Impaired neoangiogenesis in β2-adrenoceptor gene-deficient mice: Restoration by intravascular human β2-adrenoceptor gene transfer and role of NFkB and CREB transcription factors (582 views)
Br J Pharmacol British Journal Of Pharmacology (ISSN: 0007-1188), 2011; 162(3): 712-721.
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Paper type: Journal Article,
Impact factor: 4.409, 5-year impact factor: 4.635
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-78651417065&partnerID=40&md5=3e1318073584e662306eda9a6249b952
Keywords: Adrenergic Signaling, Gene Therapy, Ischaemic Hindlimb, Nfkb Activity, Adenovirus Vector, Beta 2 Adrenergic Receptor, Cyclic Amp Responsive Element Binding Protein, I Kappa B Alpha, Immunoglobulin Enhancer Binding Protein, Isoprenaline, Tumor Necrosis Factor Alpha, Vasculotropin, Angiogenesis, Animal Cell, Animal Experiment, Animal Model, Animal Tissue, Article, Controlled Study, Cytokine Production, Endothelium Cell, Limb Ischemia, Mouse, Nonhuman, Priority Journal, Receptor Density, Signal Transduction, Transcription Regulation, Upregulation, Viral Gene Therapy, Blood Flow Velocity, Cultured, Creb-Binding Protein, Disease Models, Endothelial Cells, Genetic Vectors, Luciferases, Knockout, Neovascularization, Physiologic, Nf-Kappa B, Radioligand Assay, Transfection, Vascular Endothelial Growth Factor A,
Affiliations:
*** IBB - CNR ***
Dipartimento di Medicina Clinica, Scienze Cardiovascolari Ed Immunologiche, Università Federico II, Via Pansini 5, Edificio 2, 80131 Naples, Italy
Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA, United States
References:
Not available.
Br J Pharmacol British Journal Of Pharmacology (ISSN: 0007-1188), 2011; 162(3): 712-721.
Export to BibTeX Export to EndNote
Paper type: Journal Article,
Impact factor: 4.409, 5-year impact factor: 4.635
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-78651417065&partnerID=40&md5=3e1318073584e662306eda9a6249b952
Keywords: Adrenergic Signaling, Gene Therapy, Ischaemic Hindlimb, Nfkb Activity, Adenovirus Vector, Beta 2 Adrenergic Receptor, Cyclic Amp Responsive Element Binding Protein, I Kappa B Alpha, Immunoglobulin Enhancer Binding Protein, Isoprenaline, Tumor Necrosis Factor Alpha, Vasculotropin, Angiogenesis, Animal Cell, Animal Experiment, Animal Model, Animal Tissue, Article, Controlled Study, Cytokine Production, Endothelium Cell, Limb Ischemia, Mouse, Nonhuman, Priority Journal, Receptor Density, Signal Transduction, Transcription Regulation, Upregulation, Viral Gene Therapy, Blood Flow Velocity, Cultured, Creb-Binding Protein, Disease Models, Endothelial Cells, Genetic Vectors, Luciferases, Knockout, Neovascularization, Physiologic, Nf-Kappa B, Radioligand Assay, Transfection, Vascular Endothelial Growth Factor A,
Affiliations:
*** IBB - CNR ***
Dipartimento di Medicina Clinica, Scienze Cardiovascolari Ed Immunologiche, Università Federico II, Via Pansini 5, Edificio 2, 80131 Naples, Italy
Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA, United States
References:
Not available.
Impaired neoangiogenesis in β2-adrenoceptor gene-deficient mice: Restoration by intravascular human β2-adrenoceptor gene transfer and role of NFkB and CREB transcription factors
Background and Purpose: There is much evidence supporting the role of β 2-adrenoceptors (β 2AR) in angiogenesis but the mechanisms underlying their effects have not been elucidated. Hence, we studied post-ischaemic angiogenesis in the hindlimb (HL) of β 2AR knock-out mice (β 2AR-/-) in vivo and explored possible molecular mechanisms in vitro. Experimental Approach: Femoral artery resection (FAR) was performed in wild-type and β 2AR-/-mice and adaptive responses to chronic HL ischaemia were explored; blood flow was measured by ultrasound and perfusion of dyed beads, bone rarefaction, muscle fibrosis and skin thickness were evaluated by immunoflourescence and morphometric analysis. Intrafemoral delivery of an adenovirus encoding the human β 2AR (ADβ 2AR) was used to reinstate β 2ARs in β 2AR-/-mice. Molecular mechanisms were investigated in mouse-derived aortic endothelial cells (EC) in vitro, focusing on NFκB activation and transcriptional activity. RESULTS Angiogenesis was severely impaired in β 2AR-/-mice subjected to FAR, but was restored by gene therapy with ADβ 2AR. The proangiogenic responses to a variety of stimuli were impaired in β 2AR-/-EC in vitro. Moreover, removal of β 2ARs impaired the activation of NFκB, a transcription factor that promotes angiogenesis; neither isoprenaline (stimulates βARs) nor TNFα induced NFκB activation in β 2AR -/-EC. Interestingly, cAMP response element binding protein (CREB), a transcription factor that counter regulates NFκB, was constitutively increased in β 2AR -/-ECs. ADβ 2AR administration restored β 2AR membrane density, reduced CREB activity and reinstated the NFκB response to isoprenaline and TNFα. Conclusions and Implications: Our results suggest that β 2ARs control angiogenesis through the tight regulation of nuclear transcriptional activity. © 2011 The Authors.
Background and Purpose: There is much evidence supporting the role of β 2-adrenoceptors (β 2AR) in angiogenesis but the mechanisms underlying their effects have not been elucidated. Hence, we studied post-ischaemic angiogenesis in the hindlimb (HL) of β 2AR knock-out mice (β 2AR-/-) in vivo and explored possible molecular mechanisms in vitro. Experimental Approach: Femoral artery resection (FAR) was performed in wild-type and β 2AR-/-mice and adaptive responses to chronic HL ischaemia were explored; blood flow was measured by ultrasound and perfusion of dyed beads, bone rarefaction, muscle fibrosis and skin thickness were evaluated by immunoflourescence and morphometric analysis. Intrafemoral delivery of an adenovirus encoding the human β 2AR (ADβ 2AR) was used to reinstate β 2ARs in β 2AR-/-mice. Molecular mechanisms were investigated in mouse-derived aortic endothelial cells (EC) in vitro, focusing on NFκB activation and transcriptional activity. RESULTS Angiogenesis was severely impaired in β 2AR-/-mice subjected to FAR, but was restored by gene therapy with ADβ 2AR. The proangiogenic responses to a variety of stimuli were impaired in β 2AR-/-EC in vitro. Moreover, removal of β 2ARs impaired the activation of NFκB, a transcription factor that promotes angiogenesis; neither isoprenaline (stimulates βARs) nor TNFα induced NFκB activation in β 2AR -/-EC. Interestingly, cAMP response element binding protein (CREB), a transcription factor that counter regulates NFκB, was constitutively increased in β 2AR -/-ECs. ADβ 2AR administration restored β 2AR membrane density, reduced CREB activity and reinstated the NFκB response to isoprenaline and TNFα. Conclusions and Implications: Our results suggest that β 2ARs control angiogenesis through the tight regulation of nuclear transcriptional activity. © 2011 The Authors.
Impaired neoangiogenesis in β2-adrenoceptor gene-deficient mice: Restoration by intravascular human β2-adrenoceptor gene transfer and role of NFkB and CREB transcription factors
| ▼ Evaluation of gene expression and test of new therapies by preclinical imaging in murine models |
Impaired neoangiogenesis in β2-adrenoceptor gene-deficient mice: Restoration by intravascular human β2-adrenoceptor gene transfer and role of NFkB and CREB transcription factors
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21 Records (19 excluding Abstracts).
Total impact factor: 96.601 (91.983 excluding Abstracts).
Total 5 year impact factor: 96.824 (91.372 excluding Abstracts).
Total impact factor: 96.601 (91.983 excluding Abstracts).
Total 5 year impact factor: 96.824 (91.372 excluding Abstracts).
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