ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Myeloid-derived suppressor cells are involved in lysosomal acid lipase deficiency-induced endothelial cell dysfunctions.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Limited Alleviation of Lysosomal Acid Lipase Deficiency by Deletion of Matrix Metalloproteinase 12.International journal of molecular sciences · 2024Article
- Photodynamic Therapy and Adaptive Immunity Induced by Reactive Oxygen Species: Recent Reports.Cancers · 2024Review
- LAL deficiency induced myeloid-derived suppressor cells as targets and biomarkers for lung cancer.Journal for immunotherapy of cancer · 2023Article
- IDO1 and inflammatory neovascularization: bringing new blood to tumor-promoting inflammation.Frontiers in oncology · 2023Review
- Lysosomal Acid Lipase Deficiency: Genetics, Screening, and Preclinical Study.International journal of molecular sciences · 2022Review
- Lysosomal acid lipase, CSF1R, and PD-L1 determine functions of CD11c+ myeloid-derived suppressor cells.JCI insight · 2022Article
- Article
- Lysosomal Acid Lipase Deficiency Controls T- and B-Regulatory Cell Homeostasis in the Lymph Nodes of Mice with Human Cancer Xenotransplants.The American journal of pathology · 2021Article
- A New Antitumor Direction: Tumor-Specific Endothelial Cells.Frontiers in oncology · 2021Review
- Review
- Transthyretin Stimulates Tumor Growth through Regulation of Tumor, Immune, and Endothelial Cells.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Endothelial Rab7 GTPase mediates tumor growth and metastasis in lysosomal acid lipase-deficient mice.The Journal of biological chemistry · 2017Article
- Rab7 GTPase controls lipid metabolic signaling in myeloid-derived suppressor cells.Oncotarget · 2017Article
- Metabolic reprogramming of myeloid-derived suppressive cells.Oncoscience · 2017Article
- Lysosomal acid lipase in mesenchymal stem cell stimulation of tumor growth and metastasis.Oncotarget · 2016Article
- Lung Epithelial Cell-Specific Expression of Human Lysosomal Acid Lipase Ameliorates Lung Inflammation and Tumor Metastasis in Lipa(-/-) Mice.The American journal of pathology · 2016Article
- Critical role of PPARγ in myeloid-derived suppressor cell-stimulated cancer cell proliferation and metastasis.Oncotarget · 2016Article
- Isolation of epithelial, endothelial, and immune cells from lungs of transgenic mice with oncogene-induced lung adenocarcinomas.American journal of respiratory cell and molecular biology · 2015Article
- Lysosomal acid lipase in cancer.Oncoscience · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The underlying mechanisms that lysosomal acid lipase (LAL) deficiency causes infiltration of myeloid-derived suppressor cells (MDSCs) in multiple organs and subsequent inflammation remain incompletely understood. Endothelial cells (ECs), lining the inner layer of blood vessels, constitute barriers regulating leukocytes transmigration to the site of inflammation. Therefore, we hypothesized that ECs are dysfunctional in LAL-deficient (lal(-/-)) mice. We found that Ly6G(+) cells transmigrated more efficiently across lal(-/-) ECs than wild-type (lal(+/+)) ECs, which were associated with increased levels of PECAM-1 and MCP-1 in lal(-/-) ECs. In addition, lal(-/-) ECs showed enhanced migration and proliferation, decreased apoptosis, but impaired tube formation and angiogenesis. lal(-/-) ECs also suppressed T cell proliferation in vitro. Interestingly, lal(-/-) Ly6G(+) cells promoted in vivo angiogenesis (including a tumor model), EC tube formation, and proliferation. Finally, the mammalian target of rapamycin (mTOR) pathway was activated in lal(-/-) ECs, and inhibition of mTOR reversed EC dysfunctions, including decreasing Ly6G(+) cell transmigration, delaying migration, and relieving suppression of T cell proliferation, which was mediated by decreasing production of reactive oxygen species. Our results indicate that LAL regulates EC functions through interaction with MDSCs and modulation of the mTOR pathway, which may provide a mechanistic basis for targeting MDSCs or mTOR to rejuvenate EC functions in LAL deficiency-related diseases.
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Registered trials
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