Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells’ Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 Pathway
Dexmedetomidine (DEX), which is reported to be a newly discovered, novel α-2 adrenoceptor agonist, is known to exhibit anti-inflammatory properties in several diseases. DEX regulates inflammation-related signaling pathways and genes through interactions with several miRNAs. This study verified that...
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| Format: | Article |
| Language: | English |
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Wiley
2022-01-01
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| Series: | Canadian Respiratory Journal |
| Online Access: | http://dx.doi.org/10.1155/2022/8433960 |
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| author | Xianfeng Chen Juntao Hu Jie Lai Zhiyong Zhang Zhanhong Tang |
| author_facet | Xianfeng Chen Juntao Hu Jie Lai Zhiyong Zhang Zhanhong Tang |
| author_sort | Xianfeng Chen |
| collection | DOAJ |
| description | Dexmedetomidine (DEX), which is reported to be a newly discovered, novel α-2 adrenoceptor agonist, is known to exhibit anti-inflammatory properties in several diseases. DEX regulates inflammation-related signaling pathways and genes through interactions with several miRNAs. This study verified that expression levels of miR-140-3p were diminished when alveolar type II cells were exposed to LPS. However, the levels of miR-140-3p were confirmed as showing an increase with DEX treatment. These observations revealed that the expression of miR-140-3p was related to the beneficial effects that accompanied the DEX treatment of LPS-induced ALI. In addition, PD-1/PD-L1 expression increased extensively when RLE-6TN cells were induced by LPS. The increased expression was reduced after treatment with DEX. Thus, it appears that the PD-L1 expression was targeted directly by miR-140-3p, resulting in the partial repression of PD-L1 levels, which involved the inhibition of p-JNK and Bnip3 expression. Therefore, DEX was shown to inhibit the PD-L1 expression by promoting partially increased miR-140-3p levels in RLE-6TN cells. DEX also inactivated the JNK-Bnip3 pathway, resulting in the inhibition of inflammation and alleviating alveolar type II cell injury. |
| format | Article |
| id | doaj-art-94eb99bdf2e04e5d9a049451be2d7be5 |
| institution | DOAJ |
| issn | 1916-7245 |
| language | English |
| publishDate | 2022-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Canadian Respiratory Journal |
| spelling | doaj-art-94eb99bdf2e04e5d9a049451be2d7be52025-08-20T03:19:47ZengWileyCanadian Respiratory Journal1916-72452022-01-01202210.1155/2022/8433960Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells’ Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 PathwayXianfeng Chen0Juntao Hu1Jie Lai2Zhiyong Zhang3Zhanhong Tang4Department of Intensive Care UnitDepartment of Intensive Care UnitDepartment of Intensive Care UnitDepartment of Intensive Care UnitDepartment of Intensive Care UnitDexmedetomidine (DEX), which is reported to be a newly discovered, novel α-2 adrenoceptor agonist, is known to exhibit anti-inflammatory properties in several diseases. DEX regulates inflammation-related signaling pathways and genes through interactions with several miRNAs. This study verified that expression levels of miR-140-3p were diminished when alveolar type II cells were exposed to LPS. However, the levels of miR-140-3p were confirmed as showing an increase with DEX treatment. These observations revealed that the expression of miR-140-3p was related to the beneficial effects that accompanied the DEX treatment of LPS-induced ALI. In addition, PD-1/PD-L1 expression increased extensively when RLE-6TN cells were induced by LPS. The increased expression was reduced after treatment with DEX. Thus, it appears that the PD-L1 expression was targeted directly by miR-140-3p, resulting in the partial repression of PD-L1 levels, which involved the inhibition of p-JNK and Bnip3 expression. Therefore, DEX was shown to inhibit the PD-L1 expression by promoting partially increased miR-140-3p levels in RLE-6TN cells. DEX also inactivated the JNK-Bnip3 pathway, resulting in the inhibition of inflammation and alleviating alveolar type II cell injury.http://dx.doi.org/10.1155/2022/8433960 |
| spellingShingle | Xianfeng Chen Juntao Hu Jie Lai Zhiyong Zhang Zhanhong Tang Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells’ Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 Pathway Canadian Respiratory Journal |
| title | Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells’ Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 Pathway |
| title_full | Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells’ Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 Pathway |
| title_fullStr | Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells’ Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 Pathway |
| title_full_unstemmed | Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells’ Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 Pathway |
| title_short | Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells’ Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 Pathway |
| title_sort | dexmedetomidine attenuates lps stimulated alveolar type ii cells injury through upregulation of mir 140 3p and partial suppression of pd l1 involving inactivating jnk bnip3 pathway |
| url | http://dx.doi.org/10.1155/2022/8433960 |
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