Cigarette smoke extract combined with LPS reduces ABCA3 expression in chronic pulmonary inflammation may be related to PPARγ/ P38 MAPK signaling pathway
ABCA3 (ATP-binding cassette class A3) is a transmembrane transporter that plays a positive role in chronic pulmonary inflammation by regulating lipid metabolism. However, it is not completely clear whether ABCA3 and its signaling factors are involved in chronic pulmonary inflammation induced by the...
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2022-10-01
|
| Series: | Ecotoxicology and Environmental Safety |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651322009265 |
| _version_ | 1798000586642161664 |
|---|---|
| author | Shuyi Zhang Xianwang Lu Xin Fang Zihao Wang Shihao Cheng Jue Song |
| author_facet | Shuyi Zhang Xianwang Lu Xin Fang Zihao Wang Shihao Cheng Jue Song |
| author_sort | Shuyi Zhang |
| collection | DOAJ |
| description | ABCA3 (ATP-binding cassette class A3) is a transmembrane transporter that plays a positive role in chronic pulmonary inflammation by regulating lipid metabolism. However, it is not completely clear whether ABCA3 and its signaling factors are involved in chronic pulmonary inflammation induced by the combination of CSE (cigarette smoke extract) and LPS (lipopolysaccharide). In this study, we used the method of combining CSE and LPS which was widely used to study lung inflammation-related diseases and has been proven effective in our group's studies to create in vivo and in vitro pulmonary inflammation models. The result showed that, after CSE in combination with LPS treatment, ABCA3 expression was downregulated in rat lung in vivo and in a human alveolar cell line in vitro. ABCA3 expression was upregulated, and related inflammatory factors were downregulated in the state of overexpression of PPARγ or inhibition of the p38 MAPK pathway, while PPARγ deletion or MAPK14 overexpression showed the opposite results. The level of PPARγ remained unchanged, and the expression of ABCA3 was upregulated in the state of the p38 MAPK pathway was inhibited under overexpression of PPARγ. These results indicate that CSE combined with LPS can result in downregulation of ABCA3 under conditions of inflammation, and that the p38 MAPK signaling pathway mediated by PPARγ can regulate the expression changes of ABCA3, thus providing new targets for treating chronic pulmonary inflammation. |
| first_indexed | 2024-04-11T11:22:42Z |
| format | Article |
| id | doaj.art-6b103e1270d44e1ea755792135634a1a |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-04-11T11:22:42Z |
| publishDate | 2022-10-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-6b103e1270d44e1ea755792135634a1a2022-12-22T04:26:35ZengElsevierEcotoxicology and Environmental Safety0147-65132022-10-01244114086Cigarette smoke extract combined with LPS reduces ABCA3 expression in chronic pulmonary inflammation may be related to PPARγ/ P38 MAPK signaling pathwayShuyi Zhang0Xianwang Lu1Xin Fang2Zihao Wang3Shihao Cheng4Jue Song5Institute for Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei 230032, China; Institute for the Key Laboratory of Anti-inflammatory and Immune Medicines, Ministry of Education, 230032, Hefei, ChinaInstitute for Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei 230032, China; Institute for the Key Laboratory of Anti-inflammatory and Immune Medicines, Ministry of Education, 230032, Hefei, ChinaInstitute for Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei 230032, China; Institute for the Key Laboratory of Anti-inflammatory and Immune Medicines, Ministry of Education, 230032, Hefei, ChinaInstitute for Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei 230032, China; Institute for the Key Laboratory of Anti-inflammatory and Immune Medicines, Ministry of Education, 230032, Hefei, ChinaInstitute for Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei 230032, China; Institute for the Key Laboratory of Anti-inflammatory and Immune Medicines, Ministry of Education, 230032, Hefei, ChinaInstitute for Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei 230032, China; Institute for the Key Laboratory of Anti-inflammatory and Immune Medicines, Ministry of Education, 230032, Hefei, China; Correspondence to: School of Pharmacy, Anhui Medical University, Hefei 230032, China.ABCA3 (ATP-binding cassette class A3) is a transmembrane transporter that plays a positive role in chronic pulmonary inflammation by regulating lipid metabolism. However, it is not completely clear whether ABCA3 and its signaling factors are involved in chronic pulmonary inflammation induced by the combination of CSE (cigarette smoke extract) and LPS (lipopolysaccharide). In this study, we used the method of combining CSE and LPS which was widely used to study lung inflammation-related diseases and has been proven effective in our group's studies to create in vivo and in vitro pulmonary inflammation models. The result showed that, after CSE in combination with LPS treatment, ABCA3 expression was downregulated in rat lung in vivo and in a human alveolar cell line in vitro. ABCA3 expression was upregulated, and related inflammatory factors were downregulated in the state of overexpression of PPARγ or inhibition of the p38 MAPK pathway, while PPARγ deletion or MAPK14 overexpression showed the opposite results. The level of PPARγ remained unchanged, and the expression of ABCA3 was upregulated in the state of the p38 MAPK pathway was inhibited under overexpression of PPARγ. These results indicate that CSE combined with LPS can result in downregulation of ABCA3 under conditions of inflammation, and that the p38 MAPK signaling pathway mediated by PPARγ can regulate the expression changes of ABCA3, thus providing new targets for treating chronic pulmonary inflammation.http://www.sciencedirect.com/science/article/pii/S0147651322009265Chronic pulmonary inflammationCigarette smoke extractLipid metabolismABCA3P38 MAPKPPARγ |
| spellingShingle | Shuyi Zhang Xianwang Lu Xin Fang Zihao Wang Shihao Cheng Jue Song Cigarette smoke extract combined with LPS reduces ABCA3 expression in chronic pulmonary inflammation may be related to PPARγ/ P38 MAPK signaling pathway Ecotoxicology and Environmental Safety Chronic pulmonary inflammation Cigarette smoke extract Lipid metabolism ABCA3 P38 MAPK PPARγ |
| title | Cigarette smoke extract combined with LPS reduces ABCA3 expression in chronic pulmonary inflammation may be related to PPARγ/ P38 MAPK signaling pathway |
| title_full | Cigarette smoke extract combined with LPS reduces ABCA3 expression in chronic pulmonary inflammation may be related to PPARγ/ P38 MAPK signaling pathway |
| title_fullStr | Cigarette smoke extract combined with LPS reduces ABCA3 expression in chronic pulmonary inflammation may be related to PPARγ/ P38 MAPK signaling pathway |
| title_full_unstemmed | Cigarette smoke extract combined with LPS reduces ABCA3 expression in chronic pulmonary inflammation may be related to PPARγ/ P38 MAPK signaling pathway |
| title_short | Cigarette smoke extract combined with LPS reduces ABCA3 expression in chronic pulmonary inflammation may be related to PPARγ/ P38 MAPK signaling pathway |
| title_sort | cigarette smoke extract combined with lps reduces abca3 expression in chronic pulmonary inflammation may be related to pparγ p38 mapk signaling pathway |
| topic | Chronic pulmonary inflammation Cigarette smoke extract Lipid metabolism ABCA3 P38 MAPK PPARγ |
| url | http://www.sciencedirect.com/science/article/pii/S0147651322009265 |
| work_keys_str_mv | AT shuyizhang cigarettesmokeextractcombinedwithlpsreducesabca3expressioninchronicpulmonaryinflammationmayberelatedtoppargp38mapksignalingpathway AT xianwanglu cigarettesmokeextractcombinedwithlpsreducesabca3expressioninchronicpulmonaryinflammationmayberelatedtoppargp38mapksignalingpathway AT xinfang cigarettesmokeextractcombinedwithlpsreducesabca3expressioninchronicpulmonaryinflammationmayberelatedtoppargp38mapksignalingpathway AT zihaowang cigarettesmokeextractcombinedwithlpsreducesabca3expressioninchronicpulmonaryinflammationmayberelatedtoppargp38mapksignalingpathway AT shihaocheng cigarettesmokeextractcombinedwithlpsreducesabca3expressioninchronicpulmonaryinflammationmayberelatedtoppargp38mapksignalingpathway AT juesong cigarettesmokeextractcombinedwithlpsreducesabca3expressioninchronicpulmonaryinflammationmayberelatedtoppargp38mapksignalingpathway |