a time- and dose-dependent manner. The maximum effect of IL-8 was observed directly after cell isolation, and decreased after a culture period of 10 days. Thus, our results indicate that peritoneal macrophages are the potential source of chemokines released upon GM-CSF stimulation.
Adv Perit Dial 1998
PMID:Granulocyte macrophage-colony stimulating factor stimulates secretion of chemoattractive cytokines by peritoneal macrophages of CAPD patients. 1064 17

Midkine (MK) is a multifunctional heparin-binding growth factor with migration-promoting activity for neutrophils, macrophages and neurones. Since enhanced expression of MK is observed in the tubular epithelial cells of the diseased kidney, it has been suggested that MK plays important roles in the pathogenesis of tubulointerstitial injury. The aim of this study was to determine the contribution of MK in nephrogenesis and in a murine model of ischaemic renal reperfusion injury (IRI). In the 11 day embryo, MK was expressed uniformly in both ureteric bud and metanephrogenic mesenchyme. The immature metanephros expressed both MK mRNA and MK protein more strongly than the mature metanephros. We studied the extent of tubulointerstitial injuries in MK wild-type [Mdk(+/+)] and knockout [Mdk(-/-)] mice 90 min after IRI. MK was expressed weakly in the proximal tubules in Mdk(+/+) mouse kidneys. After IRI, MK expression in proximal tubules increased and the new expression was observed in the distal tubules in Mdk(+/+) mice. Immediate induction of MK expression was observed when cultured tubular epithelial cells (TEpiCs) were exposed to 5 mM H(2)O(2). Recombinant mouse MK (10 ng/ml) induced the increased expression of macrophage inflammatory protein 2 (MIP-2) mRNA in TEpiCs. Shortly after IRI, there were significantly fewer inflammatory leukocytes such as neutrophils and macrophages in Mdk(-/-) mice than in Mdk(+/+) mice. Marked up-regulation of monocyte chemoattractant protein 1 (MCP-1) and MIP-2 expression was detected in Mdk(+/+) mouse kidneys. Tubulointerstitial damage observed after IRI was significantly more suppressed in Mdk(-/-) mice than in Mdk(+/+) mice. These results suggest an important role for MK in the molecular cascade that regulates nephrogenesis. The present work also indicates that MK induces the chemotaxis of inflammatory leukocytes into the tubulointerstitium at least partly through the induction of MCP-1 and MIP-2, and that MK contributes to the aggravation of ischaemia-induced tubulointerstitial damage.
Nephrol Dial Transplant 2002
PMID:Midkine expression in the course of nephrogenesis and its role in ischaemic reperfusion injury. 1238 88