LymphedemaV1, Ncbi, Merge, bibRecord, 005F03

Vascular endothelial growth factor-C enhances radiosensitivity of lymphatic endothelial cells

Identifieur interne : 005F03 ( Ncbi/Merge ); précédent : 005F02; suivant : 005F04

Vascular endothelial growth factor-C enhances radiosensitivity of lymphatic endothelial cells

Auteurs : Cristina T. Kesler [États-Unis] ; Angera Kuo [États-Unis] ; Hon-Kit Wong [États-Unis] ; David J. Masuck [États-Unis] ; Jennifer L. Shah [États-Unis] ; Kevin Kozak [États-Unis] ; Kathryn D. Held [États-Unis] ; Timothy P. Padera [États-Unis]

Source :

Angiogenesis [ 0969-6970 ] ; 2013.

RBID : PMC:3981926

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 :
- métabolisme : Cellules endothéliales.
- pharmacologie : Agents protecteurs, Facteur de croissance endothéliale vasculaire de type C.
- Adulte, Altération de l'ADN, Apoptose, Cellules endothéliales, Cycle cellulaire, Humains, Lymphangiogenèse, Radiotolérance, Survie cellulaire.

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 H2A.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.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3981926

DOI: 10.1007/s10456-013-9400-7
PubMed: 24201897
PubMed Central: 3981926

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PMC:3981926

Le document en format XML

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<term>Facteur de croissance endothéliale vasculaire de type C (pharmacologie)</term>
<term>Humains</term>
<term>Lymphangiogenèse ()</term>
<term>Radiotolérance ()</term>
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<front><div type="abstract" xml:lang="en"><p id="P1">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 <italic>in vitro</italic>
 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 H2A.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.</p>
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<affiliation wicri:level="1"><nlm:aff id="A1">Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA</wicri:regionArea>
<wicri:noRegion>MA</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Masuck, David J" sort="Masuck, David J" uniqKey="Masuck D" first="David J." last="Masuck">David J. Masuck</name>
<affiliation wicri:level="1"><nlm:aff id="A1">Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA</wicri:regionArea>
<wicri:noRegion>MA</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Shah, Jennifer L" sort="Shah, Jennifer L" uniqKey="Shah J" first="Jennifer L." last="Shah">Jennifer L. Shah</name>
<affiliation wicri:level="1"><nlm:aff id="A1">Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA</wicri:regionArea>
<wicri:noRegion>MA</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Kozak, Kevin" sort="Kozak, Kevin" uniqKey="Kozak K" first="Kevin" last="Kozak">Kevin Kozak</name>
<affiliation wicri:level="1"><nlm:aff id="A1">Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA</wicri:regionArea>
<wicri:noRegion>MA</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Held, Kathryn D" sort="Held, Kathryn D" uniqKey="Held K" first="Kathryn D." last="Held">Kathryn D. Held</name>
<affiliation wicri:level="1"><nlm:aff id="A1">Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA</wicri:regionArea>
<wicri:noRegion>MA</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Padera, Timothy P" sort="Padera, Timothy P" uniqKey="Padera T" first="Timothy P." last="Padera">Timothy P. Padera</name>
<affiliation wicri:level="1"><nlm:aff id="A1">Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA</wicri:regionArea>
<wicri:noRegion>MA</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series><title level="j">Angiogenesis</title>
<idno type="ISSN">0969-6970</idno>
<idno type="eISSN">1573-7209</idno>
<imprint><date when="2013">2013</date>
</imprint>
</series>
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<front><div type="abstract" xml:lang="en"><p id="P1">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 <italic>in vitro</italic>
 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 H2A.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.</p>
</div>
</front>
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<pubmed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Vascular endothelial growth factor-C enhances radiosensitivity of lymphatic endothelial cells.</title>
<author><name sortKey="Kesler, Cristina T" sort="Kesler, Cristina T" uniqKey="Kesler C" first="Cristina T" last="Kesler">Cristina T. 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>
<wicri:noRegion>02114</wicri:noRegion>
</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>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2014">2014</date>
<idno type="RBID">pubmed:24201897</idno>
<idno type="pmid">24201897</idno>
<idno type="doi">10.1007/s10456-013-9400-7</idno>
<idno type="wicri:Area/PubMed/Corpus">001853</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001853</idno>
<idno type="wicri:Area/PubMed/Curation">001853</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001853</idno>
<idno type="wicri:Area/PubMed/Checkpoint">001853</idno>
<idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001853</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Vascular endothelial growth factor-C enhances radiosensitivity of lymphatic endothelial cells.</title>
<author><name sortKey="Kesler, Cristina T" sort="Kesler, Cristina T" uniqKey="Kesler C" first="Cristina T" last="Kesler">Cristina T. 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>
<wicri:noRegion>02114</wicri:noRegion>
</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>
</double>
</record>

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Vascular endothelial growth factor-C enhances radiosensitivity of lymphatic endothelial cells

Vascular endothelial growth factor-C enhances radiosensitivity of lymphatic endothelial cells

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