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Int J Clin Exp Pathol. 2013 Nov 15;6(12):2912-8. eCollection 2013.
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Mast cells and tumour angiogenesis: new insight from experimental carcinogenesis.肥大细胞与肿瘤血管生成:实验性致癌作用的新见解
Cancer Lett. 2008 Sep 28;269(1):1-6. doi: 10.1016/j.canlet.2008.03.031. Epub 2008 May 2.
2
Hypoxia, hypoxia-inducible transcription factor, and macrophages in human atherosclerotic plaques are correlated with intraplaque angiogenesis.人类动脉粥样硬化斑块中的缺氧、缺氧诱导转录因子和巨噬细胞与斑块内血管生成相关。
J Am Coll Cardiol. 2008 Apr 1;51(13):1258-65. doi: 10.1016/j.jacc.2007.12.025.
3
Hypoxia inducible factor-1 independent pathways in tumor angiogenesis.肿瘤血管生成中缺氧诱导因子-1非依赖途径
Clin Cancer Res. 2007 Oct 1;13(19):5670-4. doi: 10.1158/1078-0432.CCR-07-0111.
4
Hyperoxia and angiogenesis.高氧与血管生成
Wound Repair Regen. 2005 Nov-Dec;13(6):558-64. doi: 10.1111/j.1524-475X.2005.00078.x.
5
Hypoxia inducible factor-1alpha and expression of vascular endothelial growth factor and its receptors in cerebral arteriovenous malformations.缺氧诱导因子-1α与脑动静脉畸形中血管内皮生长因子及其受体的表达
J Clin Neurosci. 2005 Sep;12(7):794-9. doi: 10.1016/j.jocn.2005.02.005.
6
Prostaglandin E2 induces degranulation-independent production of vascular endothelial growth factor by human mast cells.前列腺素E2诱导人肥大细胞产生不依赖于脱颗粒的血管内皮生长因子。
J Immunol. 2004 Jan 15;172(2):1227-36. doi: 10.4049/jimmunol.172.2.1227.
7
Role of blood mononuclear cells in recanalization and vascularization of thrombi: past, present, and future.血液单核细胞在血栓再通和血管化中的作用:过去、现在与未来。
Trends Cardiovasc Med. 2003 Oct;13(7):265-9. doi: 10.1016/s1050-1738(03)00108-7.
8
Vascular endothelial growth factor secretion by tumor-infiltrating macrophages essentially supports tumor angiogenesis, and IgG immune complexes potentiate the process.肿瘤浸润巨噬细胞分泌的血管内皮生长因子实质上支持肿瘤血管生成,而IgG免疫复合物会增强这一过程。
Cancer Res. 2002 Dec 1;62(23):7042-9.
9
Tumor infiltrating lymphocytes and macrophages have a potential dual role in lung cancer by supporting both host-defense and tumor progression.肿瘤浸润淋巴细胞和巨噬细胞在肺癌中可能具有双重作用,既能支持宿主防御,又能促进肿瘤进展。
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Hypoxia--a key regulatory factor in tumour growth.缺氧——肿瘤生长中的关键调节因子。
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在血管内乳头状内皮增生病例中,缺氧诱导因子-1α(HIF-1α)和血管内皮生长因子(VEGF)的表达与血栓重塑相关。

HIF-1α and VEGF expression correlates with thrombus remodeling in cases of intravascular papillary endothelial hyperplasia.

作者信息

Kim Sunzoo, Jun Jae Hun, Kim Jeongshik, Kim Do Won, Jang Yong Hyun, Lee Weon Ju, Chung Ho Yun, Lee Seok-Jong

机构信息

Department of Pathology, Kyungpook National University Hospital, Kyungpook National University School of Medicine Daegu, South Korea.

出版信息

Int J Clin Exp Pathol. 2013 Nov 15;6(12):2912-8. eCollection 2013.

PMID:24294378
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3843272/
Abstract

Intravascular papillary endothelial hyperplasia (IPEH) is histopathologically characterized by endothelium-lined papillary structures encircling an acellular fibrin core. The process of IPEH pathogenesis is unclear. The purpose of our study was to identify histopathological and immunohistochemical characteristics of IPEH to better understand the pathogenesis of this disease. After reviewing microscopic and medical records from Kyungpook National University Hospital, we selected 16 cases of IPEH. Masson's trichrome and immunohistochemical staining as well as hematoxylin-eosin staining for 16 cases of IPH were performed. Immunohistochemical studies included CD31, CD68, mast cell tryptase, hypoxia-inducible factor-1 (HIF-1α), and vascular endothelial growth factor (VEGF). Sections from all our cases showed three distinct histological regions including a papillary portion with hyalinized fibrous or fibroblastic cores, an area containing an unorganized thrombus, and organization area with an ingrowth of endothelial cells, myofibroblasts, and fibroblasts. In the organization area, HIF-1α-positive cells were identified in the loose connective tissue. Endothelial cells forming vascular channels were negative for HIF-1α while VEGF was highly expressed in both interstitial mononuclear and endothelial cells. In the papillary portion, the cellular cores were strongly positive for both HIF-1α and VEGF, but the acellular cores were negative. Our investigation confirmed that IPEH is a reactive lesion that incidentally arises during the organization process of older thrombi. It was also found that HIF-1α and VEGF expression was dependent on the thrombus remodeling stage in cases of IPEH.

摘要

血管内乳头状内皮增生(IPEH)在组织病理学上的特征是内皮细胞衬里的乳头状结构围绕无细胞纤维蛋白核心。IPEH的发病机制尚不清楚。我们研究的目的是确定IPEH的组织病理学和免疫组化特征,以更好地理解这种疾病的发病机制。在回顾庆北国立大学医院的显微镜和病历后,我们选择了16例IPEH病例。对16例IPH进行了Masson三色染色、免疫组化染色以及苏木精-伊红染色。免疫组化研究包括CD31、CD68、肥大细胞类胰蛋白酶、缺氧诱导因子-1(HIF-1α)和血管内皮生长因子(VEGF)。我们所有病例的切片显示出三个不同的组织学区域,包括一个具有透明变性纤维或成纤维细胞核心的乳头状部分、一个含有无组织血栓的区域以及一个有内皮细胞、肌成纤维细胞和成纤维细胞向内生长的机化区域。在机化区域,在疏松结缔组织中发现了HIF-1α阳性细胞。形成血管通道的内皮细胞HIF-1α呈阴性,而VEGF在间质单核细胞和内皮细胞中均高表达。在乳头状部分,细胞核心HIF-1α和VEGF均呈强阳性,但无细胞核心呈阴性。我们的研究证实,IPEH是一种在陈旧血栓机化过程中偶然出现的反应性病变。还发现,在IPEH病例中,HIF-1α和VEGF的表达取决于血栓重塑阶段。