Effect of Hypoxic Stress–Activated Polo-like Kinase 3 on Corneal Epithelial Wound Healing
Identifieur interne : 000132 ( Ncbi/Merge ); précédent : 000131; suivant : 000133Effect of Hypoxic Stress–Activated Polo-like Kinase 3 on Corneal Epithelial Wound Healing
Auteurs : Jiawei Lu ; Ling Wang ; Wei Dai ; Luo LuSource :
- Investigative Ophthalmology & Visual Science [ 0146-0404 ] ; 2010.
Abstract
Oxidative stress can affect the process of corneal epithelial wound healing. In the present study, the authors provide a new mechanism involving a hypoxic stress–activated Polo-like kinase 3 (Plk3) in the signaling pathway to elicit activation of the AP-1 transcriptional complex, affecting corneal epithelial wound healing. Removing the Plk3 gene from the mouse eye resulted in a significantly accelerated rate of corneal epithelial wound healing in the absence and presence of hypoxic stress, suggesting that Plk3 plays an important role in mediating oxidative stress–induced delay of corneal epithelial wound healing.
Url:
DOI: 10.1167/iovs.10-5501
PubMed: 20505196
PubMed Central: 3066615
Links toward previous steps (curation, corpus...)
- to stream Pmc, to step Corpus: 000309
- to stream Pmc, to step Curation: 000308
- to stream Pmc, to step Checkpoint: 000307
Links to Exploration step
PMC:3066615Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Effect of Hypoxic Stress–Activated Polo-like Kinase 3 on Corneal Epithelial Wound Healing</title><author><name sortKey="Lu, Jiawei" sort="Lu, Jiawei" uniqKey="Lu J" first="Jiawei" last="Lu">Jiawei Lu</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Wang, Ling" sort="Wang, Ling" uniqKey="Wang L" first="Ling" last="Wang">Ling Wang</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Dai, Wei" sort="Dai, Wei" uniqKey="Dai W" first="Wei" last="Dai">Wei Dai</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author><author><name sortKey="Lu, Luo" sort="Lu, Luo" uniqKey="Lu L" first="Luo" last="Lu">Luo Lu</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">20505196</idno><idno type="pmc">3066615</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3066615</idno><idno type="RBID">PMC:3066615</idno><idno type="doi">10.1167/iovs.10-5501</idno><date when="2010">2010</date><idno type="wicri:Area/Pmc/Corpus">000309</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000309</idno><idno type="wicri:Area/Pmc/Curation">000308</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000308</idno><idno type="wicri:Area/Pmc/Checkpoint">000307</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000307</idno><idno type="wicri:Area/Ncbi/Merge">000132</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Effect of Hypoxic Stress–Activated Polo-like Kinase 3 on Corneal Epithelial Wound Healing</title><author><name sortKey="Lu, Jiawei" sort="Lu, Jiawei" uniqKey="Lu J" first="Jiawei" last="Lu">Jiawei Lu</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Wang, Ling" sort="Wang, Ling" uniqKey="Wang L" first="Ling" last="Wang">Ling Wang</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Dai, Wei" sort="Dai, Wei" uniqKey="Dai W" first="Wei" last="Dai">Wei Dai</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author><author><name sortKey="Lu, Luo" sort="Lu, Luo" uniqKey="Lu L" first="Luo" last="Lu">Luo Lu</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">Investigative Ophthalmology & Visual Science</title><idno type="ISSN">0146-0404</idno><idno type="eISSN">1552-5783</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Oxidative stress can affect the process of corneal epithelial wound healing. In the present study, the authors provide a new mechanism involving a hypoxic stress–activated Polo-like kinase 3 (Plk3) in the signaling pathway to elicit activation of the AP-1 transcriptional complex, affecting corneal epithelial wound healing. Removing the Plk3 gene from the mouse eye resulted in a significantly accelerated rate of corneal epithelial wound healing in the absence and presence of hypoxic stress, suggesting that Plk3 plays an important role in mediating oxidative stress–induced delay of corneal epithelial wound healing.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Invest Ophthalmol Vis Sci</journal-id><journal-id journal-id-type="hwp">iovs</journal-id><journal-id journal-id-type="pmc">iovs</journal-id><journal-id journal-id-type="publisher-id">IOVS</journal-id><journal-title-group><journal-title>Investigative Ophthalmology & Visual Science</journal-title></journal-title-group><issn pub-type="ppub">0146-0404</issn><issn pub-type="epub">1552-5783</issn><publisher><publisher-name>Association for Research in Vision and Ophthalmology, Inc.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">20505196</article-id><article-id pub-id-type="pmc">3066615</article-id><article-id pub-id-type="publisher-id">10-5501</article-id><article-id pub-id-type="doi">10.1167/iovs.10-5501</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject><subj-group><subject>Cornea</subject></subj-group></subj-group></article-categories><title-group><article-title>Effect of Hypoxic Stress–Activated Polo-like Kinase 3 on Corneal Epithelial Wound Healing</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Lu</surname><given-names>Jiawei</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="author-notes" rid="FN1"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Ling</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="author-notes" rid="FN1"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Dai</surname><given-names>Wei</given-names></name><xref ref-type="aff" rid="aff2"><sup>3</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Lu</surname><given-names>Luo</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><aff id="aff1">From the<label>1</label>Division of Molecular Medicine, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Torrance, California; and</aff><aff id="aff2">the<label>3</label>Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York.</aff></contrib-group><author-notes><corresp>Corresponding author: Luo Lu, <addr-line>Department of Medicine, David Geffen School of Medicine at UCLA, 1124 W. Carson Street, H-H Building, Torrance, CA 90502</addr-line>; <email>lluou@ucla.edu</email>.</corresp><fn id="FN1" fn-type="equal"><label>2</label><p>These authors contributed equally to the work presented here and should therefore be regarded as equivalent authors.</p></fn></author-notes><pub-date pub-type="ppub"><month>10</month><year>2010</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>4</month><year>2011</year></pub-date><pmc-comment> PMC Release delay is 6 months and 0 days and was based on the
<volume>51</volume><issue>10</issue><fpage>5034</fpage><lpage>5040</lpage><history><date date-type="received"><day>9</day><month>3</month><year>2010</year></date><date date-type="rev-recd"><day>15</day><month>4</month><year>2010</year></date><date date-type="accepted"><day>10</day><month>5</month><year>2010</year></date></history><permissions><copyright-statement>Copyright © Association for Research in Vision and Ophthalmology</copyright-statement></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="z7g01010005034.pdf"></self-uri><abstract abstract-type="precis"><p>Oxidative stress can affect the process of corneal epithelial wound healing. In the present study, the authors provide a new mechanism involving a hypoxic stress–activated Polo-like kinase 3 (Plk3) in the signaling pathway to elicit activation of the AP-1 transcriptional complex, affecting corneal epithelial wound healing. Removing the Plk3 gene from the mouse eye resulted in a significantly accelerated rate of corneal epithelial wound healing in the absence and presence of hypoxic stress, suggesting that Plk3 plays an important role in mediating oxidative stress–induced delay of corneal epithelial wound healing.</p></abstract><abstract><sec><title>Purpose.</title><p>Hypoxia/reoxygenation conditions can generate oxidative stresses resulting in the suppression of cell proliferation and the delay of corneal epithelial wound healing. The purpose of this study was to investigate the cellular mechanism involving the role of the stress-responsive Polo-like kinase 3 (Plk3) in hypoxic stress–induced delay of corneal epithelial wound healing.</p></sec><sec><title>Methods.</title><p>Plk3 activities were determined by immunochemistry and immunocomplex kinase assay approaches. Corneal epithelial wound healing was evaluated by a whole-eye organ culture model and by scratch-induced wound closure assay. Corneal epithelial layer was removed by using a corneal rust-ring-remover in wild-type and Plk3<sup>−/−</sup> mice. Wound healing was analyzed using a confocal imaging system. Cell growth was measured by MTT assays.</p></sec><sec><title>Results.</title><p>The effect of hypoxic stress on early stages of corneal epithelial wound healing was compared with other oxidative stresses, including UV, CoCl<sub>2</sub>, and H<sub>2</sub>O<sub>2</sub> treatments. Hypoxic stress–induced delay of corneal epithelial wound healing was further evaluated in human corneal epithelial cells and in the corneas of wild-type and Plk3 knockout (Plk3<sup>−/−</sup>) mice. Hypoxic stress–induced Plk3 activation resulted in growth attenuation and delay of wound healing. Further evidence demonstrated that the increase in Plk3 activity in constitutively active Plk3-expressed cells significantly enhanced stress-induced delay of wound healing. In contrast, hypoxic stress–induced delay of wound healing was markedly diminished in the corneas of Plk3 deficient Plk3<sup>−/−</sup> mice.</p></sec><sec><title>Conclusions.</title><p>These results provide for the first time important evidence that Plk3 plays a significant role in hypoxic stress–induced attenuation of cell growth and delay of corneal epithelial wound healing.</p></sec></abstract><funding-group><award-group><funding-source id="CS100">National Institutes of Health</funding-source><award-id rid="CS100">EY15282</award-id><award-id rid="CS100">CA074229</award-id></award-group></funding-group></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Dai, Wei" sort="Dai, Wei" uniqKey="Dai W" first="Wei" last="Dai">Wei Dai</name><name sortKey="Lu, Jiawei" sort="Lu, Jiawei" uniqKey="Lu J" first="Jiawei" last="Lu">Jiawei Lu</name><name sortKey="Lu, Luo" sort="Lu, Luo" uniqKey="Lu L" first="Luo" last="Lu">Luo Lu</name><name sortKey="Wang, Ling" sort="Wang, Ling" uniqKey="Wang L" first="Ling" last="Wang">Ling Wang</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Terre/explor/CobaltMaghrebV1/Data/Ncbi/Merge
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000132 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd -nk 000132 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Terre
|area= CobaltMaghrebV1
|flux= Ncbi
|étape= Merge
|type= RBID
|clé= PMC:3066615
|texte= Effect of Hypoxic Stress–Activated Polo-like Kinase 3 on Corneal Epithelial Wound Healing
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Ncbi/Merge/RBID.i -Sk "pubmed:20505196" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd \
| NlmPubMed2Wicri -a CobaltMaghrebV1
| This area was generated with Dilib version V0.6.32. |  |