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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<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>
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<term>Carrier Proteins</term>
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<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>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term>
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<term>Human Umbilical Vein Endothelial Cells</term>
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<term>Mechanistic Target of Rapamycin Complex 2</term>
<term>Mice</term>
<term>Neovascularization, Physiologic</term>
<term>Phosphorylation</term>
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<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>
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<Title>Molecular and cellular biology</Title>
<ISOAbbreviation>Mol Cell Biol</ISOAbbreviation>
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<ArticleTitle>Regulation of endothelial cell proliferation and vascular assembly through distinct mTORC2 signaling pathways.</ArticleTitle>
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<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>
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<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>
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<ForeName>Wenqiang</ForeName>
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<AffiliationInfo><Affiliation>Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA.</Affiliation>
</AffiliationInfo>
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<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>
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</AffiliationInfo>
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<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>
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<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Jin</ForeName>
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<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>
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