Lactate dehydrogenase activity drives hair follicle stem cell activation
Although normally dormant, hair follicle stem cells (HFSCs) quickly become activated to divide during a new hair cycle. The quiescence of HFSCs is known to be regulated by a number of intrinsic and extrinsic mechanisms. Here we provide several lines of evidence to demonstrate that HFSCs utilize glyc...
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| Published in | Nature cell biology Vol. 19; no. 9; pp. 1017 - 1026 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.09.2017
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Although normally dormant, hair follicle stem cells (HFSCs) quickly become activated to divide during a new hair cycle. The quiescence of HFSCs is known to be regulated by a number of intrinsic and extrinsic mechanisms. Here we provide several lines of evidence to demonstrate that HFSCs utilize glycolytic metabolism and produce significantly more lactate than other cells in the epidermis. Furthermore, lactate generation appears to be critical for the activation of HFSCs as deletion of lactate dehydrogenase (Ldha) prevented their activation. Conversely, genetically promoting lactate production in HFSCs through mitochondrial pyruvate carrier 1 (Mpc1) deletion accelerated their activation and the hair cycle. Finally, we identify small molecules that increase lactate production by stimulating Myc levels or inhibiting Mpc1 carrier activity and can topically induce the hair cycle. These data suggest that HFSCs maintain a metabolic state that allows them to remain dormant and yet quickly respond to appropriate proliferative stimuli.
Flores
et al.
show that hair follicle stem cells rely on the production of lactate via the LDHA enzyme to become activated. Inducing Ldha through Mpc1 inhibition or Myc activation successfully reactivates the hair cycle in quiescent follicles. |
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| AbstractList | Although normally dormant, hair follicle stem cells (HFSCs) quickly become activated to divide during a new hair cycle. The quiescence of HFSCs is known to be regulated by a number of intrinsic and extrinsic mechanisms. Here we provide several lines of evidence to demonstrate that HFSCs utilize glycolytic metabolism and produce significantly more lactate than other cells in the epidermis. Furthermore, lactate generation appears to be critical for the activation of HFSCs as deletion of lactate dehydrogenase (Ldha) prevented their activation. Conversely, genetically promoting lactate production in HFSCs through mitochondrial pyruvate carrier 1 (Mpc1) deletion accelerated their activation and the hair cycle. Finally, we identify small molecules that increase lactate production by stimulating Myc levels or inhibiting Mpc1 carrier activity and can topically induce the hair cycle. These data suggest that HFSCs maintain a metabolic state that allows them to remain dormant and yet quickly respond to appropriate proliferative stimuli.Although normally dormant, hair follicle stem cells (HFSCs) quickly become activated to divide during a new hair cycle. The quiescence of HFSCs is known to be regulated by a number of intrinsic and extrinsic mechanisms. Here we provide several lines of evidence to demonstrate that HFSCs utilize glycolytic metabolism and produce significantly more lactate than other cells in the epidermis. Furthermore, lactate generation appears to be critical for the activation of HFSCs as deletion of lactate dehydrogenase (Ldha) prevented their activation. Conversely, genetically promoting lactate production in HFSCs through mitochondrial pyruvate carrier 1 (Mpc1) deletion accelerated their activation and the hair cycle. Finally, we identify small molecules that increase lactate production by stimulating Myc levels or inhibiting Mpc1 carrier activity and can topically induce the hair cycle. These data suggest that HFSCs maintain a metabolic state that allows them to remain dormant and yet quickly respond to appropriate proliferative stimuli. Although normally dormant, hair follicle stem cells (HFSCs) quickly become activated to divide during a new hair cycle. The quiescence of HFSCs is known to be regulated by a number of intrinsic and extrinsic mechanisms. Here we provide several lines of evidence to demonstrate that HFSCs utilize glycolytic metabolism and produce significantly more lactate than other cells in the epidermis. Furthermore, lactate generation appears to be critical for the activation of HFSCs as deletion of lactate dehydrogenase (Ldha) prevented their activation. Conversely, genetically promoting lactate production in HFSCs through mitochondrial pyruvate carrier 1 (Mpc1) deletion accelerated their activation and the hair cycle. Finally, we identify small molecules that increase lactate production by stimulating Myc levels or inhibiting Mpc1 carrier activity and can topically induce the hair cycle. These data suggest that HFSCs maintain a metabolic state that allows them to remain dormant and yet quickly respond to appropriate proliferative stimuli. Flores et al. show that hair follicle stem cells rely on the production of lactate via the LDHA enzyme to become activated. Inducing Ldha through Mpc1 inhibition or Myc activation successfully reactivates the hair cycle in quiescent follicles. Although normally dormant, hair follicle stem cells (HFSCs) quickly become activated to divide during a new hair cycle. The quiescence of HFSCs is known to be regulated by a number of intrinsic and extrinsic mechanisms. Here we provide several lines of evidence to demonstrate that HFSCs utilize glycolytic metabolism and produce significantly more lactate than other cells in the epidermis. Furthermore, lactate generation appears to be critical for the activation of HFSCs as deletion of lactate dehydrogenase (Ldha) prevented their activation. Conversely, genetically promoting lactate production in HFSCs through mitochondrial pyruvate carrier 1 (Mpc1) deletion accelerated their activation and the hair cycle. Finally, we identify small molecules that increase lactate production by stimulating Myc levels or inhibiting Mpc1 carrier activity and can topically induce the hair cycle. These data suggest that HFSCs maintain a metabolic state that allows them to remain dormant and yet quickly respond to appropriate proliferative stimuli. While normally dormant, Hair Follicle Stem Cells (HFSCs) quickly become activated to divide during a new hair cycle. The quiescence of HFSCs is known to be regulated by a number of intrinsic and extrinsic mechanisms. Here we provide several lines of evidence to demonstrate that HFSCs utilize glycolytic metabolism and produce significantly more lactate than other cells in the epidermis. Furthermore, lactate generation appears to be critical for the activation of HFSCs as deletion of lactate dehydrogenase (Ldha) prevented their activation. Conversely, genetically promoting lactate production in HFSCs through mitochondrial pyruvate carrier (Mpc1) deletion accelerated their activation and the hair cycle. Finally, we identify small molecules that increase lactate production by stimulating Myc levels or inhibiting Mpc1 carrier activity and can topically induce the hair cycle. These data suggest that HFSCs maintain a metabolic state that allow them to remain dormant and yet quickly respond to appropriate proliferative stimuli. |
| Audience | Academic |
| Author | Graham, Nicholas A. Graeber, Thomas Seth, Pankaj Evseenko, Denis Krall, Abigail S. Grigorian, Melina Flores, Aimee Christofk, Heather R. Zhou, Jessica L. Lowry, William E. Rutter, Jared Schell, John Jelinek, David Miranda, Matilde Coller, Hilary A. Braas, Daniel White, Andrew C. |
| AuthorAffiliation | 6 Department of Molecular and Medical Pharmacology, UCLA 10 Department of Biochemistry, University of Utah 8 Broad Center for Regenerative Medicine, University of Southern California 14 Stanford School of Medicine, UCLA 9 Mork Family Department of Chemical Engineering, University of Southern California 13 UCLA Metabolomics Center, UCLA 5 Department of Biological Chemistry, UCLA 2 Jonsson Comprehensive Cancer Center, UCLA 15 Division of Interdisciplinary Medicine and Biotechnology, Beth Israel Deaconess Cancer Center, Harvard Medical School 4 Molecular Biology Institute, UCLA 1 Department of Molecular Cell and Developmental Biology, UCLA 12 Crump Institute for Molecular Imaging, UCLA 7 School of Veterinary Medicine, Cornell University 11 Howard Hughes Medical Institute 3 Eli and Edythe Broad Center for Regenerative Medicine, UCLA |
| AuthorAffiliation_xml | – name: 7 School of Veterinary Medicine, Cornell University – name: 15 Division of Interdisciplinary Medicine and Biotechnology, Beth Israel Deaconess Cancer Center, Harvard Medical School – name: 10 Department of Biochemistry, University of Utah – name: 2 Jonsson Comprehensive Cancer Center, UCLA – name: 13 UCLA Metabolomics Center, UCLA – name: 4 Molecular Biology Institute, UCLA – name: 9 Mork Family Department of Chemical Engineering, University of Southern California – name: 1 Department of Molecular Cell and Developmental Biology, UCLA – name: 14 Stanford School of Medicine, UCLA – name: 11 Howard Hughes Medical Institute – name: 12 Crump Institute for Molecular Imaging, UCLA – name: 5 Department of Biological Chemistry, UCLA – name: 6 Department of Molecular and Medical Pharmacology, UCLA – name: 8 Broad Center for Regenerative Medicine, University of Southern California – name: 3 Eli and Edythe Broad Center for Regenerative Medicine, UCLA |
| Author_xml | – sequence: 1 givenname: Aimee surname: Flores fullname: Flores, Aimee organization: Department of Molecular Cell and Developmental Biology, UCLA, Eli and Edythe Broad Center for Regenerative Medicine, UCLA, Molecular Biology Institute, UCLA – sequence: 2 givenname: John surname: Schell fullname: Schell, John organization: Department of Biochemistry, University of Utah – sequence: 3 givenname: Abigail S. surname: Krall fullname: Krall, Abigail S. organization: Department of Molecular and Medical Pharmacology, UCLA – sequence: 4 givenname: David surname: Jelinek fullname: Jelinek, David organization: Department of Molecular Cell and Developmental Biology, UCLA – sequence: 5 givenname: Matilde surname: Miranda fullname: Miranda, Matilde organization: Department of Molecular Cell and Developmental Biology, UCLA – sequence: 6 givenname: Melina surname: Grigorian fullname: Grigorian, Melina organization: Stanford School of Medicine – sequence: 7 givenname: Daniel surname: Braas fullname: Braas, Daniel organization: Department of Molecular and Medical Pharmacology, UCLA, UCLA Metabolomics Center, UCLA – sequence: 8 givenname: Andrew C. surname: White fullname: White, Andrew C. organization: School of Veterinary Medicine, Cornell University – sequence: 9 givenname: Jessica L. surname: Zhou fullname: Zhou, Jessica L. organization: Mork Family Department of Chemical Engineering, University of Southern California – sequence: 10 givenname: Nicholas A. surname: Graham fullname: Graham, Nicholas A. organization: Department of Molecular and Medical Pharmacology, UCLA, Mork Family Department of Chemical Engineering, University of Southern California – sequence: 11 givenname: Thomas surname: Graeber fullname: Graeber, Thomas organization: Department of Molecular and Medical Pharmacology, UCLA, Crump Institute for Molecular Imaging, UCLA – sequence: 12 givenname: Pankaj surname: Seth fullname: Seth, Pankaj organization: Division of Interdisciplinary Medicine and Biotechnology, Beth Israel Deaconess Cancer Center, Harvard Medical School – sequence: 13 givenname: Denis surname: Evseenko fullname: Evseenko, Denis organization: Broad Center for Regenerative Medicine, University of Southern California – sequence: 14 givenname: Hilary A. surname: Coller fullname: Coller, Hilary A. organization: Department of Molecular Cell and Developmental Biology, UCLA, Eli and Edythe Broad Center for Regenerative Medicine, UCLA, Molecular Biology Institute, UCLA, Jonsson Comprehensive Cancer Center, UCLA, Department of Biological Chemistry, UCLA – sequence: 15 givenname: Jared orcidid: 0000-0002-2710-9765 surname: Rutter fullname: Rutter, Jared organization: Department of Biochemistry, University of Utah, Howard Hughes Medical Institute – sequence: 16 givenname: Heather R. orcidid: 0000-0002-8662-4425 surname: Christofk fullname: Christofk, Heather R. email: HChristofk@mednet.ucla.edu organization: Eli and Edythe Broad Center for Regenerative Medicine, UCLA, Department of Molecular and Medical Pharmacology, UCLA, UCLA Metabolomics Center, UCLA, Jonsson Comprehensive Cancer Center, UCLA, Department of Biological Chemistry, UCLA – sequence: 17 givenname: William E. orcidid: 0000-0003-2932-2276 surname: Lowry fullname: Lowry, William E. email: blowry@ucla.edu organization: Department of Molecular Cell and Developmental Biology, UCLA, Eli and Edythe Broad Center for Regenerative Medicine, UCLA, Molecular Biology Institute, UCLA, Jonsson Comprehensive Cancer Center, UCLA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28812580$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | Springer Nature Limited 2017 COPYRIGHT 2017 Nature Publishing Group Copyright Nature Publishing Group Sep 2017 |
| Copyright_xml | – notice: Springer Nature Limited 2017 – notice: COPYRIGHT 2017 Nature Publishing Group – notice: Copyright Nature Publishing Group Sep 2017 |
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| Snippet | Although normally dormant, hair follicle stem cells (HFSCs) quickly become activated to divide during a new hair cycle. The quiescence of HFSCs is known to be... While normally dormant, Hair Follicle Stem Cells (HFSCs) quickly become activated to divide during a new hair cycle. The quiescence of HFSCs is known to be... |
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| SubjectTerms | 13 42 42/100 631/443/319 631/532/2438 631/532/2443 631/80/642/333 64 64/60 82 82/51 82/58 Acrylates - pharmacology Animals Anion Transport Proteins - antagonists & inhibitors Anion Transport Proteins - genetics Anion Transport Proteins - metabolism Cancer Research Cell activation Cell Biology Cell metabolism Cell Proliferation - drug effects Cellular Senescence - drug effects Clonal deletion Dehydrogenase Dehydrogenases Developmental Biology Epidermis Female Genetic aspects Genotype Glycolysis Glycolysis - drug effects Hair Hair Follicle - cytology Hair Follicle - drug effects Hair Follicle - enzymology Hair follicles Health aspects Isoenzymes - deficiency Isoenzymes - genetics Isoenzymes - metabolism L-Lactate dehydrogenase L-Lactate Dehydrogenase - deficiency L-Lactate Dehydrogenase - genetics L-Lactate Dehydrogenase - metabolism Lactate dehydrogenase Lactate Dehydrogenase 5 Lactic acid Lactic Acid - metabolism Life Sciences Male Metabolism Mice, Inbred C57BL Mice, Knockout Mitochondria Mitochondrial Membrane Transport Proteins - antagonists & inhibitors Mitochondrial Membrane Transport Proteins - genetics Mitochondrial Membrane Transport Proteins - metabolism Monocarboxylic Acid Transporters Myc protein Phenotype Proto-Oncogene Proteins c-myc - metabolism Pyruvic acid Signal Transduction Stem Cells Stem Cells - drug effects Stem Cells - enzymology Time Factors |
| Title | Lactate dehydrogenase activity drives hair follicle stem cell activation |
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