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首页> 外文期刊>Cell and Tissue Research >Expression of vascular endothelial growth factor (VEGF)-B and its receptor (VEGFR1) in murine heart, lung and kidney
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Expression of vascular endothelial growth factor (VEGF)-B and its receptor (VEGFR1) in murine heart, lung and kidney

机译：血管内皮生长因子（VEGF）-B及其受体（VEGFR1）在鼠心，肺和肾中的表达

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Metabolic diseases, such as obesity and diabetes, are a serious burden for the health system. Vascular endothelial growth factor (VEGF)-B has been shown to regulate tissue uptake and accumulation of fatty acids and is thus involved in these metabolic diseases. However, the cell-type-specific expression pattern of Vegfb and its receptor (VEGFR1, gene Flt1) remains unclear. We explore the expression of Vegfb and Flt1 in the murine heart, lung and kidney by utilizing beta-galactosidase knock-in mouse models and combining the analysis of reporter gene expression and immunofluorescence microscopy. Furthermore, Flt1 heterozygous mice were analyzed with regard to muscular fatty acid accumulation and peripheral insulin sensitivity. Throughout the heart, Vegfb expression was found in cardiomyocytes with a postnatal ventricular shift corresponding to known changes in energy requirements. Vegfb expression was also found in the pulmonary myocardium of the lung and in renal epithelial cells of the thick ascending limb of Henle's loop, the connecting tubule and the collecting duct. In all analyzed organs, VEGFR1 expression was restricted to endothelial cells. We also show that reduced expression of VEGFR1 resulted in decreased cardiac fatty acid accumulation and increased peripheral insulin sensitivity, possibly as a result of attenuated VEGF-B/VEGFR1 signaling. Our data therefore support a tightly controlled, paracrine signaling mechanism of VEGF-B to VEGFR1. The identified cell-specific expression pattern of Vegfb and Flt1 might form the basis for the development of cell-type-targeted research models and contributes to the understanding of the physiological and pathological role of VEGF-B/VEGFR1 signaling.
机译：肥胖和糖尿病等代谢性疾病是卫生系统的严重负担。血管内皮生长因子（VEGF）-B已被证明可调节组织对脂肪酸的摄取和积累，因此参与了这些代谢性疾病。但是，Vegfb及其受体（VEGFR1，基因Flt1）的细胞类型特异性表达模式仍然不清楚。我们利用β-半乳糖苷酶敲入小鼠模型，并结合报告基因表达分析和免疫荧光显微镜，探讨了Vegfb和Flt1在鼠心，肺和肾中的表达。此外，分析了Flt1杂合小鼠的肌肉脂肪酸积累和外周胰岛素敏感性。在整个心脏中，发现Vegfb表达在心肌细胞中具有与已知能量需求变化相对应的出生后心室移位。 Vegfb表达还出现在肺的肺心肌和Henle环的厚上升肢，连接小管和收集管的肾上皮细胞中。在所有分析的器官中，VEGFR1的表达都局限于内皮细胞。我们还显示，VEGFR1的减少表达可能导致心脏脂肪酸蓄积减少和外周胰岛素敏感性增加，这可能是由于VEGF-B / VEGFR1信号转导减弱所致。因此，我们的数据支持了VEGF-B对VEGFR1的严格控制的旁分泌信号传导机制。鉴定的Vegfb和Flt1的细胞特异性表达模式可能构成以细胞类型为靶标的研究模型发展的基础，并且有助于理解VEGF-B / VEGFR1信号传导的生理和病理作用。

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