Редактирование: VASH1

Tubulinyl-Tyr carboxypeptidase 1 (EC 3.4.17.17) (Tubulin carboxypeptidase 1) (Tyrosine carboxypeptidase 1) (TTCP 1) (Vasohibin-1) [KIAA1036] [VASH]

==Publications==

{{medline-entry
|title=Double-Face of Vasohibin-1 for the Maintenance of Vascular Homeostasis and Healthy Longevity.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29398681
|abstract=The structural and functional integrity of endothelium is essential for the maintenance of vascular health. Vasohibin-1 ([[VASH1]]), originally isolated as an endothelium-derived angiogenesis inhibitor, has another function to promote stress tolerance of endothelial cells (ECs), and these functions are critical for the maintenance of vascular homeostasis preventing both pathological angiogenesis and stress-induced vascular diseases. The expression of [[VASH1]] is downregulated during replicative senescence of ECs by the alteration of microRNA expression, and this age-associated downregulation of [[VASH1]] might be a risk of deterioration of vascular homeostasis and age-related vascular diseases. Contrary to this expectation, the lack of Vash1 gene in mice exhibited healthy longevity. Thus, [[VASH1]] has double-face for the maintenance of vascular homeostasis and healthy longevity. This feature of [[VASH1]] and its mechanism will be described in this mini review.
|mesh-terms=* Cell Cycle Proteins
* Endothelium, Vascular
* Homeostasis
* Humans
* Longevity
* Neovascularization, Physiologic
|keywords=* , Vascular stress tolerance
* Angiogenesis inhibition
* Healthy longevity
* Vasohibin-1
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6005230
}}
{{medline-entry
|title=Age-associated downregulation of vasohibin-1 in vascular endothelial cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27325558
|abstract=Vasohibin-1 ([[VASH1]]) is an angiogenesis-inhibiting factor synthesized by endothelial cells (ECs) and it also functions to increase stress tolerance of ECs, which function is critical for the maintenance of vascular integrity. Here, we examined whether the expression of [[VASH1]] would be affected by aging. We passaged human umbilical vein endothelial cells (HUVECs) and observed that [[VASH1]] was downregulated in old HUVECs. This decrease in [[VASH1]] expression with aging was confirmed in mice. To explore the mechanism of this downregulation, we compared the expression of microRNAs between old and young HUVECs by performing microarray analysis. Among the top 20 microRNAs that were expressed at a higher level in old HUVECs, the third highest microRNA, namely miR-22-3p, had its binding site on the 3' UTR of [[VASH1]] mRNA. Experiments with microRNA mimic and anti-miR revealed that miR-22-3p was involved at least in part in the downregulation of [[VASH1]] in ECs during replicative senescence. We then clarified the significance of this defective expression of [[VASH1]] in the vasculature. When a cuff was placed around the femoral arteries of wild-type mice and [[VASH1]]-null mice, neointimal formation was augmented in the [[VASH1]]-null mice accompanied by an increase in adventitial angiogenesis, macrophage accumulation in the adventitia, and medial/neointimal proliferating cells. These results indicate that in replicative senescence, the downregulation of [[VASH1]] expression in ECs was caused, at least in part, by the alteration of microRNA expression. Such downregulation of [[VASH1]] might be involved in the acceleration of age-associated vascular diseases.
|mesh-terms=* Animals
* Apolipoproteins E
* Atherosclerosis
* Cell Cycle Proteins
* Cellular Senescence
* Down-Regulation
* Endothelial Cells
* Human Umbilical Vein Endothelial Cells
* Humans
* Mice, Inbred C57BL
* MicroRNAs
* Neointima
|keywords=* aging
* angiogenesis
* endothelial cell
* replicative senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5013028
}}