肝细胞 RXRα缺失导致小鼠血管生成抑制。
Hepatocyte RXR alpha deletion in mice leads to inhibition of angiogenesis.
机构信息
Department of Clinical Biochemistry, Jagiellonian University Medical College, Kopernika 15a Street, 31-501, Cracow, Poland,
出版信息
Genes Nutr. 2009 Mar;4(1):69-72. doi: 10.1007/s12263-009-0111-z. Epub 2009 Feb 18.
To investigate the effect of RXRalpha deficiency in liver on angiogenesis, hepatocyte RXRalpha-deficient and control wild-type mice were fed either standard or high-fat diet (HF) for 7 weeks. In the 6th week of feeding, Matrigel model of in vivo angiogenesis was applied. Matrigel plug infiltrating cells were then used for visualization of vessels (CD31 staining) as well as for gene expression analysis. HF diet appeared to decrease angiogenesis in hRXRalpha-deficient mice. Genes related to angiogenesis (Nos3, Kdr) were down-regulated, whereas genes connected with adipogenesis (Cebpb, Srebf1), apoptosis (Gzmb, Bcl2) and proinflammatory pathway (NfkappaB, Tnfalpha) were up-regulated by HF diet in hRXRalpha-deficient mice in the microarray study. Our results suggest that impaired fatty acid metabolism in liver (hRXRalpha-deficient mice) leads to impaired angiogenesis due to lipotoxicity and promotion of adipogenesis.
为了研究肝脏中 RXRα 缺乏对血管生成的影响，用标准或高脂肪饮食（HF）喂养肝细胞 RXRα 缺陷型和对照野生型小鼠 7 周。在喂养的第 6 周，应用体内血管生成的 Matrigel 模型。然后使用 Matrigel 塞浸润细胞来可视化血管（CD31 染色）以及进行基因表达分析。HF 饮食似乎减少了 hRXRα 缺陷型小鼠的血管生成。与血管生成相关的基因（Nos3、Kdr）下调，而与脂肪生成（Cebpb、Srebf1）、细胞凋亡（Gzmb、Bcl2）和促炎途径（NfkappaB、Tnfalpha）相关的基因在 hRXRα 缺陷型小鼠中被 HF 饮食上调。我们的研究结果表明，肝脏中脂肪酸代谢受损（hRXRα 缺陷型小鼠）导致脂毒性和促进脂肪生成，从而导致血管生成受损。
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