Stay Connected. Manage Your Care.
Access your health information anytime and anywhere, at home or on the go, with MyHealth.
- Message your clinic
- View your lab results
- Schedule your next appointment
- Pay your bill
The MyHealth mobile app from Stanford Health Care puts all your health information at your fingertips and makes managing your health care simple and quick.
Guest Services
24/7
We are available to assist you
whenever you need it. Give us a call at
650-498-3333 or
PHYSICIAN HELPLINE
Have a question? We're here to help! Call 1-866-742-4811
Monday - Friday, 8 a.m. - 5 p.m.
REFER A PATIENT
Fax 650-320-9443
Track your patients' progress and communicate with Stanford providers conveniently and securely.
Abstract
Emerging evidence indicates that myeloid cells are essential for promoting new blood vessel formation by secreting various angiogenic factors. Given that hypoxia-inducible factor (HIF) is a critical regulator for angiogenesis, we questioned whether HIF in myeloid cells also plays a role in promoting angiogenesis. To address this question, we generated a unique strain of myeloid-specific knockout mice targeting HIF pathways using human S100A8 as a myeloid-specific promoter. We observed that mutant mice where HIF-1 is transcriptionally activated in myeloid cells (by deletion of the von Hippel-Lindau gene) resulted in erythema, enhanced neovascularization in matrigel plugs, and increased production of vascular endothelial growth factor (VEGF) in the bone marrow, all of which were completely abrogated by either genetic or pharmacological inactivation of HIF-1. We further found that monocytes were the major effector producing VEGF and S100A8 proteins driving neovascularization in matrigel. Moreover, by using a mouse model of hindlimb ischemia we observed significantly improved blood flow in mice intramuscularly injected with HIF-1-activated monocytes. This study therefore demonstrates that HIF-1 activation in myeloid cells promotes angiogenesis through VEGF and S100A8 and that this may become an attractive therapeutic strategy to treat diseases with vascular defects.
View details for DOI 10.1073/pnas.1320243111
View details for Web of Science ID 000331396500062
View details for PubMedID 24497508