A histological study of vascular wall resident stem cells in venous malformations

A histological study of vascular wall resident stem cells in venous malformations
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静脉畸形血管壁驻留干细胞的组织学研究

DOI:
10.1007/s00441-022-03672-3
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发表时间:
2022-08-02
影响因子:
3.6
通讯作者:
Zhao,Yi-Fang
Zhao,Yi-Fang
中科院分区:
生物学3区
文献类型:
--
作者:
Xia,Hou-Fu;Lai,Wen-Qiang;Zhao,Yi-Fang

文献摘要

相似文献

血管壁驻留干细胞(VW-SCs)在生理和病理条件下的血管形成和重塑中起着关键作用。它们不仅作为一个水库,以提供所需的各种类型的血管细胞,但也通过旁分泌作用调节血管的稳态。静脉畸形是一种常见的先天性血管畸形,以血管细胞数量不足和功能异常为特征。然而,VW-SC在VM中的存在和作用目前仍不清楚。本研究采用免疫组化、免疫荧光双标记和qPCR方法检测了22例VM标本中VW-SCs的水平和分布,并进行了斯皮尔曼等级相关检验。我们发现,与正常微静脉相比,VM中CD 34、vWF、VEGFR 2、CD 44、CD 90和CD 105的蛋白和mRNA表达水平均显著下调。VW-SCs在VM内皮细胞内外散在分布,甚至不存在。VW-SC相关标志物的表达与内皮细胞和血管周围细胞的密度呈正相关。所有这些结果和现有证据表明,VW-SCs在VM中的分布更分散,数量更少,这可能是VM中血管细胞缺乏的原因。
Vascular wall resident stem cells (VW-SCs) play a key role in vascular formation and remodeling under both physiological and pathological situations. They not only serve as a reservoir to supply all types of vascular cells needed, but also regulate vascular homeostasis by paracrine effects. Venous malformations (VMs) are common congenital vascular malformations which are just characterized by the deficient quantity and abnormal function of vascular cells. However, the existence and role of VW-SCs in VMs is still unclear at present. In this study, the level and distribution of VW-SCs in 22 specimens of VMs were measured by immunochemistry, double-labeling immunofluorescence, and qPCR, followed by the Spearman rank correlation test. We found that both the protein and mRNA expression levels of CD34, vWF, VEGFR2, CD44, CD90, and CD105 were significantly downregulated in VMs compared with that in normal venules. VW-SCs were sporadically distributed or even absent within and outside the endothelium of VMs. The expression of the VW-SC-related markers was positively correlated with the density of both endothelial cells and perivascular cells. All those results and established evidence indicated that VW-SCs were more sporadically distributed with fewer amounts in VMs, which possibly contributing to the deficiency of vascular cells in VMs.