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Hypoxia-Inducible Factor-1α in Smooth Muscle Cells Protects Against Aortic Aneurysms-Brief Report. 2016

Masaki Imanishi, and Yoichi Chiba, and Noriko Tomita, and Shinji Matsunaga, and Toshitaka Nakagawa, and Masaki Ueno, and Kazuhiro Yamamoto, and Toshiaki Tamaki, and Shuhei Tomita
From the Division of Molecular Pharmacology, Faculty of Medicine, Tottori University, Japan (M.I., S.M., S.T.); Department of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Japan (Y.C., M.U.); Division of Molecular Medicine and Therapeutics, Faculty of Medicine, Tottori University, Japan (N.T., K.Y.); Life Science Research Center, Kagawa University, Japan (T.N.); Department of Pharmacology, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan (T.T.); and Department of Pharmacology, Faculty of Medicine, Osaka City University, Japan (S.T.).

The purpose of this study was to determine the role of smooth muscle cell-derived hypoxia-inducible factor-1α (Hif-1α) in the pathogenesis of aortic aneurysms. Control mice and smooth muscle cell-specific hypoxia-inducible factor-1α-deficient mice were infused with β-aminopropionitrile for 2 weeks and angiotensin II for 6 weeks to induce aortic aneurysm formation. Mutant mice experienced increased levels of aneurysm formation of the thoracic or abdominal aorta with more severe elastin disruption, compared with control mice. Smooth muscle cell-specific hypoxia-inducible factor-1α deficiency did not affect matrix metalloproteinase-2 activity; however, the activity of lysyl oxidase and the levels of tropoelastin mRNA in the angiotensin II- and β-aminopropionitrile-treated aortae, associated with elastin fiber formation, were suppressed. Furthermore, we observed reduced volumes of mature cross-linked elastin in the thoracoabdominal aorta after treatment with angiotensin II and β-aminopropionitrile. Deficiency of smooth muscle cell-derived hypoxia-inducible factor-1α augments aortic aneurysms, accompanied by disruption of elastin fiber formation, but not changes of elastin fiber degradation.

UI MeSH Term Description Entries
D008249 Protein-Lysine 6-Oxidase An enzyme oxidizing peptidyl-lysyl-peptide in the presence of water & molecular oxygen to yield peptidyl-allysyl-peptide plus ammonia & hydrogen peroxide. EC 1.4.3.13. Lysyl Oxidase,Collagen Lysyl Oxidase,6-Oxidase, Protein-Lysine,Lysyl Oxidase, Collagen,Oxidase, Collagen Lysyl,Oxidase, Lysyl,Protein Lysine 6 Oxidase
D008297 Male Males
D009131 Muscle, Smooth, Vascular The nonstriated involuntary muscle tissue of blood vessels. Vascular Smooth Muscle,Muscle, Vascular Smooth,Muscles, Vascular Smooth,Smooth Muscle, Vascular,Smooth Muscles, Vascular,Vascular Smooth Muscles
D010641 Phenotype The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment. Phenotypes
D002478 Cells, Cultured Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others. Cultured Cells,Cell, Cultured,Cultured Cell
D004108 Dilatation, Pathologic The condition of an anatomical structure's being dilated beyond normal dimensions. Ectasia,Dilatation, Pathological,Dilatations, Pathologic,Dilatations, Pathological,Pathologic Dilatation,Pathologic Dilatations,Pathological Dilatation,Pathological Dilatations
D004195 Disease Models, Animal Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases. Animal Disease Model,Animal Disease Models,Disease Model, Animal
D004547 Elastic Tissue Connective tissue comprised chiefly of elastic fibers. Elastic fibers have two components: ELASTIN and MICROFIBRILS. Elastic Fibers,Elastic Fiber,Elastic Tissues,Fiber, Elastic,Fibers, Elastic,Tissue, Elastic,Tissues, Elastic
D000629 Aminopropionitrile Reagent used as an intermediate in the manufacture of beta-alanine and pantothenic acid. beta-Aminopropionitrile,BAPN,beta Aminopropionitrile
D000804 Angiotensin II An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS. Angiotensin II, Ile(5)-,Angiotensin II, Val(5)-,5-L-Isoleucine Angiotensin II,ANG-(1-8)Octapeptide,Angiotensin II, Isoleucine(5)-,Angiotensin II, Valine(5)-,Angiotensin-(1-8) Octapeptide,Isoleucine(5)-Angiotensin,Isoleucyl(5)-Angiotensin II,Valyl(5)-Angiotensin II,5 L Isoleucine Angiotensin II,Angiotensin II, 5-L-Isoleucine

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