Regulation of endothelial cell proliferation and vascular assembly through distinct mTORC2 signaling pathways.
Identifieur interne : 000D19 ( Main/Corpus ); précédent : 000D18; suivant : 000D20Regulation of endothelial cell proliferation and vascular assembly through distinct mTORC2 signaling pathways.
Auteurs : Shan Wang ; Katherine R. Amato ; Wenqiang Song ; Victoria Youngblood ; Keunwook Lee ; Mark Boothby ; Dana M. Brantley-Sieders ; Jin ChenSource :
- Molecular and cellular biology [ 1098-5549 ] ; 2015.
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (genetics), Adaptor Proteins, Signal Transducing (metabolism), Animals (MeSH), Carrier Proteins (genetics), Carrier Proteins (metabolism), Cell Proliferation (MeSH), Cells, Cultured (MeSH), Endothelial Cells (cytology), Endothelial Cells (metabolism), Gene Deletion (MeSH), Human Umbilical Vein Endothelial Cells (MeSH), Humans (MeSH), Mechanistic Target of Rapamycin Complex 2 (MeSH), Mice (MeSH), Multiprotein Complexes (metabolism), Neovascularization, Physiologic (MeSH), Phosphorylation (MeSH), Protein Kinase C-alpha (metabolism), Proto-Oncogene Proteins c-akt (metabolism), Rapamycin-Insensitive Companion of mTOR Protein (MeSH), Regulatory-Associated Protein of mTOR (MeSH), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (metabolism), Vascular Endothelial Growth Factor A (metabolism).
- MESH :
- chemical , genetics : Adaptor Proteins, Signal Transducing, Carrier Proteins.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, Carrier Proteins, Multiprotein Complexes, Protein Kinase C-alpha, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases, Vascular Endothelial Growth Factor A.
- cytology : Endothelial Cells.
- metabolism : Endothelial Cells.
- Animals, Cell Proliferation, Cells, Cultured, Gene Deletion, Human Umbilical Vein Endothelial Cells, Humans, Mechanistic Target of Rapamycin Complex 2, Mice, Neovascularization, Physiologic, Phosphorylation, Rapamycin-Insensitive Companion of mTOR Protein, Regulatory-Associated Protein of mTOR, Signal Transduction.
Abstract
Mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates a diverse array of cellular processes, including cell growth, survival, metabolism, and cytoskeleton dynamics. mTOR functions in two distinct complexes, mTORC1 and mTORC2, whose activities and substrate specificities are regulated by complex specific cofactors, including Raptor and Rictor, respectively. Little is known regarding the relative contribution of mTORC1 versus mTORC2 in vascular endothelial cells. Using mouse models of Raptor or Rictor gene targeting, we discovered that Rictor ablation inhibited vascular endothelial growth factor (VEGF)-induced endothelial cell proliferation and assembly in vitro and angiogenesis in vivo, whereas the loss of Raptor had only a modest effect on endothelial cells (ECs). Mechanistically, the loss of Rictor reduced the phosphorylation of AKT, protein kinase Cα (PKCα), and NDRG1 without affecting the mTORC1 pathway. In contrast, the loss of Raptor increased the phosphorylation of AKT despite inhibiting the phosphorylation of S6K1, a direct target of mTORC1. Reconstitution of Rictor-null cells with myristoylated AKT (Myr-AKT) rescued vascular assembly in Rictor-deficient endothelial cells, whereas PKCα rescued proliferation defects. Furthermore, tumor neovascularization in vivo was significantly decreased upon EC-specific Rictor deletion in mice. These data indicate that mTORC2 is a critical signaling node required for VEGF-mediated angiogenesis through the regulation of AKT and PKCα in vascular endothelial cells.
DOI: 10.1128/MCB.00306-14
PubMed: 25582201
PubMed Central: PMC4355541
Links to Exploration step
pubmed:25582201Le document en format XML
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Amato</name><affiliation><nlm:affiliation>Department of Cancer Biology, Vanderbilt University, Nashville, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Song, Wenqiang" sort="Song, Wenqiang" uniqKey="Song W" first="Wenqiang" last="Song">Wenqiang Song</name><affiliation><nlm:affiliation>Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Youngblood, Victoria" sort="Youngblood, Victoria" uniqKey="Youngblood V" first="Victoria" last="Youngblood">Victoria Youngblood</name><affiliation><nlm:affiliation>Department of Cancer Biology, Vanderbilt University, Nashville, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Lee, Keunwook" sort="Lee, Keunwook" uniqKey="Lee K" first="Keunwook" last="Lee">Keunwook Lee</name><affiliation><nlm:affiliation>Department of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, Tennessee, USA Hallym University, Chuncheon, Gangwon-do, South Korea.</nlm:affiliation></affiliation></author><author><name sortKey="Boothby, Mark" sort="Boothby, Mark" uniqKey="Boothby M" first="Mark" last="Boothby">Mark Boothby</name><affiliation><nlm:affiliation>Department of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Brantley Sieders, Dana M" sort="Brantley Sieders, Dana M" uniqKey="Brantley Sieders D" first="Dana M" last="Brantley-Sieders">Dana M. Brantley-Sieders</name><affiliation><nlm:affiliation>Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Jin" sort="Chen, Jin" uniqKey="Chen J" first="Jin" last="Chen">Jin Chen</name><affiliation><nlm:affiliation>Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA Department of Cancer Biology, Vanderbilt University, Nashville, Tennessee, USA Department of Cell and Developmental Biology, Vanderbilt University, Nashville, Tennessee, USA Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, USA Veterans Affairs Medical Center, Tennessee Valley Healthcare System, Nashville, Tennessee, USA jin.chen@vanderbilt.edu.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:25582201</idno><idno type="pmid">25582201</idno><idno type="doi">10.1128/MCB.00306-14</idno><idno type="pmc">PMC4355541</idno><idno type="wicri:Area/Main/Corpus">000D19</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000D19</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Regulation of endothelial cell proliferation and vascular assembly through distinct mTORC2 signaling pathways.</title><author><name sortKey="Wang, Shan" sort="Wang, Shan" uniqKey="Wang S" first="Shan" last="Wang">Shan Wang</name><affiliation><nlm:affiliation>Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Amato, Katherine R" sort="Amato, Katherine R" uniqKey="Amato K" first="Katherine R" last="Amato">Katherine R. Amato</name><affiliation><nlm:affiliation>Department of Cancer Biology, Vanderbilt University, Nashville, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Song, Wenqiang" sort="Song, Wenqiang" uniqKey="Song W" first="Wenqiang" last="Song">Wenqiang Song</name><affiliation><nlm:affiliation>Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Youngblood, Victoria" sort="Youngblood, Victoria" uniqKey="Youngblood V" first="Victoria" last="Youngblood">Victoria Youngblood</name><affiliation><nlm:affiliation>Department of Cancer Biology, Vanderbilt University, Nashville, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Lee, Keunwook" sort="Lee, Keunwook" uniqKey="Lee K" first="Keunwook" last="Lee">Keunwook Lee</name><affiliation><nlm:affiliation>Department of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, Tennessee, USA Hallym University, Chuncheon, Gangwon-do, South Korea.</nlm:affiliation></affiliation></author><author><name sortKey="Boothby, Mark" sort="Boothby, Mark" uniqKey="Boothby M" first="Mark" last="Boothby">Mark Boothby</name><affiliation><nlm:affiliation>Department of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Brantley Sieders, Dana M" sort="Brantley Sieders, Dana M" uniqKey="Brantley Sieders D" first="Dana M" last="Brantley-Sieders">Dana M. Brantley-Sieders</name><affiliation><nlm:affiliation>Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Jin" sort="Chen, Jin" uniqKey="Chen J" first="Jin" last="Chen">Jin Chen</name><affiliation><nlm:affiliation>Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA Department of Cancer Biology, Vanderbilt University, Nashville, Tennessee, USA Department of Cell and Developmental Biology, Vanderbilt University, Nashville, Tennessee, USA Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, USA Veterans Affairs Medical Center, Tennessee Valley Healthcare System, Nashville, Tennessee, USA jin.chen@vanderbilt.edu.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Molecular and cellular biology</title><idno type="eISSN">1098-5549</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptor Proteins, Signal Transducing (genetics)</term><term>Adaptor Proteins, Signal Transducing (metabolism)</term><term>Animals (MeSH)</term><term>Carrier Proteins (genetics)</term><term>Carrier Proteins (metabolism)</term><term>Cell Proliferation (MeSH)</term><term>Cells, Cultured (MeSH)</term><term>Endothelial Cells (cytology)</term><term>Endothelial Cells (metabolism)</term><term>Gene Deletion (MeSH)</term><term>Human Umbilical Vein Endothelial Cells (MeSH)</term><term>Humans (MeSH)</term><term>Mechanistic Target of Rapamycin Complex 2 (MeSH)</term><term>Mice (MeSH)</term><term>Multiprotein Complexes (metabolism)</term><term>Neovascularization, Physiologic (MeSH)</term><term>Phosphorylation (MeSH)</term><term>Protein Kinase C-alpha (metabolism)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Rapamycin-Insensitive Companion of mTOR Protein (MeSH)</term><term>Regulatory-Associated Protein of mTOR (MeSH)</term><term>Signal Transduction (MeSH)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Vascular Endothelial Growth Factor A (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term><term>Carrier Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term><term>Carrier Proteins</term><term>Multiprotein Complexes</term><term>Protein Kinase C-alpha</term><term>Proto-Oncogene Proteins c-akt</term><term>TOR Serine-Threonine Kinases</term><term>Vascular Endothelial Growth Factor A</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelial Cells</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Proliferation</term><term>Cells, Cultured</term><term>Gene Deletion</term><term>Human Umbilical Vein Endothelial Cells</term><term>Humans</term><term>Mechanistic Target of Rapamycin Complex 2</term><term>Mice</term><term>Neovascularization, Physiologic</term><term>Phosphorylation</term><term>Rapamycin-Insensitive Companion of mTOR Protein</term><term>Regulatory-Associated Protein of mTOR</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates a diverse array of cellular processes, including cell growth, survival, metabolism, and cytoskeleton dynamics. mTOR functions in two distinct complexes, mTORC1 and mTORC2, whose activities and substrate specificities are regulated by complex specific cofactors, including Raptor and Rictor, respectively. Little is known regarding the relative contribution of mTORC1 versus mTORC2 in vascular endothelial cells. Using mouse models of Raptor or Rictor gene targeting, we discovered that Rictor ablation inhibited vascular endothelial growth factor (VEGF)-induced endothelial cell proliferation and assembly in vitro and angiogenesis in vivo, whereas the loss of Raptor had only a modest effect on endothelial cells (ECs). Mechanistically, the loss of Rictor reduced the phosphorylation of AKT, protein kinase Cα (PKCα), and NDRG1 without affecting the mTORC1 pathway. In contrast, the loss of Raptor increased the phosphorylation of AKT despite inhibiting the phosphorylation of S6K1, a direct target of mTORC1. Reconstitution of Rictor-null cells with myristoylated AKT (Myr-AKT) rescued vascular assembly in Rictor-deficient endothelial cells, whereas PKCα rescued proliferation defects. Furthermore, tumor neovascularization in vivo was significantly decreased upon EC-specific Rictor deletion in mice. These data indicate that mTORC2 is a critical signaling node required for VEGF-mediated angiogenesis through the regulation of AKT and PKCα in vascular endothelial cells. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25582201</PMID><DateCompleted><Year>2015</Year><Month>05</Month><Day>26</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5549</ISSN><JournalIssue CitedMedium="Internet"><Volume>35</Volume><Issue>7</Issue><PubDate><Year>2015</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Molecular and cellular biology</Title><ISOAbbreviation>Mol Cell Biol</ISOAbbreviation></Journal><ArticleTitle>Regulation of endothelial cell proliferation and vascular assembly through distinct mTORC2 signaling pathways.</ArticleTitle><Pagination><MedlinePgn>1299-313</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/MCB.00306-14</ELocationID><Abstract><AbstractText>Mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates a diverse array of cellular processes, including cell growth, survival, metabolism, and cytoskeleton dynamics. mTOR functions in two distinct complexes, mTORC1 and mTORC2, whose activities and substrate specificities are regulated by complex specific cofactors, including Raptor and Rictor, respectively. Little is known regarding the relative contribution of mTORC1 versus mTORC2 in vascular endothelial cells. Using mouse models of Raptor or Rictor gene targeting, we discovered that Rictor ablation inhibited vascular endothelial growth factor (VEGF)-induced endothelial cell proliferation and assembly in vitro and angiogenesis in vivo, whereas the loss of Raptor had only a modest effect on endothelial cells (ECs). Mechanistically, the loss of Rictor reduced the phosphorylation of AKT, protein kinase Cα (PKCα), and NDRG1 without affecting the mTORC1 pathway. In contrast, the loss of Raptor increased the phosphorylation of AKT despite inhibiting the phosphorylation of S6K1, a direct target of mTORC1. Reconstitution of Rictor-null cells with myristoylated AKT (Myr-AKT) rescued vascular assembly in Rictor-deficient endothelial cells, whereas PKCα rescued proliferation defects. Furthermore, tumor neovascularization in vivo was significantly decreased upon EC-specific Rictor deletion in mice. These data indicate that mTORC2 is a critical signaling node required for VEGF-mediated angiogenesis through the regulation of AKT and PKCα in vascular endothelial cells. </AbstractText><CopyrightInformation>Copyright © 2015, American Society for Microbiology. All Rights Reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Shan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Amato</LastName><ForeName>Katherine R</ForeName><Initials>KR</Initials><AffiliationInfo><Affiliation>Department of Cancer Biology, Vanderbilt University, Nashville, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Wenqiang</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Youngblood</LastName><ForeName>Victoria</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Cancer Biology, Vanderbilt University, Nashville, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Keunwook</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, Tennessee, USA Hallym University, Chuncheon, Gangwon-do, South Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boothby</LastName><ForeName>Mark</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brantley-Sieders</LastName><ForeName>Dana M</ForeName><Initials>DM</Initials><AffiliationInfo><Affiliation>Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Jin</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA Department of Cancer Biology, Vanderbilt University, Nashville, Tennessee, USA Department of Cell and Developmental Biology, Vanderbilt University, Nashville, Tennessee, USA Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, USA Veterans Affairs Medical Center, Tennessee Valley Healthcare System, Nashville, Tennessee, USA jin.chen@vanderbilt.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>CA177681</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA095004</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>I01 BX000134</GrantID><Acronym>BX</Acronym><Agency>BLRD VA</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 CA068485</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA177681</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 CA009592</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA148934</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA95004</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL106812</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>CA148934</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>01</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Cell Biol</MedlineTA><NlmUniqueID>8109087</NlmUniqueID><ISSNLinking>0270-7306</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D048868">Adaptor Proteins, Signal Transducing</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002352">Carrier 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