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Erschienen in: Clinical Rheumatology 11/2019

01.08.2019 | Original Article

LncRNA GAS5 overexpression downregulates IL-18 and induces the apoptosis of fibroblast-like synoviocytes

verfasst von: Cuili Ma, Weigang Wang, Ping Li

Erschienen in: Clinical Rheumatology | Ausgabe 11/2019

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Abstract

Background

Long non-coding RNA (lncRNA) growth arrest specific transcript 5 (GAS5) negatively regulates interleukin-18 (IL-18) in ovarian cancer, while IL-18 contributes to the development of rheumatoid arthritis (RA). Therefore, GAS5 may also participate in RA.

Methods

GAS5 and IL-18 in plasma of RA patients (n = 60) and healthy controls (n = 60) were measured by RT-qPCR and ELISA, respectively. Linear regression was performed to analyze the correlations between plasma levels of IL-18 and GAS5 in both RA patients and healthy controls.

Results

In the present study, we found that plasma GAS5 was downregulated, while IL-18 was upregulated in RA patients than in healthy controls. A significant and inverse correlation between GAS5 and IL-18 was found in RA patients but not in healthy controls. IL-18 treatment did not significantly alter the expression of GAS5 in fibroblast-like synoviocytes, while GAS5 overexpression led to the inhibited expression of IL-18. GAS5 overexpression also resulted in the promoted apoptosis of fibroblast-like synoviocytes.

Conclusions

Therefore, GAS5 overexpression may improve RA by downregulating IL-18 and inducing the apoptosis of fibroblast-like synoviocytes.
Key points
The present study mainly showed that overexpression of GAS5 may assist the treatment of RA.
The mechanism of GAS5 for the treatment of RA involves the downregulating inflammatory IL-18 and mediating the apoptosis of fibroblast-like synoviocytes.
GAS5 and IL-8 were correlated in RA patients but not in healthy controls.
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Metadaten
Titel
LncRNA GAS5 overexpression downregulates IL-18 and induces the apoptosis of fibroblast-like synoviocytes
verfasst von
Cuili Ma
Weigang Wang
Ping Li
Publikationsdatum
01.08.2019
Verlag
Springer London
Erschienen in
Clinical Rheumatology / Ausgabe 11/2019
Print ISSN: 0770-3198
Elektronische ISSN: 1434-9949
DOI
https://doi.org/10.1007/s10067-019-04691-2

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