Contribution of Thrombospondin-1 and -2 to Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome
Thrombospondin (TSP) proteins have been shown to impact T-cell adhesion, migration, differentiation, and apoptosis. Thrombospondin-1 (TSP-1) is specifically upregulated in several inflammatory diseases and can effectively promote lipopolysaccharide- (LPS-) induced inflammation. In contrast, thrombos...
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| Format: | Article |
| Language: | English |
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Wiley
2021-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2021/8876484 |
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| author | Qiang Li Xiaoxiao Fu Jiang Yuan Shu Han |
| author_facet | Qiang Li Xiaoxiao Fu Jiang Yuan Shu Han |
| author_sort | Qiang Li |
| collection | DOAJ |
| description | Thrombospondin (TSP) proteins have been shown to impact T-cell adhesion, migration, differentiation, and apoptosis. Thrombospondin-1 (TSP-1) is specifically upregulated in several inflammatory diseases and can effectively promote lipopolysaccharide- (LPS-) induced inflammation. In contrast, thrombospondin-2 (TSP-2) has been associated with activation of “anti-inflammatory” T-regulatory cells (Tregs). In this study, we investigated the effects of both TSP-1 and TSP-2 overexpression on macrophage polarization and activation in vitro and in vivo. We analyzed the effects of TSP-1 and TSP-2 on inflammation, vascular endothelial permeability, edema, ultrastructural morphology, and apoptosis in lung tissues of an ARDS mouse model and cultured macrophages. Our results demonstrated that TSP-2 overexpression effectively attenuated LPS-induced ARDS in vivo and promoted M2 macrophage phenotype polarization in vitro. Furthermore, TSP-2 played a role in regulating pulmonary vascular barrier leakage by activating the PI3K/Akt pathway. Overall, our findings indicate that TSP-2 can modulate inflammation and could therefore be a potential therapeutic target against LPS-induced ARDS. |
| format | Article |
| id | doaj-art-071a0be4fcc8456cbc16666fa3bc1166 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-071a0be4fcc8456cbc16666fa3bc11662025-08-20T03:55:24ZengWileyMediators of Inflammation0962-93511466-18612021-01-01202110.1155/2021/88764848876484Contribution of Thrombospondin-1 and -2 to Lipopolysaccharide-Induced Acute Respiratory Distress SyndromeQiang Li0Xiaoxiao Fu1Jiang Yuan2Shu Han3The Emergency Department, The Second Affiliated Hospital Zhejiang University School of Medicine (SAHZU), Hangzhou, ChinaInstitute of Anatomy and Cell Biology, Medical College, Zhejiang University, Hangzhou, ChinaDepartment of Pulmonology, The Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, ChinaInstitute of Anatomy and Cell Biology, Medical College, Zhejiang University, Hangzhou, ChinaThrombospondin (TSP) proteins have been shown to impact T-cell adhesion, migration, differentiation, and apoptosis. Thrombospondin-1 (TSP-1) is specifically upregulated in several inflammatory diseases and can effectively promote lipopolysaccharide- (LPS-) induced inflammation. In contrast, thrombospondin-2 (TSP-2) has been associated with activation of “anti-inflammatory” T-regulatory cells (Tregs). In this study, we investigated the effects of both TSP-1 and TSP-2 overexpression on macrophage polarization and activation in vitro and in vivo. We analyzed the effects of TSP-1 and TSP-2 on inflammation, vascular endothelial permeability, edema, ultrastructural morphology, and apoptosis in lung tissues of an ARDS mouse model and cultured macrophages. Our results demonstrated that TSP-2 overexpression effectively attenuated LPS-induced ARDS in vivo and promoted M2 macrophage phenotype polarization in vitro. Furthermore, TSP-2 played a role in regulating pulmonary vascular barrier leakage by activating the PI3K/Akt pathway. Overall, our findings indicate that TSP-2 can modulate inflammation and could therefore be a potential therapeutic target against LPS-induced ARDS.http://dx.doi.org/10.1155/2021/8876484 |
| spellingShingle | Qiang Li Xiaoxiao Fu Jiang Yuan Shu Han Contribution of Thrombospondin-1 and -2 to Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome Mediators of Inflammation |
| title | Contribution of Thrombospondin-1 and -2 to Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome |
| title_full | Contribution of Thrombospondin-1 and -2 to Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome |
| title_fullStr | Contribution of Thrombospondin-1 and -2 to Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome |
| title_full_unstemmed | Contribution of Thrombospondin-1 and -2 to Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome |
| title_short | Contribution of Thrombospondin-1 and -2 to Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome |
| title_sort | contribution of thrombospondin 1 and 2 to lipopolysaccharide induced acute respiratory distress syndrome |
| url | http://dx.doi.org/10.1155/2021/8876484 |
| work_keys_str_mv | AT qiangli contributionofthrombospondin1and2tolipopolysaccharideinducedacuterespiratorydistresssyndrome AT xiaoxiaofu contributionofthrombospondin1and2tolipopolysaccharideinducedacuterespiratorydistresssyndrome AT jiangyuan contributionofthrombospondin1and2tolipopolysaccharideinducedacuterespiratorydistresssyndrome AT shuhan contributionofthrombospondin1and2tolipopolysaccharideinducedacuterespiratorydistresssyndrome |