Intervertebral disc and endplate cells response to IL-1β inflammatory cell priming and identification of molecular targets of tissue degeneration Article Swipe
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· 2020
· Open Access
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· DOI: https://doi.org/10.22203/ecm.v039a15
Inflammation represents an important factor leading to metabolic imbalance within the intervertebral disc (IVD), conducive to degenerative changes. Therefore, a thorough knowledge of the IVD and endplate (EP) cell behaviour in such pathological environments is essential when designing regenerative therapeutic strategies. The present study aimed at assessing the molecular response of the IVD constitutive nucleus pulposus (NPCs)-, annulus fibrosus (AFCs)- and endplate (EPCs)-derived cells to interleukin (IL)-1β treatment, through large-scale, high-throughput microarray and protein analysis, identifying the differentially expressed genes and released proteins. Overall, the inflammatory stimulus downregulated stemness genes while upregulating pro-inflammatory, pro-angiogenic and catabolic genes, including matrix metalloproteases, which were not balanced by a concomitant upregulation of their inhibitors. Upregulation of anti-inflammatory and anabolic tumour necrosis factor inducible gene 6 protein (TNFAIP6), of IL-1 receptor antagonist (IL-1Ra) (at gene and protein levels) and of trophic insulin-like growth factor 1 (IGF1) was also observed in all cell types; IGF1 particularly in AFCs. An overall inhibitory effect of tumour necrosis factor alpha (TNFα) signal was observed in all cell types; however, EPCs showed the strongest anti-inflammatory behaviour. AFCs and EPCs shared the ability to limit the activation of the signalling mediated by specific chemokines. AFCs showed a slightly senescent attitude, with a downregulation of genes related to DNA repair or pro-mitosis. Results allowed for the identification of specific molecular targets in IVD and EP cells that respond to an inflammatory environment. Such targets can be either silenced (when pathological targets) or stimulated to counteract the inflammation.
Related Topics
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.22203/ecm.v039a15
- https://doi.org/10.22203/ecm.v039a15
- OA Status
- gold
- Cited By
- 21
- References
- 73
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W3031926748
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W3031926748Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.22203/ecm.v039a15Digital Object Identifier
- Title
-
Intervertebral disc and endplate cells response to IL-1β inflammatory cell priming and identification of molecular targets of tissue degenerationWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2020Year of publication
- Publication date
-
2020-06-02Full publication date if available
- Authors
-
Paola De Luca, Laura de Girolamo, Dimitrios Kouroupis, Mauro Castagnetta, Carlotta Perucca Orfei, Domenico Coviello, Simona Coco, Diego Correa, Marco Brayda‐Bruno, Alessandra ColombiniList of authors in order
- Landing page
-
https://doi.org/10.22203/ecm.v039a15Publisher landing page
- PDF URL
-
https://doi.org/10.22203/ecm.v039a15Direct link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://doi.org/10.22203/ecm.v039a15Direct OA link when available
- Concepts
-
Downregulation and upregulation, Cell biology, Biology, Tumor necrosis factor alpha, Inflammation, Intervertebral disc, Aggrecan, ADAMTS, Cancer research, Immunology, Gene, Medicine, Pathology, Matrix metalloproteinase, Genetics, Osteoarthritis, Metalloproteinase, Anatomy, Thrombospondin, Alternative medicine, Articular cartilageTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
21Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 4, 2024: 4, 2023: 2, 2022: 7, 2021: 4Per-year citation counts (last 5 years)
- References (count)
-
73Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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