YANG Gui-tang, HAN Ya-ling, YAN Cheng-hui. Expression of cellular repressor of E1A-stimulated genes in atherosclerotic artery and its relationship with inflammatory factors[J]. Chinese Heart Journal, 2016, 28(1): 7-10,24. DOI: 10.13191/j.chj.2016.0002
    Citation: YANG Gui-tang, HAN Ya-ling, YAN Cheng-hui. Expression of cellular repressor of E1A-stimulated genes in atherosclerotic artery and its relationship with inflammatory factors[J]. Chinese Heart Journal, 2016, 28(1): 7-10,24. DOI: 10.13191/j.chj.2016.0002

    Expression of cellular repressor of E1A-stimulated genes in atherosclerotic artery and its relationship with inflammatory factors

    • AIM To investigate the effects of cellular repressor of E1A-stimulated genes( CREG) on atherosclerotic lesion formation and its relation with inflammatory factors. METHODS Immunofluorescence and Western blot was used to detect the expression of CREG in atherosclerotic arteries. The morphology of the artery and expressions of CREG and smooth muscle α-actin( SMα-actin) on natural atherosclerotic formation were observed in Apo E(-/-) knockout mice fed with high-fat diet. RESULTS From 1 to 8 weeks of atherogenic diet,CREG expression in arterial wall of Apo E(-/-) mice did not decrease at the early stage of AS. However,its expression obviously increased within 2 weeks of atherogenic diet. At the fourth week of atherogenic diet,CREG expression decreased rapidly and later increased gradually until the 8th week. But the expression of CREG did not reach the normal level. At the same time,the change of nuclear factor-kappa B( NF-κB) expression,an inflammatory marker,was observed in a time-dependent fashion. Within 8 weeks of atherogenic diet,NF-κB increased gradually,indicating that inflammation continued and became more serious throughout atherosclerosis. CONCLUSION The phenotype of VSMCs changes from differentiation to synthesis in atherosclerotic formation. CREG expression decreases with the development of atherosclerosis,suggesting that CREG is associated with atherosclerosis and inflammation.
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