Vascular endothelial growth factor-C enhances radiosensitivity of lymphatic endothelial cells.
Identifieur interne : 001853 ( PubMed/Curation ); précédent : 001852; suivant : 001854Vascular endothelial growth factor-C enhances radiosensitivity of lymphatic endothelial cells.
Auteurs : Cristina T. Kesler [États-Unis] ; Angera H. Kuo ; Hon-Kit Wong ; David J. Masuck ; Jennifer L. Shah ; Kevin R. Kozak ; Kathryn D. Held ; Timothy P. PaderaSource :
- Angiogenesis [ 1573-7209 ] ; 2014.
Descripteurs français
- KwdFr :
- Adulte, Agents protecteurs (pharmacologie), Altération de l'ADN, Apoptose (), Cellules endothéliales (), Cellules endothéliales (métabolisme), Cycle cellulaire (), Facteur de croissance endothéliale vasculaire de type C (pharmacologie), Humains, Lymphangiogenèse (), Radiotolérance (), Survie cellulaire ().
- MESH :
English descriptors
- KwdEn :
- Adult, Apoptosis (drug effects), Cell Cycle (drug effects), Cell Survival (drug effects), DNA Damage, Endothelial Cells (drug effects), Endothelial Cells (metabolism), Humans, Lymphangiogenesis (drug effects), Protective Agents (pharmacology), Radiation Tolerance (drug effects), Vascular Endothelial Growth Factor C (pharmacology).
- MESH :
- chemical , pharmacology : Protective Agents, Vascular Endothelial Growth Factor C.
- drug effects : Apoptosis, Cell Cycle, Cell Survival, Endothelial Cells, Lymphangiogenesis, Radiation Tolerance.
- metabolism : Endothelial Cells.
- Adult, DNA Damage, Humans.
Abstract
Radiation therapy after lymph node dissection increases the risk of developing painful and incurable lymphedema in breast cancer patients. Lymphedema occurs when lymphatic vessels become unable to maintain proper fluid balance. The sensitivity of lymphatic endothelial cells (LECs) to ionizing radiation has not been reported to date. Here, the radiosensitivity of LECs in vitro has been determined using clonogenic survival assays. The ability of various growth factors to alter LEC radiosensitivity was also examined. Vascular endothelial growth factor (VEGF)-C enhanced radiosensitivity when LECs were treated prior to radiation. VEGF-C-treated LECs exhibited higher levels of entry into the cell cycle at the time of radiation, with a greater number of cells in the S and G2/M phases. These LECs showed higher levels of γH2A.X-an indicator of DNA damage-after radiation. VEGF-C did not increase cell death as a result of radiation. Instead, it increased the relative number of quiescent LECs. These data suggest that abundant VEGF-C or lymphangiogenesis may predispose patients to radiation-induced lymphedema by impairing lymphatic vessel repair through induction of LEC quiescence.
DOI: 10.1007/s10456-013-9400-7
PubMed: 24201897
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Kuo</name></author><author><name sortKey="Wong, Hon Kit" sort="Wong, Hon Kit" uniqKey="Wong H" first="Hon-Kit" last="Wong">Hon-Kit Wong</name></author><author><name sortKey="Masuck, David J" sort="Masuck, David J" uniqKey="Masuck D" first="David J" last="Masuck">David J. Masuck</name></author><author><name sortKey="Shah, Jennifer L" sort="Shah, Jennifer L" uniqKey="Shah J" first="Jennifer L" last="Shah">Jennifer L. Shah</name></author><author><name sortKey="Kozak, Kevin R" sort="Kozak, Kevin R" uniqKey="Kozak K" first="Kevin R" last="Kozak">Kevin R. Kozak</name></author><author><name sortKey="Held, Kathryn D" sort="Held, Kathryn D" uniqKey="Held K" first="Kathryn D" last="Held">Kathryn D. Held</name></author><author><name sortKey="Padera, Timothy P" sort="Padera, Timothy P" uniqKey="Padera T" first="Timothy P" last="Padera">Timothy P. 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Kesler</name><affiliation wicri:level="1"><nlm:affiliation>Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Cox-7, 100 Blossom St., Boston, MA, 02114, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Cox-7, 100 Blossom St., Boston, MA, 02114</wicri:regionArea></affiliation></author><author><name sortKey="Kuo, Angera H" sort="Kuo, Angera H" uniqKey="Kuo A" first="Angera H" last="Kuo">Angera H. Kuo</name></author><author><name sortKey="Wong, Hon Kit" sort="Wong, Hon Kit" uniqKey="Wong H" first="Hon-Kit" last="Wong">Hon-Kit Wong</name></author><author><name sortKey="Masuck, David J" sort="Masuck, David J" uniqKey="Masuck D" first="David J" last="Masuck">David J. Masuck</name></author><author><name sortKey="Shah, Jennifer L" sort="Shah, Jennifer L" uniqKey="Shah J" first="Jennifer L" last="Shah">Jennifer L. Shah</name></author><author><name sortKey="Kozak, Kevin R" sort="Kozak, Kevin R" uniqKey="Kozak K" first="Kevin R" last="Kozak">Kevin R. Kozak</name></author><author><name sortKey="Held, Kathryn D" sort="Held, Kathryn D" uniqKey="Held K" first="Kathryn D" last="Held">Kathryn D. Held</name></author><author><name sortKey="Padera, Timothy P" sort="Padera, Timothy P" uniqKey="Padera T" first="Timothy P" last="Padera">Timothy P. Padera</name></author></analytic><series><title level="j">Angiogenesis</title><idno type="eISSN">1573-7209</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Apoptosis (drug effects)</term><term>Cell Cycle (drug effects)</term><term>Cell Survival (drug effects)</term><term>DNA Damage</term><term>Endothelial Cells (drug effects)</term><term>Endothelial Cells (metabolism)</term><term>Humans</term><term>Lymphangiogenesis (drug effects)</term><term>Protective Agents (pharmacology)</term><term>Radiation Tolerance (drug effects)</term><term>Vascular Endothelial Growth Factor C (pharmacology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte</term><term>Agents protecteurs (pharmacologie)</term><term>Altération de l'ADN</term><term>Apoptose ()</term><term>Cellules endothéliales ()</term><term>Cellules endothéliales (métabolisme)</term><term>Cycle cellulaire ()</term><term>Facteur de croissance endothéliale vasculaire de type C (pharmacologie)</term><term>Humains</term><term>Lymphangiogenèse ()</term><term>Radiotolérance ()</term><term>Survie cellulaire ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Protective Agents</term><term>Vascular Endothelial Growth Factor C</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Cell Cycle</term><term>Cell Survival</term><term>Endothelial Cells</term><term>Lymphangiogenesis</term><term>Radiation Tolerance</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules endothéliales</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Agents protecteurs</term><term>Facteur de croissance endothéliale vasculaire de type C</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>DNA Damage</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Altération de l'ADN</term><term>Apoptose</term><term>Cellules endothéliales</term><term>Cycle cellulaire</term><term>Humains</term><term>Lymphangiogenèse</term><term>Radiotolérance</term><term>Survie cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Radiation therapy after lymph node dissection increases the risk of developing painful and incurable lymphedema in breast cancer patients. Lymphedema occurs when lymphatic vessels become unable to maintain proper fluid balance. The sensitivity of lymphatic endothelial cells (LECs) to ionizing radiation has not been reported to date. Here, the radiosensitivity of LECs in vitro has been determined using clonogenic survival assays. The ability of various growth factors to alter LEC radiosensitivity was also examined. Vascular endothelial growth factor (VEGF)-C enhanced radiosensitivity when LECs were treated prior to radiation. VEGF-C-treated LECs exhibited higher levels of entry into the cell cycle at the time of radiation, with a greater number of cells in the S and G2/M phases. These LECs showed higher levels of γH2A.X-an indicator of DNA damage-after radiation. VEGF-C did not increase cell death as a result of radiation. Instead, it increased the relative number of quiescent LECs. These data suggest that abundant VEGF-C or lymphangiogenesis may predispose patients to radiation-induced lymphedema by impairing lymphatic vessel repair through induction of LEC quiescence.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24201897</PMID><DateCreated><Year>2014</Year><Month>04</Month><Day>08</Day></DateCreated><DateCompleted><Year>2014</Year><Month>11</Month><Day>26</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1573-7209</ISSN><JournalIssue CitedMedium="Internet"><Volume>17</Volume><Issue>2</Issue><PubDate><Year>2014</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Angiogenesis</Title><ISOAbbreviation>Angiogenesis</ISOAbbreviation></Journal><ArticleTitle>Vascular endothelial growth factor-C enhances radiosensitivity of lymphatic endothelial cells.</ArticleTitle><Pagination><MedlinePgn>419-27</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s10456-013-9400-7</ELocationID><Abstract><AbstractText>Radiation therapy after lymph node dissection increases the risk of developing painful and incurable lymphedema in breast cancer patients. Lymphedema occurs when lymphatic vessels become unable to maintain proper fluid balance. The sensitivity of lymphatic endothelial cells (LECs) to ionizing radiation has not been reported to date. Here, the radiosensitivity of LECs in vitro has been determined using clonogenic survival assays. The ability of various growth factors to alter LEC radiosensitivity was also examined. Vascular endothelial growth factor (VEGF)-C enhanced radiosensitivity when LECs were treated prior to radiation. VEGF-C-treated LECs exhibited higher levels of entry into the cell cycle at the time of radiation, with a greater number of cells in the S and G2/M phases. These LECs showed higher levels of γH2A.X-an indicator of DNA damage-after radiation. VEGF-C did not increase cell death as a result of radiation. Instead, it increased the relative number of quiescent LECs. These data suggest that abundant VEGF-C or lymphangiogenesis may predispose patients to radiation-induced lymphedema by impairing lymphatic vessel repair through induction of LEC quiescence.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kesler</LastName><ForeName>Cristina T</ForeName><Initials>CT</Initials><AffiliationInfo><Affiliation>Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Cox-7, 100 Blossom St., Boston, MA, 02114, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kuo</LastName><ForeName>Angera H</ForeName><Initials>AH</Initials></Author><Author ValidYN="Y"><LastName>Wong</LastName><ForeName>Hon-Kit</ForeName><Initials>HK</Initials></Author><Author ValidYN="Y"><LastName>Masuck</LastName><ForeName>David J</ForeName><Initials>DJ</Initials></Author><Author ValidYN="Y"><LastName>Shah</LastName><ForeName>Jennifer L</ForeName><Initials>JL</Initials></Author><Author ValidYN="Y"><LastName>Kozak</LastName><ForeName>Kevin R</ForeName><Initials>KR</Initials></Author><Author ValidYN="Y"><LastName>Held</LastName><ForeName>Kathryn D</ForeName><Initials>KD</Initials></Author><Author ValidYN="Y"><LastName>Padera</LastName><ForeName>Timothy P</ForeName><Initials>TP</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>UL1 TR000427</GrantID><Acronym>TR</Acronym><Agency>NCATS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R00CA137167</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R00 CA137167</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>C06 CA059267</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>DP2OD008780</GrantID><Acronym>OD</Acronym><Agency>NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>DP2 OD008780</GrantID><Acronym>OD</Acronym><Agency>NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K99 CA137167</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>2013</Year><Month>11</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Angiogenesis</MedlineTA><NlmUniqueID>9814575</NlmUniqueID><ISSNLinking>0969-6970</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020011">Protective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042582">Vascular Endothelial Growth Factor C</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8868-73</RefSource><PMID Version="1">12070340</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 2002 Jun 7;296(5574):1811-2</RefSource><PMID Version="1">12052939</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cold Spring Harb Symp Quant Biol. 2002;67:227-37</RefSource><PMID Version="1">12858545</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Immunol. 2004 Jan;5(1):74-80</RefSource><PMID Version="1">14634646</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Surg Oncol. 2004 Jun;11(6):573-80</RefSource><PMID Version="1">15172932</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Radiat Res. 1986 May;106(2):182-9</RefSource><PMID 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RefType="Cites"><RefSource>Cancer Res. 2003 Jul 1;63(13):3755-63</RefSource><PMID Version="1">12839971</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002453" MajorTopicYN="N">Cell Cycle</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004249" MajorTopicYN="N">DNA Damage</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020011" MajorTopicYN="N">Protective Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011836" MajorTopicYN="N">Radiation Tolerance</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042582" MajorTopicYN="N">Vascular Endothelial Growth Factor C</DescriptorName><QualifierName UI="Q000494" 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