scholarly journals Bone Marrow Cell Recruitment Mediated by Inducible Nitric Oxide Synthase/Stromal Cell-Derived Factor-1α Signaling Repairs the Acoustically Damaged Cochlear Blood-Labyrinth Barrier

2010 ◽  
Vol 177 (6) ◽  
pp. 3089-3099 ◽  
Author(s):  
Min Dai ◽  
Yue Yang ◽  
Irina Omelchenko ◽  
Alfred L. Nuttall ◽  
Allan Kachelmeier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Bone Marrow ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Stromal Cell ◽  
Marrow Cell ◽  
Cell Recruitment ◽  
Stromal Cell Derived Factor ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The role of SHIP1 in macrophage programming and activation

2004 ◽  
Vol 32 (5) ◽  
pp. 785-788 ◽  
Author(s):  
M.J. Rauh ◽  
L.M. Sly ◽  
J. Kalesnikoff ◽  
M.R. Hughes ◽  
L.-P. Cao ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Bone Marrow ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Endotoxin Tolerance ◽  
Negative Regulator ◽  
Collagen Formation ◽  
Phosphoinositide 3 Kinase ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The SHIP1 (SH2-containing inositol-5′-phosphatase 1) acts as a negative regulator of proliferation, survival and end cell activation in haemopoietic cells. It does so, at least in part, by translocating to membranes after extracellular stimulation and hydrolysing the phosphoinositide 3-kinase-generated second messenger, PtdIns(3,4,5)P3 to PtdIns(3,4)P2. SHIP1−/− mice have, as a result, an increased number of neutrophils and monocyte/macrophages because their progenitors display enhanced survival and proliferation. These mice also suffer from osteoporosis because of an increased number of hyperactive osteoclasts and a significant neutrophil infiltration of the lungs. Interestingly, SHIP1−/− mice do not display endotoxin tolerance and we have found that lipopolysaccharide-induced endotoxin tolerance is contingent on up-regulating SHIP1, through the production of autocrine-acting transforming growth factor-β, in bone-marrow-derived macrophages and mast cells. Intriguingly, unlike bone-marrow-derived macrophages, SHIP1−/− peritoneal and alveolar macrophages produce 10-fold less NO than wild-type macrophages because these in vivo-generated macrophages have very high arginase I levels and this enzyme competes with inducible nitric oxide synthase for the substrate L-arginine. It is probable that, in the face of chronically increased PtdIns(3,4,5)P3 levels in their myeloid progenitors, SHIP1−/− mice display a skewed development away from M1 (killer) macrophages (which have high inducible nitric oxide synthase levels and produce NO to kill microorganisms and tumour cells), towards M2 (healing) macrophages (which have high arginase levels and produce ornithine to promote host-cell growth and collagen formation). This skewing probably occurs to avoid septic shock and suggests that the phosphoinositide 3-kinase pathway plays a critical role in programming macrophages.

Inducible Nitric Oxide Synthase/CD95L-dependent Suppression of Pulmonary and Bone Marrow Eosinophilia by Diethylcarbamazine

2010 ◽  
Vol 181 (5) ◽  
pp. 429-437 ◽  
Author(s):  
Tulio Queto ◽  
Pedro Xavier-Elsas ◽  
Marcelo Aranha Gardel ◽  
Bianca de Luca ◽  
Mônica Barradas ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Bone Marrow ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide
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