Journal article
Myofibroblast in the ligamentum flavum hypertrophic activity
European spine journal, Vol.26(8), pp.2021-2030
08/01/2017
DOI: 10.1007/s00586-017-4981-2
PMID: 28180980
Abstract
Majority of the previous studies compared lumbar spinal stenosis (LSS) and lumbar disc herniation (LDH) patients for analyses of LFH. However, the separation of normal/hypertrophied LF has often been ambiguous and the severity of hypertrophic activity differed. Here, we present a novel analysis scheme for LFH in which myofibroblast is proposed as a major etiological factor for LFH study.
Seventy-one LF patient tissue samples were used for this study. Initially, mRNA levels of the samples were assessed by qRT-PCR: angiopoietin-like protein-2 (ANGPTL2), transforming growth factor-beta1 (TGF-β1), vascular endothelial growth factor (VEGF), interleukin-6, collagen-1, 3, 4, 5, and 11, and elastin. Myofibroblasts were detected by immune stain using α-smooth muscle actin (αSMA) as a marker. To study the myofibroblast in TGF-β pathway, LF tissues were analyzed for protein levels of αSMA/TGF-β1 by Western blot. In addition, from LF cells cultured with exogenous TGF-β1 conditioned medium, expression of αSMA/collagen-1 was assessed and the cell morphology was identified.
The comparative analysis of mRNA expression levels (LSS vs LDH) failed to show significant differences in TGF-β1 (p = 0.08); however, we found a significant positive correlation among ANGPTL2, VEGF, TGF-β1, and collagen-1 and 3, which represent common trends in hypertrophic activity (p < 0.05). We detected myofibroblast in the patient samples by αSMA staining, and the protein levels of αSMA were positively correlated with TGF-β1. In LF cell culture, exogenous TGF-β1 upregulated αSMA/collagen-1 mRNA levels and facilitated trans-differentiation to myofibroblast.
We conclude that the transition of fibroblast to myofibroblasts via TGF-β pathway is a key linker between inflammation and fibrosis in LFH mechanism.
Details
- Title: Subtitle
- Myofibroblast in the ligamentum flavum hypertrophic activity
- Creators
- Junseok W Hur - Institute for Basic ScienceTaegeun Bae - Institute for Basic ScienceSunghyeok Ye - Korea University of Science and TechnologyJoo-Hyun Kim - Korea UniversitySunhye Lee - University of SeoulKyoungmi Kim - Institute for Basic ScienceSeung-Hwan Lee - Institute for Basic ScienceJin-Soo Kim - Seoul National UniversityJang-Bo Lee - Korea UniversityTai-Hyoung Cho - Korea UniversityJung-Yul Park - University of SeoulJunho K Hur - Korea University Anam Hospital, 73, Inchon-ro, Seongbuk-gu, Seoul, 02841, Republic of Korea. jh0210@gmail.com
- Resource Type
- Journal article
- Publication Details
- European spine journal, Vol.26(8), pp.2021-2030
- DOI
- 10.1007/s00586-017-4981-2
- PMID
- 28180980
- ISSN
- 0940-6719
- eISSN
- 1432-0932
- Grant note
- name: Hanmi Pharm Co., Ltd.; DOI: 10.13039/501100010446, name: Institute for Basic Science, award: IBS-R021-D1
- Language
- English
- Date published
- 08/01/2017
- Academic Unit
- Neurosurgery
- Record Identifier
- 9984459620902771
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