CD24 is expressed specifically in the nucleus pulposus of intervertebral discs

Fujita, Nobuyuki; Miyamoto, Takeshi; Imai, Jun; Hosogane, Naobumi; Suzuki, T.; Yagi, Mitsuru; Morita, Kozo; Ninomiya, Ken; Miyamoto, Kana; Takaishi, Hironari; Matsumoto, Morio; Morioka, Hideo; Yabe, Hiroo; Chiba, Kazuhiro; Watanabe, Shinya; Toyama, Yoshiaki; Suda, Toshio

doi:10.1016/j.bbrc.2005.10.166

Cited by 132 publications

(136 citation statements)

References 14 publications

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“…A variety of animal models including bovine, canine, rabbit, rat, and mouse have been used to study IVD degeneration or regeneration in place of human samples [28][29][30]. In vitro studies that identify potential catabolic mechanisms involved in deserve consideration when formulating a clinical solution to degenerative disc disease.…”

Section: Discussionmentioning

confidence: 99%

Nerve growth factor increases MMP9 activity in annulus fibrosus cells by upregulating lipocalin 2 expression

et al. 2014

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Purpose Nerve growth factor (NGF) expression and activity is important in chronic lower back pain but may also act as a pro-catabolic factor in the pathogenesis of intervertebral disc (IVD) degeneration. Lipocalin 2 (Lcn2) expression in IVD was upregulated by NGF stimulation in our previous study. The current study was undertaken to identify potential mechanisms of the latter effect including potential interactions between Lcn2 and matrix metalloproteinase 9 (MMP9). Methods Rat annulus fibrosus (AF) cells were stimulated by NGF and subjected to microarray analysis, subsequent real-time PCR, western immunoblotting, and immunofluorescence. Cells were treated with NGF in the absence or presence of the NGF inhibitor Ro 08-2750. Zymography and functional MMP9 assays were used to determine MMP9 activity, whilst the dimethyl-methylene blue assay was used to quantify the release of glycosaminoglycans (GAGs) reflecting catabolic effects following NGF treatment. Immunoprecipitation with immunoblotting was used to identify interactions between MMP9 and Lcn2. Results Increased expression of Lcn2 gene and protein following NGF stimulation was confirmed by microarray analysis, real-time PCR, western blot and immunofluorescence. Zymography showed that NGF enhanced 125-kDa gelatinase activity, identified as a Lcn2/MMP9 complex by immunoprecipitation and immunoblotting. Functional assays showed increased MMP9 activity and GAG release in the presence of NGF. The effects of NGF were neutralized by the presence of Ro 08-2750. Conclusions NGF upregulates Lcn2 expression and increases MMP9 activity in AF cells; processes which are likely to potentiate degeneration of AF tissue in vivo. Anti-NGF treatment may have benefit for management of pain Electronic supplementary material The online version of this article

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Section: Discussionmentioning

confidence: 99%

Nerve growth factor increases MMP9 activity in annulus fibrosus cells by upregulating lipocalin 2 expression

et al. 2014

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“…Although different markers have been suggested for NP cells in the last few years, no ideal single marker has been identified so far, thus leading to the conclusion that the expression of a set of genes needs to be analyzed, such as HIF-1 (hypoxia induced factor) (Rajpurohit et al, 2002), GLUT-1 (glucose transporter) (Rajpurohit et al, 2002), MMP2 (matrix metalloproteinase 2) (Rajpurohit et al, 2002), CD24 (glycosylphosphat-idylinositol-anchored cell surface protein) (Fujita et al, 2005) and Sox9 (Paul et al, 2003). Both HIF-1 and GLUT-1 are related to the NP metabolic activity.…”

Section: Discussionmentioning

confidence: 99%

“…RNA concentrations were assessed spectrophotometrically (UV-visible spectrophotometer, Cary 50 Scan, Varian) at 260nm. 400ng of total RNA was reverse transcribed (Superscript TM II, Invitrogen) and analyzed by Reverse Transcriptase-PCR (RT-PCR) (Hotstar Taq DNA polymerase; Qiagen, Hilden, Germany) using genespecific primers (Table 1) for collagen 1 (Col1α1), collagen II (Col2α1), aggrecan and transcription factor Sox9 , hypoxia inducible factor-1 (HIF) 1α isoform (Gao et al, 2005), metalloproteinase-2 (MMP2) (Shan et al, 2005), glycosylphosphatidylinositol-anchored cell surface protein CD24 (Fujita et al, 2005), glucose transporter (GLUT-1) (Robey et al, 2005), and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as a housekeeping gene (Sanchez et al, 2005). The PCR fragments were resolved on a 1.5% agarose gel and stained with ethidium bromide.…”

Section: Gene Expression Analysismentioning

confidence: 99%

Cell-seeded polyurethane-fibrin structures – A possible system for intervertebral disc regeneration

Mauth

Bono²,

Haas³

et al. 2009

eCM

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Nowadays, intervertebral disc (IVD) degeneration is one of the principal causes of low back pain involving high expense within the health care system. The long-term goal is the development of a medical treatment modality focused on a more biological regeneration of the inner nucleus pulposus (NP). Hence, interest in the endoscopic implantation of an injectable material took center stage in the recent past. We report on the development of a novel polyurethane (PU) scaffold as a mechanically stable carrier system for the reimplantation of expanded autologous IVDderived cells (disc cells) to stimulate regenerative processes and restore the chondrocyte-like tissue within the NP. Primary human disc cells were seeded into newly developed PU spheroids which were subsequently encapsulated in fibrin hydrogel. The study aims to analyze adhesion properties, proliferation capacity and phenotypic characterization of these cells. Polymerase chain reaction was carried out to detect the expression of genes specifically expressed by native IVD cells. Biochemical analyses showed an increased DNA content, and a progressive enhancement of total collagen and glycosaminoglycans (GAG) was observed during cell culture. The results suggest the synthesis of an appropriate extracellular matrix as well as a stable mRNA expression of chondrogenic and/or NP specific markers. In conclusion, the data presented indicate an alternative medical approach to current treatment options of degenerated IVD tissue.

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“…Currently, there are no definitive cellular biomarkers which can be used to define a normal AF or NP cell to differentiate these from one another or from an articular chondrocyte. Micro-array and RT-PCR approaches have been used to determine which disc cell markers are most appropriate as phenotypic markers in rat IVDs [28,67]. In an initial study, CD-24 was suggested as an NP cell marker [28].…”

Section: Integration Of Engineered Annular Constructs In Repair Envirmentioning

confidence: 99%

Recent advances in annular pathobiology provide insights into rim-lesion mediated intervertebral disc degeneration and potential new approaches to annular repair strategies

et al. 2008

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The objective of this study was to assess the impact of a landmark annular lesion model on our understanding of the etiopathogenesis of IVD degeneration and to appraise current IVD repairative strategies. A number of studies have utilised the Osti sheep model since its development in 1990. The experimental questions posed at that time are covered in this review, as are significant recent advances in annular repair strategies. The ovine model has provided important spatial and temporal insights into the longitudinal development of annular lesions and how they impact on other discal and paradiscal components such as the NP, cartilaginous end plates, zygapophyseal joints and vertebral bone and blood vessels. Important recent advances have been made in biomatrix design for IVD repair and in the oriented and dynamic culture of annular fibrochondrocytes into planar, spatially relevant, annular type structures.

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CD24 is expressed specifically in the nucleus pulposus of intervertebral discs

Cited by 132 publications

References 14 publications

Nerve growth factor increases MMP9 activity in annulus fibrosus cells by upregulating lipocalin 2 expression

Nerve growth factor increases MMP9 activity in annulus fibrosus cells by upregulating lipocalin 2 expression

Cell-seeded polyurethane-fibrin structures – A possible system for intervertebral disc regeneration

Recent advances in annular pathobiology provide insights into rim-lesion mediated intervertebral disc degeneration and potential new approaches to annular repair strategies

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