TRPML1 acts as a predisposing factor in lymphedema development by regulating the subcellular localization of aquaporin-3, -5.
An imbalance in lymphatic fluid, whether it is caused by generation, transport, outflow, or dysfunctional vessels, can lead to lymphedema; however, the exact pathogenesis of this disease remains unclear. To explore the mechanism, we focused on the association among TRPML1, aquaporin-3 (AQP3), and aq...
Saved in:
| Main Authors: | , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2024-01-01
|
| Series: | PLoS ONE |
| Online Access: | https://doi.org/10.1371/journal.pone.0310653 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1846129376850083840 |
|---|---|
| author | Lijie Yang Guanzheng Wang Yuan Ma Qiancheng Zhao He Zhao Qi Wang Chonghua Zhong Chunmei Zhang Yiming Yang |
| author_facet | Lijie Yang Guanzheng Wang Yuan Ma Qiancheng Zhao He Zhao Qi Wang Chonghua Zhong Chunmei Zhang Yiming Yang |
| author_sort | Lijie Yang |
| collection | DOAJ |
| description | An imbalance in lymphatic fluid, whether it is caused by generation, transport, outflow, or dysfunctional vessels, can lead to lymphedema; however, the exact pathogenesis of this disease remains unclear. To explore the mechanism, we focused on the association among TRPML1, aquaporin-3 (AQP3), and aquaporin-5 (AQP5) in human lymphatic endothelial cells (HLECs). We explored the role of TRPML1 in altering the permeability of HLECs in lymphedema. Meanwhile, we constructed a disease model using gene-knockout mice to observe the effect of TRPML1 on inflammation and fibrosis in lymphedema sites. Our results indicate that TRPML1 not only regulates the localization of AQP3, -5 to the cell membrane but also increases HLEC permeability, disrupts lymphatic fluid transport, and mediates the development of chronic inflammation at the site of lymphedema. Our study suggests that TRPML1 is a precipitating factor in lymphedema. Our findings improve the understanding of TRPML1 and aquaporins in secondary lymphedema, providing valuable insights for future research. |
| format | Article |
| id | doaj-art-3fe2cef83aeb4ddeb0138bc0a7390b9a |
| institution | Kabale University |
| issn | 1932-6203 |
| language | English |
| publishDate | 2024-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-3fe2cef83aeb4ddeb0138bc0a7390b9a2024-12-10T05:32:23ZengPublic Library of Science (PLoS)PLoS ONE1932-62032024-01-011912e031065310.1371/journal.pone.0310653TRPML1 acts as a predisposing factor in lymphedema development by regulating the subcellular localization of aquaporin-3, -5.Lijie YangGuanzheng WangYuan MaQiancheng ZhaoHe ZhaoQi WangChonghua ZhongChunmei ZhangYiming YangAn imbalance in lymphatic fluid, whether it is caused by generation, transport, outflow, or dysfunctional vessels, can lead to lymphedema; however, the exact pathogenesis of this disease remains unclear. To explore the mechanism, we focused on the association among TRPML1, aquaporin-3 (AQP3), and aquaporin-5 (AQP5) in human lymphatic endothelial cells (HLECs). We explored the role of TRPML1 in altering the permeability of HLECs in lymphedema. Meanwhile, we constructed a disease model using gene-knockout mice to observe the effect of TRPML1 on inflammation and fibrosis in lymphedema sites. Our results indicate that TRPML1 not only regulates the localization of AQP3, -5 to the cell membrane but also increases HLEC permeability, disrupts lymphatic fluid transport, and mediates the development of chronic inflammation at the site of lymphedema. Our study suggests that TRPML1 is a precipitating factor in lymphedema. Our findings improve the understanding of TRPML1 and aquaporins in secondary lymphedema, providing valuable insights for future research.https://doi.org/10.1371/journal.pone.0310653 |
| spellingShingle | Lijie Yang Guanzheng Wang Yuan Ma Qiancheng Zhao He Zhao Qi Wang Chonghua Zhong Chunmei Zhang Yiming Yang TRPML1 acts as a predisposing factor in lymphedema development by regulating the subcellular localization of aquaporin-3, -5. PLoS ONE |
| title | TRPML1 acts as a predisposing factor in lymphedema development by regulating the subcellular localization of aquaporin-3, -5. |
| title_full | TRPML1 acts as a predisposing factor in lymphedema development by regulating the subcellular localization of aquaporin-3, -5. |
| title_fullStr | TRPML1 acts as a predisposing factor in lymphedema development by regulating the subcellular localization of aquaporin-3, -5. |
| title_full_unstemmed | TRPML1 acts as a predisposing factor in lymphedema development by regulating the subcellular localization of aquaporin-3, -5. |
| title_short | TRPML1 acts as a predisposing factor in lymphedema development by regulating the subcellular localization of aquaporin-3, -5. |
| title_sort | trpml1 acts as a predisposing factor in lymphedema development by regulating the subcellular localization of aquaporin 3 5 |
| url | https://doi.org/10.1371/journal.pone.0310653 |
| work_keys_str_mv | AT lijieyang trpml1actsasapredisposingfactorinlymphedemadevelopmentbyregulatingthesubcellularlocalizationofaquaporin35 AT guanzhengwang trpml1actsasapredisposingfactorinlymphedemadevelopmentbyregulatingthesubcellularlocalizationofaquaporin35 AT yuanma trpml1actsasapredisposingfactorinlymphedemadevelopmentbyregulatingthesubcellularlocalizationofaquaporin35 AT qianchengzhao trpml1actsasapredisposingfactorinlymphedemadevelopmentbyregulatingthesubcellularlocalizationofaquaporin35 AT hezhao trpml1actsasapredisposingfactorinlymphedemadevelopmentbyregulatingthesubcellularlocalizationofaquaporin35 AT qiwang trpml1actsasapredisposingfactorinlymphedemadevelopmentbyregulatingthesubcellularlocalizationofaquaporin35 AT chonghuazhong trpml1actsasapredisposingfactorinlymphedemadevelopmentbyregulatingthesubcellularlocalizationofaquaporin35 AT chunmeizhang trpml1actsasapredisposingfactorinlymphedemadevelopmentbyregulatingthesubcellularlocalizationofaquaporin35 AT yimingyang trpml1actsasapredisposingfactorinlymphedemadevelopmentbyregulatingthesubcellularlocalizationofaquaporin35 |