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首页> 外文期刊>Endocrine Research >Paracrine control of the adult adrenal cortex vasculature by vascular endothelial growth factor.
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Paracrine control of the adult adrenal cortex vasculature by vascular endothelial growth factor.

机译：通过血管内皮生长因子对成人肾上腺皮质血管的旁分泌控制。

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The extensive vascular network that irrigates the adult adrenal cortex is essential for both the delivery of oxygen and nutrients to glandular steroidogenic cells and for the rapid and efficient export of corticosteroid products from these cells into the blood flow. During experimental and pathological changes in adrenal cortex size caused by ACTH overproduction or deficiency, the vasculature evolves in a coordinated manner with the mass of glandular cells so that blood vessel formation/regression and cortical gowth/atrophy are respectively synchronized. In addition to its previously reported expression in human fetal adrenocortical cells, the angiogenic factor VEGF-A appears also to be strongly expressed by both glomerulosa and fasciculata cells of the adult bovine adrenal cortex, when the endothelium is quiescent. Moreover, the expression of the two major transcripts encoding the 121 and the 165 amino acid-long isoforms of VEGF-A was observed to be rapidly (within 2-4 h) up-regulated (2-3 fold) by ACTH in primary cultures of bovine fasciculata and glomerulosa cells. The expression of the signalling VEGF receptors R1 (flt-1) and R2 (flk-1) was restricted to the endothelial cells of the cortex whereas neuropilin-1 was expressed by both endothelial and steroidogenic cells. This suggests that, under the control of the pituitary hormone ACTH, VEGF exerts a paracrine control over the vasculature of the adult adrenal cortex. Given its known effects as an anti-apoptotic agent and an inducer of endothelial fenestration, VEGF is likely to play a role in the maintenance of the dense and fenestrated vascular bed of the adrenal cortex. The vasculature thus appears as an important secondary target of ACTH action in the physiological control of adrenal cortex homeostasis.
机译：灌溉成年肾上腺皮质的广泛的血管网络对于将氧气和营养物质输送至腺类固醇生成细胞以及将皮质类固醇产品从这些细胞快速有效地输出到血流中都是至关重要的。在由ACTH过度生产或缺乏引起的肾上腺皮质大小的实验和病理变化期间，脉管系统与腺细胞的质量以协调的方式演化，从而使血管的形成/消退和皮质的生长/萎缩分别同步。除了先前报道的在人胎儿肾上腺皮质细胞中的表达外，当内皮静止时，血管生成因子VEGF-A似乎也由成年牛肾上腺皮质的肾小球和筋膜细胞强烈表达。此外，在原代培养物中，ACTH迅速（2-4小时内）上调了（2-3倍）编码VEGF-A 121和165个氨基酸长的亚型的两个主要转录物的表达。牛fasciculata和肾小球细胞VEGF信号受体R1（flt-1）和R2（flk-1）的表达仅限于皮层内皮细胞​​，而内皮细胞和类固醇生成细胞均表达Neuropilin-1。这表明，在垂体激素ACTH的控制下，VEGF对成年肾上腺皮质的脉管系统发挥旁分泌控制作用。鉴于其作为抗凋亡剂和内皮开窗诱导剂的已知作用，VEGF可能在维持肾上腺皮质致密和开窗的血管床中发挥作用。因此，在肾上腺皮质稳态的生理控制中，脉管系统似乎是ACTH作用的重要次要靶标。

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