Abstract

Aims Intervertebral disc (IVD) degeneration was believed to contribute to lower back pain. The aim of the study was to investigate the pathogenesis and regulatory mechanism of puncture-induced IVD degeneration. Main methods We established a rat-tail puncture model using Kirschner wire and a homemade stopper. The progress of disc degeneration was evaluated by histological examination and the quantitative measurement of type I, type II collagen and other factors expression at 0.5, 1, 2, 6, and 12 weeks after puncture and was compared with control rats of the same age. Key findings Histological examination and Safranin-O staining revealed progressive degeneration of the punctured disc. Matrix metalloproteinase 13 (MMP13) was increased at 1 week after puncture but did not change in the control group. The interleukin-1 beta (IL-1β) mRNA expression level was elevated at the acute stage after puncture compared with the control group. The hypoxia inducible factor 2 (HIF-2) increased expression in punctured groups. Additionally, compare to adjacent non-punctured segments, HIF-2α expression level transiently increased and then decreased in the nucleus pulposus immediately following puncture, and it then increased 12 weeks after puncture. Significance The degenerative changes observed in this rat-tail puncture model are similar to human disc degeneration and that this model may be valuable for elucidating the molecular mechanisms and pathways underlying disc degeneration.

Original languageEnglish
Pages (from-to)15-20
Number of pages6
JournalLife Sciences
Volume156
DOIs
Publication statusPublished - Jul 1 2016

Fingerprint

Intervertebral Disc Degeneration
Punctures
Tail
Rats
Rat control
Matrix Metalloproteinase 13
Collagen Type II
Interleukin-1beta
Wire
Messenger RNA
Bone Wires
Control Groups
Collagen Type I
Low Back Pain
endothelial PAS domain-containing protein 1
Staining and Labeling

Keywords

  • HIF-2
  • Intervertebral disc degeneration
  • Nucleus pulposus
  • Rat-tail puncture model

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Time course investigation of intervertebral disc degeneration in a rat-tail puncture model. / Chen, Chia Hsian; Chiang, Chang Jung; Wu, Lien Chen; Yang, Chih Hong; Kuo, Yi Jie; Tsuang, Yang Hwei; Tsai, Tung Hu.

In: Life Sciences, Vol. 156, 01.07.2016, p. 15-20.

Research output: Contribution to journalArticle

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abstract = "Aims Intervertebral disc (IVD) degeneration was believed to contribute to lower back pain. The aim of the study was to investigate the pathogenesis and regulatory mechanism of puncture-induced IVD degeneration. Main methods We established a rat-tail puncture model using Kirschner wire and a homemade stopper. The progress of disc degeneration was evaluated by histological examination and the quantitative measurement of type I, type II collagen and other factors expression at 0.5, 1, 2, 6, and 12 weeks after puncture and was compared with control rats of the same age. Key findings Histological examination and Safranin-O staining revealed progressive degeneration of the punctured disc. Matrix metalloproteinase 13 (MMP13) was increased at 1 week after puncture but did not change in the control group. The interleukin-1 beta (IL-1β) mRNA expression level was elevated at the acute stage after puncture compared with the control group. The hypoxia inducible factor 2 (HIF-2) increased expression in punctured groups. Additionally, compare to adjacent non-punctured segments, HIF-2α expression level transiently increased and then decreased in the nucleus pulposus immediately following puncture, and it then increased 12 weeks after puncture. Significance The degenerative changes observed in this rat-tail puncture model are similar to human disc degeneration and that this model may be valuable for elucidating the molecular mechanisms and pathways underlying disc degeneration.",
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author = "Chen, {Chia Hsian} and Chiang, {Chang Jung} and Wu, {Lien Chen} and Yang, {Chih Hong} and Kuo, {Yi Jie} and Tsuang, {Yang Hwei} and Tsai, {Tung Hu}",
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AU - Chiang, Chang Jung

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AU - Yang, Chih Hong

AU - Kuo, Yi Jie

AU - Tsuang, Yang Hwei

AU - Tsai, Tung Hu

PY - 2016/7/1

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N2 - Aims Intervertebral disc (IVD) degeneration was believed to contribute to lower back pain. The aim of the study was to investigate the pathogenesis and regulatory mechanism of puncture-induced IVD degeneration. Main methods We established a rat-tail puncture model using Kirschner wire and a homemade stopper. The progress of disc degeneration was evaluated by histological examination and the quantitative measurement of type I, type II collagen and other factors expression at 0.5, 1, 2, 6, and 12 weeks after puncture and was compared with control rats of the same age. Key findings Histological examination and Safranin-O staining revealed progressive degeneration of the punctured disc. Matrix metalloproteinase 13 (MMP13) was increased at 1 week after puncture but did not change in the control group. The interleukin-1 beta (IL-1β) mRNA expression level was elevated at the acute stage after puncture compared with the control group. The hypoxia inducible factor 2 (HIF-2) increased expression in punctured groups. Additionally, compare to adjacent non-punctured segments, HIF-2α expression level transiently increased and then decreased in the nucleus pulposus immediately following puncture, and it then increased 12 weeks after puncture. Significance The degenerative changes observed in this rat-tail puncture model are similar to human disc degeneration and that this model may be valuable for elucidating the molecular mechanisms and pathways underlying disc degeneration.

AB - Aims Intervertebral disc (IVD) degeneration was believed to contribute to lower back pain. The aim of the study was to investigate the pathogenesis and regulatory mechanism of puncture-induced IVD degeneration. Main methods We established a rat-tail puncture model using Kirschner wire and a homemade stopper. The progress of disc degeneration was evaluated by histological examination and the quantitative measurement of type I, type II collagen and other factors expression at 0.5, 1, 2, 6, and 12 weeks after puncture and was compared with control rats of the same age. Key findings Histological examination and Safranin-O staining revealed progressive degeneration of the punctured disc. Matrix metalloproteinase 13 (MMP13) was increased at 1 week after puncture but did not change in the control group. The interleukin-1 beta (IL-1β) mRNA expression level was elevated at the acute stage after puncture compared with the control group. The hypoxia inducible factor 2 (HIF-2) increased expression in punctured groups. Additionally, compare to adjacent non-punctured segments, HIF-2α expression level transiently increased and then decreased in the nucleus pulposus immediately following puncture, and it then increased 12 weeks after puncture. Significance The degenerative changes observed in this rat-tail puncture model are similar to human disc degeneration and that this model may be valuable for elucidating the molecular mechanisms and pathways underlying disc degeneration.

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