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首页> 外文期刊>Molecular and Cellular Biology >CYR61 (CCN1) Is Essential for Placental Development and Vascular Integrity
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CYR61 (CCN1) Is Essential for Placental Development and Vascular Integrity

机译：CYR61（CCN1）对胎盘发育和血管完整性至关重要

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CYR61 (CCN1) is a member of the CCN family of secreted matricellular proteins that includes connective tissue growth factor (CCN2), NOV (CCN3), WISP-1 (CCN4), WISP-2 (CCN5), and WISP-3 (CCN6). First identified as the product of a growth factor-inducible immediate-early gene, CYR61 is an extracellular matrix-associated angiogenic inducer that functions as a ligand of integrin receptors to promote cell adhesion, migration, and proliferation. Aberrant expression of Cyr61 is associated with breast cancer, wound healing, and vascular diseases such as atherosclerosis and restenosis. To understand the functions of CYR61 during development, we have disrupted the Cyr61 gene in mice. We show here that Cyr61-null mice suffer embryonic death: ～30% succumbed to a failure in chorioallantoic fusion, and the reminder perished due to placental vascular insufficiency and compromised vessel integrity. These findings establish CYR61 as a novel and essential regulator of vascular development. CYR61 deficiency results in a specific defect in vessel bifurcation (nonsprouting angiogenesis) at the chorioallantoic junction, leading to an undervascularization of the placenta without affecting differentiation of the labyrinthine syncytiotrophoblasts. This unique phenotype is correlated with impaired Vegf-C expression in the allantoic mesoderm, suggesting that CYR61-regulated expression of Vegf-C plays a role in vessel bifurcation. The genetic and molecular basis of vessel bifurcation is presently unknown, and these findings provide new insight into this aspect of angiogenesis.
机译：CYR61（CCN1）是分泌型基质细胞蛋白CCN家族的成员，包括结缔组织生长因子（CCN2），NOV（CCN3），WISP-1（CCN4），WISP-2（CCN5）和WISP-3（CCN6） ）。 CYR61首先被鉴定为生长因子诱导的立即早期基因的产物，是一种与细胞外基质相关的血管生成诱导剂，其作为整联蛋白受体的配体起作用，以促进细胞粘附，迁移和增殖。 Cyr61 的异常表达与乳腺癌，伤口愈合以及血管疾病（如动脉粥样硬化和再狭窄）有关。为了了解CYR61在发育过程中的功能，我们破坏了小鼠的 Cyr61 基因。我们在这里显示 Cyr61 -null小鼠遭受胚胎死亡：约30％的患者因绒毛膜尿囊融合失败而死亡，并且由于胎盘血管功能不全和血管完整性受损而使提醒消失。这些发现将CYR61确立为新颖且必要的血管发育调节剂。 CYR61缺乏症会导致绒毛膜尿囊连接处的血管分叉（非发芽性血管生成）出现特定缺陷，从而导致胎盘血管生成不足，而不会影响迷路合胞体滋养层细胞的分化。这种独特的表型与尿囊中膜中 Vegf-C 表达受损有关，表明CYR61调控的 Vegf-C 表达在血管分叉中起作用。血管分叉的遗传和分子基础目前未知，这些发现为血管生成的这一方面提供了新的见识。

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