GRβ Regulates Glucocorticoid Resistance in Sudden Sensorineural Hearing Loss
Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net..
BACKGROUND: In recent years, the incidence of sudden deafness has gradually increased, with a very limited understanding of its etiology and pathogenesis. Glucocorticoids are the first choice of the treatment, but some hormone-resistant patients are not sensitive to glucocorticoid therapy. The pathogenesis is not yet known. In this study, we aim to construct the HEI-OC1 cell line stably overexpressing Glucocorticoid Receptor Beta (GRβ), and identify its exact role in the cases of glucocorticoidresistant sudden deafness.
METHODS: We used the endotoxin lipopolysaccharide-stimulated cochlear hair cells (HEI-OC1) to investigate the relationship of inflammation factor IL-2, TNF alpha, and SRp30c with the high expression GRβ. We built a stable GRβ high expression HEI-OC1 cell line and clarified its effects on the therapeutic effect of dexamethasone. MTT assay, colony formation assay, CCK-8 assay, Western blot, and RT-qPCR were utilized for characterizations.
RESULTS: Dexamethasone reduced the LPS-induced inflammatory response from HEI-OC1 cells (p<0.05), detected by MTT assay. Dexamethasone could protect HEI-OC1 cells, but its protective effect was weakened due to the transfection of SRp30c over-expression plasmid (p<0.05). The transfection of SRp30c over-expression plasmid in HEI-OC1 cells could elevate the expressions of GRβ (p<0.05).
CONCLUSION: We clarified the mechanisms of high expression of GRβ in glucocorticoid-resistant sudden sensorineural hearing loss, and proved that the inhibition of SRp30c may act as a new treatment way of glucocorticoid-resistant sudden sensorineural hearing loss.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:22 |
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| Enthalten in: |
Current pharmaceutical biotechnology - 22(2021), 9 vom: 20., Seite 1206-1215 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Chen, Xubo [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 10.08.2021 Date Revised 10.08.2021 published: Print Citation Status MEDLINE |
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| doi: |
10.2174/1389201021666201008163534 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM316025402 |
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| 245 | 1 | 0 | |a GRβ Regulates Glucocorticoid Resistance in Sudden Sensorineural Hearing Loss |
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| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net. | ||
| 520 | |a BACKGROUND: In recent years, the incidence of sudden deafness has gradually increased, with a very limited understanding of its etiology and pathogenesis. Glucocorticoids are the first choice of the treatment, but some hormone-resistant patients are not sensitive to glucocorticoid therapy. The pathogenesis is not yet known. In this study, we aim to construct the HEI-OC1 cell line stably overexpressing Glucocorticoid Receptor Beta (GRβ), and identify its exact role in the cases of glucocorticoidresistant sudden deafness | ||
| 520 | |a METHODS: We used the endotoxin lipopolysaccharide-stimulated cochlear hair cells (HEI-OC1) to investigate the relationship of inflammation factor IL-2, TNF alpha, and SRp30c with the high expression GRβ. We built a stable GRβ high expression HEI-OC1 cell line and clarified its effects on the therapeutic effect of dexamethasone. MTT assay, colony formation assay, CCK-8 assay, Western blot, and RT-qPCR were utilized for characterizations | ||
| 520 | |a RESULTS: Dexamethasone reduced the LPS-induced inflammatory response from HEI-OC1 cells (p<0.05), detected by MTT assay. Dexamethasone could protect HEI-OC1 cells, but its protective effect was weakened due to the transfection of SRp30c over-expression plasmid (p<0.05). The transfection of SRp30c over-expression plasmid in HEI-OC1 cells could elevate the expressions of GRβ (p<0.05) | ||
| 520 | |a CONCLUSION: We clarified the mechanisms of high expression of GRβ in glucocorticoid-resistant sudden sensorineural hearing loss, and proved that the inhibition of SRp30c may act as a new treatment way of glucocorticoid-resistant sudden sensorineural hearing loss | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a GRβ | |
| 650 | 4 | |a Glucocorticoid resistance | |
| 650 | 4 | |a LPS | |
| 650 | 4 | |a SRp30c | |
| 650 | 4 | |a dexamethasone | |
| 650 | 4 | |a sudden sensorineural hearing loss | |
| 650 | 7 | |a Glucocorticoids |2 NLM | |
| 650 | 7 | |a Interleukin-2 |2 NLM | |
| 650 | 7 | |a Lipopolysaccharides |2 NLM | |
| 650 | 7 | |a Receptors, Glucocorticoid |2 NLM | |
| 650 | 7 | |a SRSF9 protein, human |2 NLM | |
| 650 | 7 | |a Tumor Necrosis Factor-alpha |2 NLM | |
| 650 | 7 | |a glucocorticoid receptor beta |2 NLM | |
| 650 | 7 | |a Serine-Arginine Splicing Factors |2 NLM | |
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| 650 | 7 | |a Dexamethasone |2 NLM | |
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| 700 | 1 | |a Zhang, Qi |e verfasserin |4 aut | |
| 700 | 1 | |a Yang, Chunping |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Yuehui |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Lihua |e verfasserin |4 aut | |
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