Photodermatology, photoimmunology & photomedicine · 2021
Up-regulation of hsa-miR-221-3p induced by UVB affects proliferation and apoptosis of keratinocytes via Bcl-xL/Bax pathway.
СтатьяНазвание и аннотация: Перевод в очереди
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Tu Yunhua, Wu Wenjuan, Guo Yanni, Lu Fengyan, Li Xing, Xu Dan, Zou Dandan, Tu Ying, Chai Yanjie, He Li
Аннотация
BACKGROUND: Chronic actinic dermatitis (CAD) is a photoallergic skin disease with abnormal hyperplasia. At present, the mechanism of abnormal proliferation is not clear.
OBJECTIVE: To explore possible mechanism of CAD proliferative lesions.
METHODS: Immunohistochemistry (IHC) assay and small RNA sequencing were carried out. Quantitative real-time PCR (qRT-PCR) analysis was performed to evaluate expression levels of hsa-miR-221-3p and FOS. The interaction between hsa-miR-221-3p and FOS was identified by dual-luciferase reporter assay. Expression of hsa-miR-221-3p also was detected by qRT-PCR after UVB irradiation. Influences of hsa-miR-221-3p and FOS on cell viability and apoptosis were assessed through a series of functional experiments and rescue experiments. Western blot analysis was used to detect protein expression of fos, Bax, Bcl-xL, and caspase-3.
RESULTS: Patients with CAD had marked epidermal hyperplasia. The expression of hsa-miR-221-3p was up-regulated in CAD while FOS was significantly down-regulated. Dual-luciferase reporter assay confirmed that hsa-miR-221-3p targeted FOS 3'UTR. Hsa-miR-221-3p induced by UVB ranged from 0 to 30 mJ. Moreover, hsa-miR-221-3p overexpression or FOS knockdown promoted cell proliferation and reduced cell apoptosis. Western blot showed that hsa-miR-221-3p negatively regulated fos, which regulated Bcl-xL/Bax. Cell proliferation caused by hsa-miR-221-3p overexpression or FOS knockdown could be reversed by Bcl-xL inhibitor.
CONCLUSION: Hsa-miR-221-3p induced by UVB targeted FOS 3'UTR, which played an important role in regulating proliferation and apoptosis of keratinocytes via Bcl-xL/Bax pathway; this may provide a new insight for CAD proliferative lesions.
OBJECTIVE: To explore possible mechanism of CAD proliferative lesions.
METHODS: Immunohistochemistry (IHC) assay and small RNA sequencing were carried out. Quantitative real-time PCR (qRT-PCR) analysis was performed to evaluate expression levels of hsa-miR-221-3p and FOS. The interaction between hsa-miR-221-3p and FOS was identified by dual-luciferase reporter assay. Expression of hsa-miR-221-3p also was detected by qRT-PCR after UVB irradiation. Influences of hsa-miR-221-3p and FOS on cell viability and apoptosis were assessed through a series of functional experiments and rescue experiments. Western blot analysis was used to detect protein expression of fos, Bax, Bcl-xL, and caspase-3.
RESULTS: Patients with CAD had marked epidermal hyperplasia. The expression of hsa-miR-221-3p was up-regulated in CAD while FOS was significantly down-regulated. Dual-luciferase reporter assay confirmed that hsa-miR-221-3p targeted FOS 3'UTR. Hsa-miR-221-3p induced by UVB ranged from 0 to 30 mJ. Moreover, hsa-miR-221-3p overexpression or FOS knockdown promoted cell proliferation and reduced cell apoptosis. Western blot showed that hsa-miR-221-3p negatively regulated fos, which regulated Bcl-xL/Bax. Cell proliferation caused by hsa-miR-221-3p overexpression or FOS knockdown could be reversed by Bcl-xL inhibitor.
CONCLUSION: Hsa-miR-221-3p induced by UVB targeted FOS 3'UTR, which played an important role in regulating proliferation and apoptosis of keratinocytes via Bcl-xL/Bax pathway; this may provide a new insight for CAD proliferative lesions.