Control of endothelial quiescence by FOXO-regulated metabolites.


Journal

Nature cell biology
ISSN: 1476-4679
Titre abrégé: Nat Cell Biol
Pays: England
ID NLM: 100890575

Informations de publication

Date de publication:
04 2021
Historique:
received: 05 02 2020
accepted: 21 01 2021
pubmed: 3 4 2021
medline: 29 6 2021
entrez: 2 4 2021
Statut: ppublish

Résumé

Endothelial cells (ECs) adapt their metabolism to enable the growth of new blood vessels, but little is known how ECs regulate metabolism to adopt a quiescent state. Here, we show that the metabolite S-2-hydroxyglutarate (S-2HG) plays a crucial role in the regulation of endothelial quiescence. We find that S-2HG is produced in ECs after activation of the transcription factor forkhead box O1 (FOXO1), where it limits cell cycle progression, metabolic activity and vascular expansion. FOXO1 stimulates S-2HG production by inhibiting the mitochondrial enzyme 2-oxoglutarate dehydrogenase. This inhibition relies on branched-chain amino acid catabolites such as 3-methyl-2-oxovalerate, which increase in ECs with activated FOXO1. Treatment of ECs with 3-methyl-2-oxovalerate elicits S-2HG production and suppresses proliferation, causing vascular rarefaction in mice. Our findings identify a metabolic programme that promotes the acquisition of a quiescent endothelial state and highlight the role of metabolites as signalling molecules in the endothelium.

Identifiants

pubmed: 33795871
doi: 10.1038/s41556-021-00637-6
pii: 10.1038/s41556-021-00637-6
pmc: PMC8032556
doi:

Substances chimiques

Forkhead Box Protein O1 0
Glutarates 0
Valerates 0
Proto-Oncogene Proteins c-akt EC 2.7.11.1

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

413-423

Subventions

Organisme : Medical Research Council
ID : MRC_MC_UU_12022/6
Pays : United Kingdom
Organisme : European Research Council
ID : 773047
Pays : International
Organisme : Medical Research Council
ID : MC_UU_12022/6
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UP_1101/3
Pays : United Kingdom
Organisme : NCI NIH HHS
ID : P30 CA045508
Pays : United States

Commentaires et corrections

Type : CommentIn

Références

Augustin, H. G. & Koh, G. Y. Organotypic vasculature: from descriptive heterogeneity to functional pathophysiology. Science 357, eaal2379 (2017).
pubmed: 28775214 doi: 10.1126/science.aal2379
Potente, M. & Makinen, T. Vascular heterogeneity and specialization in development and disease. Nat. Rev. Mol. Cell Biol. 18, 477–494 (2017).
pubmed: 28537573 doi: 10.1038/nrm.2017.36
Paik, J. H. et al. FoxOs are lineage-restricted redundant tumor suppressors and regulate endothelial cell homeostasis. Cell 128, 309–323 (2007).
pubmed: 17254969 pmcid: 1855089 doi: 10.1016/j.cell.2006.12.029
Wilhelm, K. et al. FOXO1 couples metabolic activity and growth state in the vascular endothelium. Nature 529, 216–220 (2016).
pubmed: 26735015 pmcid: 5380221 doi: 10.1038/nature16498
Salih, D. A. & Brunet, A. FoxO transcription factors in the maintenance of cellular homeostasis during aging. Curr. Opin. Cell Biol. 20, 126–136 (2008).
pubmed: 18394876 pmcid: 2387118 doi: 10.1016/j.ceb.2008.02.005
Eijkelenboom, A. & Burgering, B. M. FOXOs: signalling integrators for homeostasis maintenance. Nat. Rev. Mol. Cell Biol. 14, 83–97 (2013).
pubmed: 23325358 doi: 10.1038/nrm3507
Sengupta, A., Chakraborty, S., Paik, J., Yutzey, K. E. & Evans-Anderson, H. J. FoxO1 is required in endothelial but not myocardial cell lineages during cardiovascular development. Dev. Dyn. 241, 803–813 (2012).
pubmed: 22411556 doi: 10.1002/dvdy.23759
Dharaneeswaran, H. et al. FOXO1-mediated activation of Akt plays a critical role in vascular homeostasis. Circ. Res. 115, 238–251 (2014).
pubmed: 24874427 pmcid: 4961050 doi: 10.1161/CIRCRESAHA.115.303227
De Bock, K. et al. Role of PFKFB3-driven glycolysis in vessel sprouting. Cell 154, 651–663 (2013).
pubmed: 23911327 doi: 10.1016/j.cell.2013.06.037
Schoors, S. et al. Fatty acid carbon is essential for dNTP synthesis in endothelial cells. Nature 520, 192–197 (2015).
pubmed: 25830893 pmcid: 4413024 doi: 10.1038/nature14362
Kim, B., Li, J., Jang, C. & Arany, Z. Glutamine fuels proliferation but not migration of endothelial cells. EMBO J. 36, 2321–2333 (2017).
pubmed: 28659379 pmcid: 5556269 doi: 10.15252/embj.201796436
Huang, H. et al. Role of glutamine and interlinked asparagine metabolism in vessel formation. EMBO J. 36, 2334–2352 (2017).
pubmed: 28659375 pmcid: 5556263 doi: 10.15252/embj.201695518
Yu, P. et al. FGF-dependent metabolic control of vascular development. Nature 545, 224–228 (2017).
pubmed: 28467822 pmcid: 5427179 doi: 10.1038/nature22322
Kim, B. et al. Endothelial pyruvate kinase M2 maintains vascular integrity. J. Clin. Invest. 128, 4543–4556 (2018).
pubmed: 30222136 pmcid: 6159968 doi: 10.1172/JCI120912
Stone, O. A. et al. Loss of pyruvate kinase M2 limits growth and triggers innate immune signaling in endothelial cells. Nat. Commun. 9, 4077 (2018).
pubmed: 30301887 pmcid: 6177464 doi: 10.1038/s41467-018-06406-8
Bruning, U. et al. Impairment of angiogenesis by fatty acid synthase inhibition involves mTOR malonylation. Cell Metab. 28, 866–880.e15 (2018).
pubmed: 30146486 doi: 10.1016/j.cmet.2018.07.019 pmcid: 8057116
Vandekeere, S. et al. Serine synthesis via PHGDH is essential for heme production in endothelial cells. Cell Metab. 28, 573–587.e13 (2018).
pubmed: 30017355 doi: 10.1016/j.cmet.2018.06.009
Eelen, G. et al. Role of glutamine synthetase in angiogenesis beyond glutamine synthesis. Nature 561, 63–69 (2018).
pubmed: 30158707 doi: 10.1038/s41586-018-0466-7
Kalucka, J. et al. Quiescent endothelial cells upregulate fatty acid β-oxidation for vasculoprotection via redox homeostasis. Cell Metab. 28, 881–894.e13 (2018).
pubmed: 30146488 doi: 10.1016/j.cmet.2018.07.016
Coller, H. A., Sang, L. & Roberts, J. M. A new description of cellular quiescence. PLoS Biol. 4, e83 (2006).
pubmed: 16509772 pmcid: 1393757 doi: 10.1371/journal.pbio.0040083
Liu, H., Adler, A. S., Segal, E. & Chang, H. Y. A transcriptional program mediating entry into cellular quiescence. PLoS Genet. 3, e91 (2007).
pubmed: 17559306 pmcid: 1904355 doi: 10.1371/journal.pgen.0030091
Schlereth, K. et al. The transcriptomic and epigenetic map of vascular quiescence in the continuous lung endothelium. eLife 7, e34423 (2018).
pubmed: 29749927 pmcid: 5947988 doi: 10.7554/eLife.34423
van Velthoven, C. T. J. & Rando, T. A. Stem cell quiescence: dynamism, restraint, and cellular idling. Cell Stem Cell 24, 213–225 (2019).
pubmed: 30735649 pmcid: 6413865 doi: 10.1016/j.stem.2019.01.001
Kaelin, W. G. Jr. & McKnight, S. L. Influence of metabolism on epigenetics and disease. Cell 153, 56–69 (2013).
pubmed: 23540690 pmcid: 3775362 doi: 10.1016/j.cell.2013.03.004
Metallo, C. M. & Vander Heiden, M. G. Understanding metabolic regulation and its influence on cell physiology. Mol. Cell 49, 388–398 (2013).
pubmed: 23395269 pmcid: 3569837 doi: 10.1016/j.molcel.2013.01.018
Ryan, D. G. et al. Coupling Krebs cycle metabolites to signalling in immunity and cancer. Nat. Metab. 1, 16–33 (2019).
pubmed: 31032474 pmcid: 6485344 doi: 10.1038/s42255-018-0014-7
Losman, J. A., Koivunen, P. & Kaelin, W. G. 2-Oxoglutarate-dependent dioxygenases in cancer. Nat. Rev. Cancer 20, 710–726 (2020).
pubmed: 33087883 doi: 10.1038/s41568-020-00303-3
Xu, W. et al. Oncometabolite 2-hydroxyglutarate is a competitive inhibitor of α-ketoglutarate-dependent dioxygenases. Cancer Cell 19, 17–30 (2011).
pubmed: 21251613 pmcid: 3229304 doi: 10.1016/j.ccr.2010.12.014
Dang, L. et al. Cancer-associated IDH1 mutations produce 2-hydroxyglutarate. Nature 462, 739–744 (2009).
pubmed: 19935646 pmcid: 2818760 doi: 10.1038/nature08617
Chowdhury, R. et al. The oncometabolite 2-hydroxyglutarate inhibits histone lysine demethylases. EMBO Rep. 12, 463–469 (2011).
pubmed: 21460794 pmcid: 3090014 doi: 10.1038/embor.2011.43
Koivunen, P. et al. Transformation by the (R)-enantiomer of 2-hydroxyglutarate linked to EGLN activation. Nature 483, 484–488 (2012).
pubmed: 22343896 pmcid: 3656605 doi: 10.1038/nature10898
Losman, J. A. et al. (R)-2-hydroxyglutarate is sufficient to promote leukemogenesis and its effects are reversible. Science 339, 1621–1625 (2013).
pubmed: 23393090 doi: 10.1126/science.1231677
Burr, S. P. et al. Mitochondrial protein lipoylation and the 2-oxoglutarate dehydrogenase complex controls HIF1α stability in aerobic conditions. Cell Metab. 24, 740–752 (2016).
pubmed: 27923773 pmcid: 5106373 doi: 10.1016/j.cmet.2016.09.015
Nadtochiy, S. M. et al. Acidic pH is a metabolic switch for 2-hydroxyglutarate generation and signaling. J. Biol. Chem. 291, 20188–20197 (2016).
pubmed: 27510037 pmcid: 5025701 doi: 10.1074/jbc.M116.738799
Intlekofer, A. M. et al. L-2-Hydroxyglutarate production arises from noncanonical enzyme function at acidic pH. Nat. Chem. Biol. 13, 494–500 (2017).
pubmed: 28263965 pmcid: 5516644 doi: 10.1038/nchembio.2307
Graham, S. M., Vass, J. K., Holyoake, T. L. & Graham, G. J. Transcriptional analysis of quiescent and proliferating CD34
pubmed: 17717066 doi: 10.1634/stemcells.2007-0250
Intlekofer, A. M. et al. Hypoxia induces production of L-2-hydroxyglutarate. Cell Metab. 22, 304–311 (2015).
pubmed: 26212717 pmcid: 4527873 doi: 10.1016/j.cmet.2015.06.023
Oldham, W. M., Clish, C. B., Yang, Y. & Loscalzo, J. Hypoxia-mediated increases in L-2-hydroxyglutarate coordinate the metabolic response to reductive stress. Cell Metab. 22, 291–303 (2015).
pubmed: 26212716 pmcid: 4526408 doi: 10.1016/j.cmet.2015.06.021
Tyrakis, P. A. et al. S-2-Hydroxyglutarate regulates CD8
pubmed: 27798602 pmcid: 5149074 doi: 10.1038/nature20165
Anso, E. et al. The mitochondrial respiratory chain is essential for haematopoietic stem cell function. Nat. Cell Biol. 19, 614–625 (2017).
pubmed: 28504706 pmcid: 5474760 doi: 10.1038/ncb3529
Weinberg, S. E. et al. Mitochondrial complex III is essential for suppressive function of regulatory T cells. Nature 565, 495–499 (2019).
pubmed: 30626970 pmcid: 6345596 doi: 10.1038/s41586-018-0846-z
Ni, M. et al. Functional assessment of lipoyltransferase-1 deficiency in cells, mice, and humans. Cell Rep. 27, 1376–1386.e6 (2019).
pubmed: 31042466 pmcid: 7351313 doi: 10.1016/j.celrep.2019.04.005
Bailey, P. S. J. et al. ABHD11 maintains 2-oxoglutarate metabolism by preserving functional lipoylation of the 2-oxoglutarate dehydrogenase complex. Nat. Commun. 11, 4046 (2020).
pubmed: 32792488 pmcid: 7426941 doi: 10.1038/s41467-020-17862-6
Patel, M. S. Inhibition by the branched-chain 2-oxo acids of the 2-oxoglutarate dehydrogenase complex in developing rat and human brain. Biochem. J. 144, 91–97 (1974).
pubmed: 4462577 pmcid: 1168468 doi: 10.1042/bj1440091
Gibson, G. E. & Blass, J. P. Inhibition of acetylcholine synthesis and of carbohydrate utilization by maple-syrup-urine disease metabolites. J. Neurochem. 26, 1073–1078 (1976).
pubmed: 945329 doi: 10.1111/j.1471-4159.1976.tb06988.x
Lynch, C. J. & Adams, S. H. Branched-chain amino acids in metabolic signalling and insulin resistance. Nat. Rev. Endocrinol. 10, 723–736 (2014).
pubmed: 25287287 pmcid: 4424797 doi: 10.1038/nrendo.2014.171
Ilic, N. et al. PIK3CA mutant tumors depend on oxoglutarate dehydrogenase. Proc. Natl Acad. Sci. USA 114, e3434–e3443 (2017).
pubmed: 28396387 doi: 10.1073/pnas.1617922114 pmcid: 5410781
Su, R. et al. R-2HG exhibits anti-tumor activity by targeting FTO/m
pubmed: 29249359 doi: 10.1016/j.cell.2017.11.031
Fu, X. et al. 2-Hydroxyglutarate inhibits ATP synthase and mTOR signaling. Cell Metab. 22, 508–515 (2015).
pubmed: 26190651 pmcid: 4663076 doi: 10.1016/j.cmet.2015.06.009
Goda, N. et al. Hypoxia-inducible factor 1α is essential for cell cycle arrest during hypoxia. Mol. Cell. Biol. 23, 359–369 (2003).
pubmed: 12482987 pmcid: 140666 doi: 10.1128/MCB.23.1.359-369.2003
Manalo, D. J. et al. Transcriptional regulation of vascular endothelial cell responses to hypoxia by HIF-1. Blood 105, 659–669 (2005).
pubmed: 15374877 doi: 10.1182/blood-2004-07-2958
Mazzone, M. et al. Heterozygous deficiency of PHD2 restores tumor oxygenation and inhibits metastasis via endothelial normalization. Cell 136, 839–851 (2009).
pubmed: 19217150 pmcid: 4037868 doi: 10.1016/j.cell.2009.01.020
Chen, F. et al. Oncometabolites D- and L-2-hydroxyglutarate Inhibit the AlkB family DNA repair enzymes under physiological conditions. Chem. Res. Toxicol. 30, 1102–1110 (2017).
pubmed: 28269980 pmcid: 5498157 doi: 10.1021/acs.chemrestox.7b00009
Guarani, V. et al. Acetylation-dependent regulation of endothelial notch signalling by the SIRT1 deacetylase. Nature 473, 234–238 (2011).
pubmed: 21499261 pmcid: 4598045 doi: 10.1038/nature09917
Schmidt, E. K., Clavarino, G., Ceppi, M. & Pierre, P. SUnSET, a nonradioactive method to monitor protein synthesis. Nat. Methods 6, 275–277 (2009).
pubmed: 19305406 doi: 10.1038/nmeth.1314
Sakaue-Sawano, A. et al. Visualizing spatiotemporal dynamics of multicellular cell-cycle progression. Cell 132, 487–498 (2008).
pubmed: 18267078 doi: 10.1016/j.cell.2007.12.033
Luo, W. et al. Arterialization requires the timely suppression of cell growth. Nature 589, 437–441 (2021).
pubmed: 33299176 doi: 10.1038/s41586-020-3018-x
Cantelmo, A. R. et al. Inhibition of the glycolytic activator PFKFB3 in endothelium induces tumor vessel normalization, impairs metastasis, and improves chemotherapy. Cancer Cell 30, 968–985 (2016).
pubmed: 27866851 pmcid: 5675554 doi: 10.1016/j.ccell.2016.10.006
Lim, R. et al. Deubiquitinase USP10 regulates Notch signaling in the endothelium. Science 364, 188–193 (2019).
pubmed: 30975888 doi: 10.1126/science.aat0778
Struys, E. A., Jansen, E. E., Verhoeven, N. M. & Jakobs, C. Measurement of urinary D- and L-2-hydroxyglutarate enantiomers by stable-isotope-dilution liquid chromatography-tandem mass spectrometry after derivatization with diacetyl-L-tartaric anhydride. Clin. Chem. 50, 1391–1395 (2004).
pubmed: 15166110 doi: 10.1373/clinchem.2004.033399
Zhang, T. et al. Prmt5 is a regulator of muscle stem cell expansion in adult mice. Nat. Commun. 6, 7140 (2015).
pubmed: 26028225 doi: 10.1038/ncomms8140
Subramanian, A. et al. Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles. Proc. Natl Acad. Sci. USA 102, 15545–15550 (2005).
pubmed: 16199517 doi: 10.1073/pnas.0506580102 pmcid: 1239896
Li, H. & Durbin, R. Fast and accurate short read alignment with Burrows–Wheeler transform. Bioinformatics 25, 1754–1760 (2009).
pubmed: 19451168 pmcid: 2705234 doi: 10.1093/bioinformatics/btp324
Zhang, Y. et al. Model-based analysis of ChIP-seq (MACS). Genome Biol. 9, R137 (2008).
pubmed: 18798982 pmcid: 2592715 doi: 10.1186/gb-2008-9-9-r137
Heinz, S. et al. Simple combinations of lineage-determining transcription factors prime cis-regulatory elements required for macrophage and B cell identities. Mol. Cell 38, 576–589 (2010).
pubmed: 20513432 pmcid: 2898526 doi: 10.1016/j.molcel.2010.05.004
Koni, P. A. et al. Conditional vascular cell adhesion molecule 1 deletion in mice: impaired lymphocyte migration to bone marrow. J. Exp. Med. 193, 741–754 (2001).
pubmed: 11257140 pmcid: 2193418 doi: 10.1084/jem.193.6.741
Okabe, K. et al. Neurons limit angiogenesis by titrating VEGF in retina. Cell 159, 584–596 (2014).
pubmed: 25417109 doi: 10.1016/j.cell.2014.09.025
Lee, J. et al. Angiopoietin-1 guides directional angiogenesis through integrin alphavbeta5 signaling for recovery of ischemic retinopathy. Sci. Transl. Med. 5, 203ra127 (2013).
pubmed: 24048525
Pitulescu, M. E., Schmidt, I., Benedito, R. & Adams, R. H. Inducible gene targeting in the neonatal vasculature and analysis of retinal angiogenesis in mice. Nat. Protoc. 5, 1518–1534 (2010).
pubmed: 20725067 doi: 10.1038/nprot.2010.113

Auteurs

Jorge Andrade (J)

Angiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Chenyue Shi (C)

Angiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Ana S H Costa (ASH)

Medical Research Council Cancer Unit, University of Cambridge, Cambridge, UK.
Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.

Jeongwoon Choi (J)

Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Korea.
Center for Vascular Research, Institute for Basic Science (IBS), Daejeon, Korea.

Jaeryung Kim (J)

Center for Vascular Research, Institute for Basic Science (IBS), Daejeon, Korea.
Department of Oncology and Ludwig Institute for Cancer Research, University of Lausanne and Centre Hospitalier Universitaire Vaudois, Epalinges, Switzerland.

Anuradha Doddaballapur (A)

Angiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Toshiya Sugino (T)

Angiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Yu Ting Ong (YT)

Angiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Marco Castro (M)

Angiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Barbara Zimmermann (B)

Angiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Manuel Kaulich (M)

Gene Editing Group, Institute of Biochemistry II, Goethe University, Frankfurt (Main), Germany.

Stefan Guenther (S)

Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Kerstin Wilhelm (K)

Angiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Yoshiaki Kubota (Y)

Department of Anatomy, Keio University School of Medicine, Tokyo, Japan.

Thomas Braun (T)

Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Gou Young Koh (GY)

Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Korea.
Center for Vascular Research, Institute for Basic Science (IBS), Daejeon, Korea.

Ana Rita Grosso (AR)

UCIBIO-Unidade de Ciências Biomoleculares Aplicadas, Departamento Ciências da Vida, Faculdade de Ciências e Tecnologia-Universidade Nova de Lisboa Campus de Caparica, Caparica, Portugal.
Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.

Christian Frezza (C)

Medical Research Council Cancer Unit, University of Cambridge, Cambridge, UK.

Michael Potente (M)

Angiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany. michael.potente@mpi-bn.mpg.de.
Berlin Institute of Health (BIH) at Charité-Universitätsmedizin Berlin, Berlin, Germany. michael.potente@mpi-bn.mpg.de.
Max Delbrück Center for Molecular Medicine (MDC), Berlin, Germany. michael.potente@mpi-bn.mpg.de.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH