Alterations in Polyamine Metabolism in Patients With Lymphangioleiomyomatosis and Tuberous Sclerosis Complex 2-Deficient Cells.
Identifieur interne : 000045 ( PubMed/Corpus ); précédent : 000044; suivant : 000046Alterations in Polyamine Metabolism in Patients With Lymphangioleiomyomatosis and Tuberous Sclerosis Complex 2-Deficient Cells.
Auteurs : Yan Tang ; Souheil El-Chemaly ; Angelo Taveira-Dasilva ; Hilary J. Goldberg ; Shefali Bagwe ; Ivan O. Rosas ; Joel Moss ; Carmen Priolo ; Elizabeth P. HenskeSource :
- Chest [ 1931-3543 ] ; 2019.
Abstract
Lymphangioleiomyomatosis (LAM), a destructive lung disease that affects primarily women, is caused by loss-of-function mutations in TSC1 or TSC2, leading to hyperactivation of mechanistic/mammalian target of rapamycin complex 1 (mTORC1). Rapamycin (sirolimus) treatment suppresses mTORC1 but also induces autophagy, which promotes the survival of TSC2-deficient cells. Based on the hypothesis that simultaneous inhibition of mTORC1 and autophagy would limit the availability of critical nutrients and inhibit LAM cells, we conducted a phase 1 clinical trial of sirolimus and hydroxychloroquine for LAM. Here, we report the analyses of plasma metabolomic profiles from the clinical trial.
DOI: 10.1016/j.chest.2019.05.038
PubMed: 31299246
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<front><div type="abstract" xml:lang="en">Lymphangioleiomyomatosis (LAM), a destructive lung disease that affects primarily women, is caused by loss-of-function mutations in TSC1 or TSC2, leading to hyperactivation of mechanistic/mammalian target of rapamycin complex 1 (mTORC1). Rapamycin (sirolimus) treatment suppresses mTORC1 but also induces autophagy, which promotes the survival of TSC2-deficient cells. Based on the hypothesis that simultaneous inhibition of mTORC1 and autophagy would limit the availability of critical nutrients and inhibit LAM cells, we conducted a phase 1 clinical trial of sirolimus and hydroxychloroquine for LAM. Here, we report the analyses of plasma metabolomic profiles from the clinical trial.</div>
</front>
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<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>22</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1931-3543</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>156</Volume>
<Issue>6</Issue>
<PubDate><Year>2019</Year>
<Month>Dec</Month>
</PubDate>
</JournalIssue>
<Title>Chest</Title>
<ISOAbbreviation>Chest</ISOAbbreviation>
</Journal>
<ArticleTitle>Alterations in Polyamine Metabolism in Patients With Lymphangioleiomyomatosis and Tuberous Sclerosis Complex 2-Deficient Cells.</ArticleTitle>
<Pagination><MedlinePgn>1137-1148</MedlinePgn>
</Pagination>
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<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.chest.2019.05.038</ELocationID>
<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Lymphangioleiomyomatosis (LAM), a destructive lung disease that affects primarily women, is caused by loss-of-function mutations in TSC1 or TSC2, leading to hyperactivation of mechanistic/mammalian target of rapamycin complex 1 (mTORC1). Rapamycin (sirolimus) treatment suppresses mTORC1 but also induces autophagy, which promotes the survival of TSC2-deficient cells. Based on the hypothesis that simultaneous inhibition of mTORC1 and autophagy would limit the availability of critical nutrients and inhibit LAM cells, we conducted a phase 1 clinical trial of sirolimus and hydroxychloroquine for LAM. Here, we report the analyses of plasma metabolomic profiles from the clinical trial.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">We analyzed the plasma metabolome in samples obtained before, during, and after 6 months of treatment with sirolimus and hydroxychloroquine, using univariate statistical models and machine learning approaches. Metabolites and metabolic pathways were validated in TSC2-deficient cells derived from patients with LAM. Single-cell RNA-Seq was employed to assess metabolic enzymes in an early-passage culture from an LAM lung.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Metabolomic profiling revealed changes in polyamine metabolism during treatment, with 5'-methylthioadenosine and arginine among the most highly upregulated metabolites. Similar findings were observed in TSC2-deficient cells derived from patients with LAM. Single-cell transcriptomic profiling of primary LAM cultured cells revealed that mTORC1 inhibition upregulated key enzymes in the polyamine metabolism pathway, including adenosylmethionine decarboxylase 1.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our data demonstrate that polyamine metabolic pathways are targeted by the combination of rapamycin and hydroxychloroquine, leading to upregulation of 5'-methylthioadenosine and arginine in the plasma of patients with LAM and in TSC2-deficient cells derived from a patient with LAM upon treatment with this drug combination.</AbstractText>
<AbstractText Label="TRIAL REGISTRY" NlmCategory="BACKGROUND">ClinicalTrials.gov; No.: NCT01687179; URL: www.clinicaltrials.gov. Partners Human Research Committee, protocol No. 2012P000669.</AbstractText>
<CopyrightInformation>Copyright © 2019 American College of Chest Physicians. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tang</LastName>
<ForeName>Yan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Pulmonary and Critical Care Medicine Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>El-Chemaly</LastName>
<ForeName>Souheil</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Pulmonary and Critical Care Medicine Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Taveira-Dasilva</LastName>
<ForeName>Angelo</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Goldberg</LastName>
<ForeName>Hilary J</ForeName>
<Initials>HJ</Initials>
<AffiliationInfo><Affiliation>Pulmonary and Critical Care Medicine Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Bagwe</LastName>
<ForeName>Shefali</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Pulmonary and Critical Care Medicine Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Rosas</LastName>
<ForeName>Ivan O</ForeName>
<Initials>IO</Initials>
<AffiliationInfo><Affiliation>Pulmonary and Critical Care Medicine Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Moss</LastName>
<ForeName>Joel</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Priolo</LastName>
<ForeName>Carmen</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Pulmonary and Critical Care Medicine Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA. Electronic address: Carmen_priolo@dfci.harvard.edu.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Henske</LastName>
<ForeName>Elizabeth P</ForeName>
<Initials>EP</Initials>
<AffiliationInfo><Affiliation>Pulmonary and Critical Care Medicine Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
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<AccessionNumberList><AccessionNumber>NCT01687179</AccessionNumber>
</AccessionNumberList>
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<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2019</Year>
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<CitationSubset>AIM</CitationSubset>
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<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">5′-methylthioadenosine</Keyword>
<Keyword MajorTopicYN="N">angiomyolipoma</Keyword>
<Keyword MajorTopicYN="N">arginine</Keyword>
<Keyword MajorTopicYN="N">autophagy</Keyword>
<Keyword MajorTopicYN="N">hydroxychloroquine</Keyword>
<Keyword MajorTopicYN="N">lymphangioleiomyomatosis</Keyword>
<Keyword MajorTopicYN="N">mechanistic/mammalian target of rapamycin complex 1</Keyword>
<Keyword MajorTopicYN="N">metabolomics</Keyword>
<Keyword MajorTopicYN="N">polyamines</Keyword>
<Keyword MajorTopicYN="N">rapamycin</Keyword>
<Keyword MajorTopicYN="N">single-cell transcriptomics</Keyword>
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