Analysis Tools
cardiovascular system
|
• heterozygotes exhibit abnormal thinning of the medial and adventitial layers of the aortic wall
|
|
• in the cuff-injured femoral artery model, heterozygotes display reduced cardiovascular remodeling and angiogenesis relative to wild-type mice
• in addition, heterozygotes show impaired angiogenic activity in a hind-limb ischemia model (where femoral arteries are ablated), and significantly attenuated angiogenic responses to implanted tumors
|
|
• in response to external stress (cuff-injured femoral artery model), heterozygotes exhibit decreased arterial-wall thickening with no evidence of intimal hyperplasia, as well as reduced levels of angiogenesis, cardiac hypertrophy, and interstitial fibrosis relative to wild-type mice
• similarly attenuated responses to vascular injury are observed in the wire-injured femoral artery model
• following a continuous, 14-day infusion of angiotensin II, heterozygotes display significantly reduced cardiac hypertrophy, with thinner ventricular walls and lower heart weight to body weight ratios, as well as significantly reduced interstitial and perivascular fibrosis relative to wild-type mice
• attenuation of cardiovascular remodeling is associated with reduced expression of both activated platelet-derived growth factor-A (PDGF-A) and transforming growth factor-beta (TGF-beta)
|
|
• in the cuff-injured femoral artery model, heterozygotes show impaired activation and proliferation of smooth muscle cells and fibroblasts, whereas wild-type mice display thickening of the medial and intimal layers and high proliferation of smooth muscle cells
|
|
• in the cuff-injured femoral artery model, heterozygotes display smaller areas of neointima and granulation tissue around the cuff relative to wild-type mice
• administration of LE135, a synthetic retinoic-acid receptor (RAR) antagonist, to heterozygotes with cuffed femoral arteries incrementally increases formation of granulation tissue and neointima to nearly wild-type levels
|
homeostasis/metabolism
|
• in response to external stress (cuff-injured femoral artery model), heterozygotes exhibit decreased arterial-wall thickening with no evidence of intimal hyperplasia, as well as reduced levels of angiogenesis, cardiac hypertrophy, and interstitial fibrosis relative to wild-type mice
• similarly attenuated responses to vascular injury are observed in the wire-injured femoral artery model
• following a continuous, 14-day infusion of angiotensin II, heterozygotes display significantly reduced cardiac hypertrophy, with thinner ventricular walls and lower heart weight to body weight ratios, as well as significantly reduced interstitial and perivascular fibrosis relative to wild-type mice
• attenuation of cardiovascular remodeling is associated with reduced expression of both activated platelet-derived growth factor-A (PDGF-A) and transforming growth factor-beta (TGF-beta)
|
|
• in the cuff-injured femoral artery model, heterozygotes display smaller areas of neointima and granulation tissue around the cuff relative to wild-type mice
• administration of LE135, a synthetic retinoic-acid receptor (RAR) antagonist, to heterozygotes with cuffed femoral arteries incrementally increases formation of granulation tissue and neointima to nearly wild-type levels
|
muscle
|
• in the cuff-injured femoral artery model, heterozygotes show impaired activation and proliferation of smooth muscle cells and fibroblasts, whereas wild-type mice display thickening of the medial and intimal layers and high proliferation of smooth muscle cells
|
digestive/alimentary system
|
• heterozygotes display abnormally shaped villi, a lower number of mesenchymal cells, and a reduced amount of extracellular matrix in the GI tract relative to wild-type mice
• administration of LE135 increases the mesenchymal components and thickness of villi in the GI tracts of heterozygous mice, making the structure of the GI mucosa comparable to that in wild-type mice
|
|
• heterozygotes display abnormally shaped villi in the jejunum
|
