建立基因敲除小鼠颈动脉粥样硬化模型英文教学提纲.pptVIP

Lipoprotein Lipase (LPL) Deficiency Increases Plasma Lipid Level and Enhances Neointima Formation After Carotid Artery Injury in apoE Knock-out Mice Candidate genes in lipoprotein metabolism Lusis et al Circulation. 2004 Lipoprotein Lipase in the Arterial Wall Pentik?inen et al Arterioscler Thromb Vasc Biol. 2002 Hypothesis LPL Arterial response to injury hyperlipidemic conditions ？ A 1x2-mm strip of filter paper saturated with 10% FeCl3 solution was applied to the adventitial surface of the surgically exposed carotid artery for 3.0 minutes, then removed. The surgical incision was sutured with 4–0 monofilament, and the animal was returned to its cage. Common carotid arteries of apoE-/-, LPL+/- (ELK)mice (A) and apoE-/-, LPL+/+ (EK)mice (B) 8 weeks after ferric chloride injury neointima formation after carotid artery injury by FeCl3 for 8 weeks ELK carotid artery stained with HE EK noninjured injured neointima formation after carotid artery injury by FeCl3 for 8 weeks carotid artery stained with HE ELK EK noninjured injured Mean Intimal and Medial Cross-sectional Areas of EK and ELK Mice 8 Weeks after Injury EK ELK ** * EK ELK media 2.95x104±2000 5.98x104±1000 intimal 4.01x104±6000 8.15x104±2000 lipid deposit after carotid artery injury by FeCl3 for 8 weeks ELK EK control carotid artery stained with ORO noninjured injured lipid deposit after carotid artery injury by FeCl3 for 8 weeks ELK EK carotid artery stained with ORO noninjured injured lipid deposit after carotid artery injury by FeCl3 for 8 weeks ELK EK carotid artery counterstained with ORO and haematoxylin injured noninjured lipid deposit after carotid artery injury by FeCl3 for 8 weeks ELK EK carotid artery counterstained with ORO and haematoxylin noninjured injured Macrophage stain for 8 weeks ELK EK ELK EK Von Willebrand Factor Stain for 8 weeks 0 week 4 weeks 8 weeks ELK（n=4） 61.52±11.09 113.9±5.98 270.17±24.29 EK（n=3） 53.96±18.17 61.61±3.14 85.07±9.40 P value 0.76 0.0015 0.0