Influences of Nutrition Supply and Pathways on the Degenerative Patterns in Human Intervertebral Disc

Zhu, Qiaoqiao; Gao, Xin; Levene, Howard; Brown, Mark D.; Gu, Weiyong

doi:10.1097/brs.0000000000001292

Cited by 45 publications

(37 citation statements)

References 39 publications

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“…Above and below intervertebral discs, a layer of hydrated biological tissue exists, called the cartilaginous endplate (CEP). Since nucleus pulposus and annulus fibrosus tissues do not have their own vascular supply, the CEP is the main nutritional supply route for intervertebral discs . Loss of nutrient supply may lead to increased cell death, matrix degradation as well as decreased matrix production in intervertebral discs, which further lead to disc degeneration .…”

Section: Introductionmentioning

confidence: 99%

“…Since nucleus pulposus and annulus fibrosus tissues do not have their own vascular supply, the CEP is the main nutritional supply route for intervertebral discs . Loss of nutrient supply may lead to increased cell death, matrix degradation as well as decreased matrix production in intervertebral discs, which further lead to disc degeneration . Therefore, CEP dysfunction, which may block the nutritional supply for disc tissues, is believed to play a vital role in IDD pathogenesis .…”

Section: Introductionmentioning

confidence: 99%

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Melatonin protects vertebral endplate chondrocytes against apoptosis and calcification via the Sirt1‐autophagy pathway

Zhang

Lin

Tian

et al. 2018

J Cellular Molecular Medi

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Melatonin is reportedly associated with intervertebral disc degeneration (IDD). Endplate cartilage is vitally important to intervertebral discs in physiological and pathological conditions. However, the effects and mechanism of melatonin on endplate chondrocytes (EPCs) are still unclear. Herein, we studied the effects of melatonin on EPC apoptosis and calcification and elucidated the underlying mechanism. Our study revealed that melatonin treatment decreases the incidence of apoptosis and inhibits EPC calcification in a dose‐dependent manner. We also found that melatonin upregulates Sirt1 expression and activity and promotes autophagy in EPCs. Autophagy inhibition by 3‐methyladenine reversed the protective effect of melatonin on apoptosis and calcification, while the Sirt1 inhibitor EX‐527 suppressed melatonin‐induced autophagy and the protective effects of melatonin against apoptosis and calcification, indicating that the beneficial effects of melatonin in EPCs are mediated through the Sirt1‐autophagy pathway. Furthermore, melatonin may ameliorate IDD in vivo in rats. Collectively, this study revealed that melatonin reduces EPC apoptosis and calcification and that the underlying mechanism may be related to Sirt1‐autophagy pathway regulation, which may help us better understand the association between melatonin and IDD.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Melatonin protects vertebral endplate chondrocytes against apoptosis and calcification via the Sirt1‐autophagy pathway

Zhang

Lin

Tian

et al. 2018

J Cellular Molecular Medi

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“…It seems that the appearance of the bright spot in the posterior region (Fig. 2b) may be related to the nutrition level in this particular region, 33 where the change in relative tissue volume (i.e., dilation) is found to be small (data not shown) and there is no cell death for the nutrition boundary condition in the case of mildly degenerated disc. This may be partially attributed to the relatively short diffusion distance between this region and nutrition supply source at the disc edge.…”

Section: Discussionmentioning

confidence: 94%

Simulation of water content distributions in degenerated human intervertebral discs

Zhu

Gao

Brown

et al. 2016

Journal Orthopaedic Research

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The objective of this study was to investigate the spatial and temporal variations of water content in intervertebral discs during degeneration and repair processes. We hypothesized that the patterns of water content distribution in the discs are related to the intensity patterns observed in T2-weighted MRI images. Water content distributions in the mildly (e.g., 80% viable cells in the disc, 2.3% decrease in disc height) and moderately (e.g., 40% viable cells in the disc, 9.3% decrease in disc height) degenerated discs were predicted using a finite element model. The variation of water content in the degenerated discs treated with three biological therapies [i.e., increasing the cell density in the NP (Case I), increasing glycosaminoglycan synthesis rate in the nucleus pulposus (Case II), and decreasing glycosaminoglycan degradation rate in the nucleus pulposus (Case III)] were also predicted. It was found that two patterns of water content distributions, a horizontal region with lower water content at the mid-axial plane of nucleus pulposus and a spot with higher water content at the posterior region, were shown during the degeneration progress for the disc simulated in this study. These two patterns disappeared after treatment in Case I, but in Case II and Case III. The implication of these patterns for the horizontal gray band and high intensity zone in T2-weighted MRI images was discussed. This study provided new guidance to develop a novel method for diagnosing disc degeneration and assessing outcomes of biological therapies with MRI techniques.

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“…Intervertebral discs consist of cartilage endplate and nucleus pulposus (NP) and annulus fibrosus (AF) cells. Cartilage endplates are required for stress distribution and nutrient transport to the intervertebral discs (2,3). It has been reported that degeneration of the endplates may result in IDD (4,5).…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA MALAT1 promotes high glucose‑induced rat cartilage endplate cell apoptosis via the p38/MAPK signalling pathway

Jiang

Zeng

et al. 2020

Mol Med Report

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diabetes mellitus (dM) contributes to intervertebral disc degeneration (idd). The long non-coding rna MalaT1 has been revealed to play an important role in diabetes-associated complications. However, the specific role of MALAT1 in diabetes-associated idd has not been determined. The aim of the present study was to evaluate the roles of MALAT1 in the apoptosis of cartilage endplate (CEP) cells induced by high glucose and to explore the mechanisms underlying this effect. rat ceP cells were cultured in high-glucose medium (25 mM glucose) for 24 or 72 h. Cells cultured in medium containing 5 mM glucose were used as a control. Flow cytometry was used to detect the degree of apoptosis. Reverse transcription-quantitative PCR was used to measure the expression of MALAT1 mRNA. In addition, CEP cells were treated with different conditions (high glucose, high glucose + MalaT1 negative control, high glucose + MALAT1 RNAi, normal control) for 72 h. Flow cytometry was subsequently used to detect apoptosis and western blotting was used to measure the expression levels of total and phosphorylated p38. The results revealed that high glucose concentration promoted apoptosis and enhanced expression of MALAT1 in CEP cells. Furthermore, MALAT1 knockout decreased the expression levels of total and phosphorylated p38 and reduced the apoptosis of rat CEP cells. The results obtained in the present study indicated that MALAT1 may serve as an important therapeutic target for curing or delaying idd in patients with diabetes.

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Influences of Nutrition Supply and Pathways on the Degenerative Patterns in Human Intervertebral Disc

Cited by 45 publications

References 39 publications

Melatonin protects vertebral endplate chondrocytes against apoptosis and calcification via the Sirt1‐autophagy pathway

Melatonin protects vertebral endplate chondrocytes against apoptosis and calcification via the Sirt1‐autophagy pathway

Simulation of water content distributions in degenerated human intervertebral discs

Long non‑coding RNA MALAT1 promotes high glucose‑induced rat cartilage endplate cell apoptosis via the p38/MAPK signalling pathway

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