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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Adenoviridae, Animals, Bradykinin Receptor Antagonists, Capillaries, Disease Models, Animal, Gene Expression, Genetic Therapy, Hindlimb, Humans, Immunohistochemistry, Injections, Intramuscular, Ischemia, Male, Mice, Muscle, Skeletal, Neovascularization, Physiologic, Peripheral Vascular Diseases, Receptor, Bradykinin B1, Receptor, Bradykinin B2, Receptors, Bradykinin, Regional Blood Flow, Reverse Transcriptase Polymerase Chain Reaction, Tissue Kallikreins, Transgenes.
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Does local delivery of human tissue kallikrein gene accelerate spontaneous angiogenesis in mouse model of hindlimb ischemia? Context: Human tissue kallikrein (HK) releases kinins from kininogen. We investigated whether adenovirus-mediated HK gene delivery is angiogenic in the context of ischemia. Hindlimb ischemia, caused by femoral artery excision, increased muscular capillary density (P:<0.001) and induced the expression of kinin B(1) receptor gene (P:<0.05). Pharmacological blockade of B(1) receptors blunted ischemia-induced angiogenesis (P:<0.01), whereas kinin B(2) receptor antagonism was ineffective. Intramuscular delivery of adenovirus containing the HK gene (Ad. CMV-cHK) enhanced the increase in capillary density caused by ischemia (969+/-32 versus 541+/-18 capillaries/mm(2) for control, P:<0.001), accelerated blood flow recovery (P:<0.01), and preserved energetic charge of ischemic muscle (P:<0.01). Chronic blockade of kinin B(1) or B(2) receptors prevented HK-induced angiogenesis.
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HK gene delivery enhances the native angiogenic response to ischemia. Angiogenesis gene therapy with HK might be applicable to peripheral occlusive vascular disease. Final Decision: yes