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TRAIL、DR5 和 caspase 3 依赖性凋亡在病变的人颞下颌关节盘血管中的作用。一项免疫组化研究。

TRAIL, DR5 and caspase 3-dependent apoptosis in vessels of diseased human temporomandibular joint disc. An immunohistochemical study.

机构信息

Department of Anatomy, Diagnostic Pathology, Forensic Medicine, Hygiene and Public Health, University of Catania, via S. Sofia 87, Catania, Italy.

出版信息

Eur J Histochem. 2010;54(3):e40. doi: 10.4081/ejh.2010.e40.

DOI:10.4081/ejh.2010.e40
PMID:20839416
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3167309/
Abstract

To evaluate the apoptosis involvement in the angiogenesis as a self-limiting process in patients with temporomandibular joint (TMJ) degenerated disc vessels, we assessed, by immunohistochemistry, the detection of TRAIL, its death receptor DR5 and caspase 3. TRAIL, its death receptor DR5 and caspase 3 expression were studied by immunohistochemistry in 15 TMJ discs displaced without reduction and in 4 unaffected discs. These apoptosis molecules were detected in the intima and media layers of newly formed vessels affected discs. In conclusion, vessels apoptosis activation in TMJ disc with ID could be regarded as a self-limiting process that try to leads to vessel regression; in this way an inhibition of angiogenic vessels may prove a key strategy in limiting pathological angiogenesis, by cutting off blood supply to tumors, or by reducing harmful inflammation.

摘要

为了评估细胞凋亡在颞下颌关节(TMJ)退行性盘血管中作为一个自限性过程的参与,我们通过免疫组织化学评估了 TRAIL、其死亡受体 DR5 和半胱氨酸蛋白酶 3 的检测。在 15 个无复位脱位的 TMJ 盘和 4 个未受影响的盘中,通过免疫组织化学研究了 TRAIL、其死亡受体 DR5 和半胱氨酸蛋白酶 3 的表达。这些凋亡分子在受影响的新形成血管的内膜和中膜层中被检测到。总之,TMJ 盘 ID 中血管的细胞凋亡激活可以被视为一种自限性过程,试图导致血管退化;通过抑制血管生成,可能会通过切断肿瘤的血液供应,或减少有害炎症,从而成为限制病理性血管生成的关键策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2050/3167309/15b2e2c74920/ejh-2010-3-e40-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2050/3167309/13d36e92e881/ejh-2010-3-e40-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2050/3167309/3093d1ab2fad/ejh-2010-3-e40-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2050/3167309/15b2e2c74920/ejh-2010-3-e40-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2050/3167309/13d36e92e881/ejh-2010-3-e40-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2050/3167309/3093d1ab2fad/ejh-2010-3-e40-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2050/3167309/15b2e2c74920/ejh-2010-3-e40-g003.jpg

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本文引用的文献

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2-DG-Regulated RIP and c-FLIP Effect on Liver Cancer Cell Apoptosis Induced by TRAIL.2-脱氧葡萄糖调节的RIP和c-FLIP对TRAIL诱导的肝癌细胞凋亡的影响
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