<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Duong HT</submitter><funding>NCRR NIH HHS</funding><funding>Howard Hughes Medical Institute</funding><funding>NHLBI NIH HHS</funding><pagination>411-22</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3725463</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(4)</volume><pubmed_abstract>Dysregulation of angiogenesis is a common feature of many disease processes. Vascular remodeling is believed to depend on the participation of endothelial progenitor cells, but the identification of endothelial progenitors in postnatal neovascularization remains elusive. Current understanding posits a role for circulating pro-angiogenic hematopoietic cells that interact with local endothelial cells to establish an environment that favors angiogenesis in physiologic and pathophysiologic responses. In the lung, increased and dysregulated angiogenesis is a hallmark of diseases of the bronchial and pulmonary circulations, manifested by asthma and pulmonary arterial hypertension (PAH), respectively. In asthma, T(Helper)-2 immune cells produce angiogenic factors that mobilize and recruit pro-inflammatory and pro-angiogenic precursors from the bone marrow into the airway wall where they induce angiogenesis and fuel inflammation. In contrast, in PAH, upregulation of hypoxia-inducible factor (HIF) in vascular cells leads to the production of bone marrow-mobilizing factors that recruit pro-angiogenic progenitor cells to the pulmonary circulation where they contribute to angiogenic remodeling of the vessel wall. This review focuses on current knowledge of pro-angiogenic progenitor cells in the pathogenesis of asthma and PAH.</pubmed_abstract><journal>Angiogenesis</journal><pubmed_title>Pro-angiogenic hematopoietic progenitor cells and endothelial colony-forming cells in pathological angiogenesis of bronchial and pulmonary circulation.</pubmed_title><pmcid>PMC3725463</pmcid><funding_grant_id>UL1 RR024989</funding_grant_id><funding_grant_id>R37 HL060917</funding_grant_id><funding_grant_id>RC37 HL060917</funding_grant_id><funding_grant_id>P01 HL103453</funding_grant_id><funding_grant_id>U10 HL109250</funding_grant_id><pubmed_authors>Duong HT</pubmed_authors><pubmed_authors>Erzurum SC</pubmed_authors><pubmed_authors>Asosingh K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pro-angiogenic hematopoietic progenitor cells and endothelial colony-forming cells in pathological angiogenesis of bronchial and pulmonary circulation.</name><description>Dysregulation of angiogenesis is a common feature of many disease processes. Vascular remodeling is believed to depend on the participation of endothelial progenitor cells, but the identification of endothelial progenitors in postnatal neovascularization remains elusive. Current understanding posits a role for circulating pro-angiogenic hematopoietic cells that interact with local endothelial cells to establish an environment that favors angiogenesis in physiologic and pathophysiologic responses. In the lung, increased and dysregulated angiogenesis is a hallmark of diseases of the bronchial and pulmonary circulations, manifested by asthma and pulmonary arterial hypertension (PAH), respectively. In asthma, T(Helper)-2 immune cells produce angiogenic factors that mobilize and recruit pro-inflammatory and pro-angiogenic precursors from the bone marrow into the airway wall where they induce angiogenesis and fuel inflammation. In contrast, in PAH, upregulation of hypoxia-inducible factor (HIF) in vascular cells leads to the production of bone marrow-mobilizing factors that recruit pro-angiogenic progenitor cells to the pulmonary circulation where they contribute to angiogenic remodeling of the vessel wall. This review focuses on current knowledge of pro-angiogenic progenitor cells in the pathogenesis of asthma and PAH.</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Dec</publication><modification>2021-02-19T10:22:59Z</modification><creation>2019-03-27T01:13:43Z</creation></dates><accession>S-EPMC3725463</accession><cross_references><pubmed>21796417</pubmed><doi>10.1007/s10456-011-9228-y</doi></cross_references></HashMap>