Suppr超能文献

脊髓型颈椎病患者后纵韧带中与转化生长因子-β1相关的炎症

TGF-β1 related inflammation in the posterior longitudinal ligament of cervical spondylotic myelopathy patients.

作者信息

Wang Jia-Zeng, Fang Xiu-Tong, Lv E, Yu Fang, Wang Zhen-Wei, Song Hong-Xing

机构信息

Department of Orthopaedics, Beijing Shijitan Hospital, Capital Medical University Beijing 100038, China ; Shandong Medical College Linyi 276000, Shandong, China.

Department of Orthopaedics, Beijing Shijitan Hospital, Capital Medical University Beijing 100038, China.

出版信息

Int J Clin Exp Med. 2015 Feb 15;8(2):2233-9. eCollection 2015.

Abstract

AIM

This study aimed to elucidate the pathogenesis of posterior longitudinal ligament (PLL) hypertrophy.

METHODS

Cervical PLL specimens were collected from CSM patients during surgery (n = 30) and during routine autopsy (n = 14), and processed for histological examination (HE staining and Masson's Trichrome staining) and IHC (CD3, CD68, CD31, TGF-β1 and collagen II). In addition, the mRNA expression of collagen I was detected in cervical PLL specimens from 16 CSM patients (n = 16) and from routine autopsy (n = 16) by RT-PCR.

RESULTS

Obvious fibrosis, cartilage metaplasia and calcification were found in the cervical PLL of CSM patients. In the degenerated PLL, CD68(+) macrophages were frequently identified, CD3(+) T lymphocytes were occasionally found, and many newly generated small vessels were also present. In the degenerated PLL, of the number of TGF-β1 positive cells increased markedly when compared with control group. IHC indicated TGF-β1 was secreted by macrophages. RT-PCR showed a significantly lower mRNA expression of collagen I in the PLL of CSM patients as compared to control group.

CONCLUSIONS

Macrophages are the major type of inflammatory cells involved in the cervical PLL degeneration, and TGF-β1 is related to the cervical PLL degeneration. TGF-β1 is mainly secreted by macrophages. Anti-inflammation may serve as an alternative non-surgical treatment and prophylactic strategy for PLL degeneration.

摘要

目的

本研究旨在阐明后纵韧带(PLL)肥厚的发病机制。

方法

在手术过程中从脊髓型颈椎病(CSM)患者中收集颈椎PLL标本(n = 30),并在常规尸检时收集(n = 14),进行组织学检查(苏木精-伊红染色和Masson三色染色)以及免疫组化(CD3、CD68、CD31、转化生长因子-β1(TGF-β1)和胶原蛋白II)。此外,通过逆转录-聚合酶链反应(RT-PCR)检测16例CSM患者(n = 16)和常规尸检(n = 16)的颈椎PLL标本中I型胶原蛋白的mRNA表达。

结果

在CSM患者的颈椎PLL中发现明显的纤维化、软骨化生和钙化。在退变的PLL中,经常鉴定出CD68(+)巨噬细胞,偶尔发现CD3(+)T淋巴细胞,并且还存在许多新生成的小血管。在退变的PLL中,与对照组相比,TGF-β1阳性细胞数量明显增加。免疫组化表明TGF-β1由巨噬细胞分泌。RT-PCR显示,与对照组相比,CSM患者PLL中I型胶原蛋白的mRNA表达明显降低。

结论

巨噬细胞是参与颈椎PLL退变的主要炎症细胞类型,TGF-β1与颈椎PLL退变有关。TGF-β1主要由巨噬细胞分泌。抗炎可能是PLL退变的一种替代性非手术治疗和预防策略。

相似文献

3
Removal of posterior longitudinal ligament in anterior decompression for cervical spondylotic myelopathy.
J Spinal Disord Tech. 2009 Aug;22(6):404-7. doi: 10.1097/BSD.0b013e318187039f.
9
Analysis of hypertrophy of the posterior longitudinal ligament of the cervical spine, on the basis of clinical and experimental studies.
Neurosurgery. 2001 Nov;49(5):1091-7; discussion 1097-8. doi: 10.1097/00006123-200111000-00013.
10
Arthroplasty for cervical spondylotic myelopathy: similar results to patients with only radiculopathy at 3 years' follow-up.
J Neurosurg Spine. 2014 Sep;21(3):400-10. doi: 10.3171/2014.3.SPINE13387. Epub 2014 Jun 13.

引用本文的文献

本文引用的文献

1
Pathophysiology and natural history of cervical spondylotic myelopathy.
Spine (Phila Pa 1976). 2013 Oct 15;38(22 Suppl 1):S21-36. doi: 10.1097/BRS.0b013e3182a7f2c3.
2
Ossification of the posterior longitudinal ligament of the cervical spine: etiology and natural history.
Spine (Phila Pa 1976). 2012 Mar 1;37(5):E309-14. doi: 10.1097/BRS.0b013e318241ad33.
5
Is platelet-derived growth factor-BB expression proportional to fibrosis in the hypertrophied lumber ligamentum flavum?
Spine (Phila Pa 1976). 2010 Dec 1;35(25):E1479-86. doi: 10.1097/BRS.0b013e3181f3d2df.
6
Removal of posterior longitudinal ligament in anterior decompression for cervical spondylotic myelopathy.
J Spinal Disord Tech. 2009 Aug;22(6):404-7. doi: 10.1097/BSD.0b013e318187039f.
7
Growth factors and cytokines in wound healing.
Wound Repair Regen. 2008 Sep-Oct;16(5):585-601. doi: 10.1111/j.1524-475X.2008.00410.x.
8
Novel therapies for scar reduction and regenerative healing of skin wounds.
Trends Biotechnol. 2008 Apr;26(4):173-80. doi: 10.1016/j.tibtech.2007.12.007. Epub 2008 Mar 4.
9
Fragments of extracellular matrix as mediators of inflammation.
Int J Biochem Cell Biol. 2008;40(6-7):1101-10. doi: 10.1016/j.biocel.2007.12.005. Epub 2007 Dec 24.
10
TGF-beta-induced fibrosis and SMAD signaling: oligo decoys as natural therapeutics for inhibition of tissue fibrosis and scarring.
Wound Repair Regen. 2007 Sep-Oct;15 Suppl 1:S54-60. doi: 10.1111/j.1524-475X.2007.00226.x.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验