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Tie2-dependent knockout of HIF-1 impairs burn wound vascularization and homing of bone marrow-derived angiogenic cells
Author(s) -
Kakali Sarkar,
Sergio Rey,
Xianjie Zhang,
Raul Sebastian,
Guy P. Marti,
Karen Fox-Talbot,
Amanda V. Cardona,
Junkai Du,
Yee Sun Tan,
Lixin Liu,
Frank Lay,
Frank J. Gonzalez,
John W. Harmon,
Gregg L. Semenza
Publication year - 2011
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvr282
Subject(s) - homing (biology) , bone marrow , angiopoietin receptor , neovascularization , knockout mouse , angiogenesis , microbiology and biotechnology , cancer research , immunology , medicine , pathology , biology , receptor , ecology
Hypoxia-inducible factor 1 (HIF-1) is a heterodimer composed of HIF-1α and HIF-1β subunits. HIF-1 is known to promote tissue vascularization by activating the transcription of genes encoding angiogenic factors, which bind to receptors on endothelial cells (ECs) and bone marrow-derived angiogenic cells (BMDACs). In this study, we analysed whether HIF-1 activity in the responding ECs and BMDACs is also required for cutaneous vascularization during burn wound healing.

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