Format

Send to

Choose Destination
Proc Natl Acad Sci U S A. 2009 Oct 13;106(41):17511-6. doi: 10.1073/pnas.0907359106. Epub 2009 Sep 25.

Reticulon 4B (Nogo-B) is necessary for macrophage infiltration and tissue repair.

Author information

1
Department of Pharmacology, Amistad Research Building, Yale University School of Medicine, New Haven, CT 06519, USA.

Abstract

Blood vessel formation during ischemia and wound healing requires coordination of the inflammatory response with genes that regulate blood vessel assembly. Here we show that the reticulon family member 4B, aka Nogo-B, is upregulated in response to ischemia and is necessary for blood flow recovery secondary to ischemia and wound healing. Mice lacking Nogo-B exhibit reduced arteriogenesis and angiogenesis that are linked to a decrease in macrophage infiltration and inflammatory gene expression in vivo. Bone marrow-derived macrophages isolated from Nogo knock-out mice have reduced spreading and chemotaxis due to impaired Rac activation. Bone marrow reconstitution experiments show that Nogo in myeloid cells is necessary to promote macrophage homing and functional recovery after limb ischemia. Thus, endogenous Nogo coordinates macrophage-mediated inflammation with arteriogenesis, wound healing, and blood flow control.

PMID:
19805174
PMCID:
PMC2762666
DOI:
10.1073/pnas.0907359106
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for HighWire Icon for PubMed Central
Loading ...
Support Center