XXXX is required for @entity5 @entity3 and angiogenesis.

@entity309 @entity634 @entity635 @entity19 @entity5 @entity5003 @entity3 @entity320
Here, we describe that microenvironmental @entity635 and, to a lesser extent, @entity634 are required for in vivo angiogenesis and @entity3 of different @entity5 cells. In @entity635 knockout (KO) @entity19 , local @entity5 or lung metastases of B16 @entity320 cells were not observed compared with WT @entity19 . Angiogenesis was assessed by the recruitment of blood vessel networks into Matrigel plugs containing B16 @entity320 cells; vascularization of the plugs was present in WT @entity19 , but was absent in @entity635 KO @entity19 . The addition of exogenous @entity5003 into B16-containing Matrigel plugs in @entity635 KO @entity19 partially restored the angiogenic response. Moreover, the incorporation of @entity5003 receptor antagonist to B16-containing plugs in WT @entity19 inhibited the ingrowth of blood vessel networks into Matrigel plugs. In @entity5003 alpha KO @entity19 , local @entity5 development and induction of an angiogenic response in Matrigel plugs was less pronounced than in WT @entity19 , but significantly higher than in @entity635 KO @entity19 . These effects of host-derived @entity634 and @entity635 were not restricted to the @entity320 model, but were also observed in @entity19 mammary and prostate @entity5 cell models. In addition to the in vivo findings, @entity5003 contributed to the production of vascular endothelial cell growth factor and @entity5 necrosis factor in cocultures of peritoneal macrophages and @entity5 cells. Host-derived @entity5003 seems to control @entity5 angiogenesis and @entity3 . Furthermore, the anti-angiogenic effects of @entity5003 receptor antagonist, shown here, suggest a possible therapeutic role in @entity5 , in addition to its current use in @entity309 .
