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TRAIL 和死亡受体 DR4 在 Palmer Ⅱ型 TFCC 病变中的表达。

Expression of TRAIL and death receptor DR4 in Palmer type 2 TFCC lesions.

机构信息

Department of Plastic and Hand Surgery, University Erlangen, Krankenhausstrasse 12, Erlangen, Germany.

出版信息

Arch Orthop Trauma Surg. 2010 Oct;130(10):1215-20. doi: 10.1007/s00402-009-0988-4. Epub 2009 Nov 13.

Abstract

INTRODUCTION

Degenerative articular disc perforations of the triangular fibrocartilage (TFC) of the wrist are characterized by fibrocartilage cell loss and are often associated with ulna-plus situations. Apoptosis has been found to play a crucial role in fibrocartilage cell loss, however, the molecular mechanism and mediators are still poorly understood.

AIM

The purpose of this study was to identify receptors to apoptosis in degenerative disc lesions.

PATIENTS

Included in the study were 17 patients with degenerative articular disc tears of the TFC (Palmer type 2C). Following arthroscopic debridement of the TFC, histological sections were examined to assess the presence of apoptosis. Apoptosis was determined using TRAIL and death receptor DR4 agonists for immunohistochemical analyses. The number of cells positive for apoptosis was then correlated with ulna length.

RESULTS

Cells positive for TRAIL and DR4 were found in all specimens. The number of cells positive for TRAIL was significantly increased in specimens of patients with an ulna positive variance (P = 0.040). However, DR4 was not significantly increased in ulna plus (P > 0.05). Both, TRAIL and DR4 positive cells were found to be evenly distributed throughout each specimen. There was no accumulation of any type of cells in any particular zone of the biopsies.

CONCLUSION

This is the first study that shows that TFCC cells express TRAIL and DR4, which suggests that apoptosis, as well as, mechanical trauma are involved in the development of disc perforation. The TRAIL/DR4 receptor system is a molecular mediator of apoptosis induction in TFC cells and therefore plays a role in cell loss in degenerative disc lesions.

摘要

简介

腕关节三角纤维软骨(TFCC)的退行性关节盘穿孔的特征是纤维软骨细胞丢失,并且常与尺骨阳性情况相关。凋亡已被发现对纤维软骨细胞丢失起关键作用,然而,其分子机制和介质仍知之甚少。

目的

本研究旨在鉴定退行性椎间盘病变中凋亡的受体。

患者

本研究纳入了 17 例 TFCC 退行性关节盘撕裂的患者(Palmer 2C 型)。在 TFCC 关节镜清创后,通过组织学切片评估凋亡的存在。使用 TRAIL 和死亡受体 DR4 激动剂进行免疫组织化学分析,确定凋亡。然后将凋亡阳性细胞的数量与尺骨长度相关联。

结果

所有标本中均发现 TRAIL 和 DR4 阳性细胞。在尺骨阳性方差的患者标本中,TRAIL 阳性细胞的数量显著增加(P=0.040)。然而,DR4 在尺骨阳性中并未显著增加(P>0.05)。TRAIL 和 DR4 阳性细胞在每个标本中均匀分布。在活检的任何特定区域均未发现任何类型细胞的堆积。

结论

这是第一项表明 TFCC 细胞表达 TRAIL 和 DR4 的研究,这表明凋亡以及机械创伤参与了椎间盘穿孔的发生。TRAIL/DR4 受体系统是 TFC 细胞凋亡诱导的分子介质,因此在退行性椎间盘病变中的细胞丢失中起作用。

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