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myocardial hypertrophy overrides the angiogenic response to hypoxia心肌肥厚覆盖血管生成对缺氧的反应
Myocardial Hypertrophy Overrides the Angiogenic Response to Hypoxia 1¤ 2 1 2 1 Yeong-Hoon Choi *, Douglas B. Cowan , Meena Nathan , Dimitrios Poutias , Christof Stamm , Pedro J. del Nido1, Francis X. McGowan, Jr.2 1 Department of Cardiac Surgery, Children’s Hospital Boston and Harvard Medical School, Boston, Massachusetts, United States of America, 2 Department of Anesthesiology, Perioperative and Pain Medicine, Children’s Hospital Boston and Harvard Medical School, Boston, Massachusetts, United States of America Abstract Background: Cyanosis and myocardial hypertrophy frequently occur in combination. Hypoxia or cyanosis can be potent inducers of angiogenesis, regulating the expression of hypoxia-inducible factors (HIF), vascular endothelial growth factors (VEGF), and VEGF receptors (VEGFR-1 and 2); in contrast, pressure overload hypertrophy is often associated with impaired pro- angiogenic signaling and decreased myocardial capillary density. We hypothesized that the physiological pro-angiogenic response to cyanosis in the hypertrophied myocardium is blunted through differential HIF and VEGF-associated signaling. Methods and Results: Newborn rabbits underwent aortic banding and, together with sham-operated littermates, were transferred into a hypoxic chamber (FiO2 = 0.12) at 3 weeks of age. Control banded or sham-operated rabbits were housed in normoxia. Systemic cyanosis was confirmed (hematocrit, arterial oxygen saturation, and serum erythropoietin). Myocardial tissue was assayed for low oxygen concentrations using a pimonidazole adduct. At 4 weeks of age, HIF-1a and HIF-2a protein levels, HIF-1a DNA-binding activity, and expression of VEGFR-1, VEGFR-2, and VEGF were determined in hypoxic
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