Extended stability of cyclin D1 contributes to limited cell cycle arrest at G1-phase in BHK-21 cells with Japanese encephalitis virus persistent infection
Identifieur interne : 000278 ( Pmc/Corpus ); précédent : 000277; suivant : 000279Extended stability of cyclin D1 contributes to limited cell cycle arrest at G1-phase in BHK-21 cells with Japanese encephalitis virus persistent infection
Auteurs : Ji Young Kim ; Soo Young Park ; Hey Rhyoung Lyoo ; Eung Seo Koo ; Man Su Kim ; Yong Seok JeongSource :
- Journal of Microbiology (Seoul, Korea) [ 1225-8873 ] ; 2015.
Abstract
There is increasing evidence that many RNA viruses manipulate cell cycle control to achieve favorable cellular environments for their efficient replication during infection. Although virus-induced G0/G1 arrest often delays early apoptosis temporarily, a prolonged replication of the infected virus leads host cells to eventual death. In contrast, most mammalian cells with RNA virus persistent infection often escape cytolysis in the presence of productive viral replication. In this study, we demonstrated that the extended endurance of cyclin D1 was clearly associated with the suppression of glycogen synthase kinase-3ß (GSK-3ß) expression in BHK-21 cells that are persistently infected with Japanese encephalitis virus (JEV). The G0/G1 arrest of these cells turned much loose compared to the normal BHK-21 cells with JEV acute infection. After cycloheximide treatment, cyclin D1 in the persistently infected cells lasted several hours longer than those in acutely infected cells. Furthermore, both p21Cip1 and p27Kip1, positive regulators for cyclin D1 accumulation in the nucleus, were suppressed in their expression, which contrasts with those in JEV acute infection. Inhibition of the GSK-3ß by lithium chloride treatment rescued a significant number of cells from cytolysis in JEV acute infection, which coincided with the levels of cyclin D1 that escaped from proteolysis. Therefore, the limitation of G1/S arrest in the BHK-21 cells with JEV persistent infection is associated with the suppression of GSK-3ß expression, resulting in the extended duration of cyclin D1.
Url:
DOI: 10.1007/s12275-015-4661-z
PubMed: 25557483
PubMed Central: 7090764
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PMC:7090764Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Extended stability of cyclin D1 contributes to limited cell cycle arrest at G1-phase in BHK-21 cells with Japanese encephalitis virus persistent infection</title><author><name sortKey="Kim, Ji Young" sort="Kim, Ji Young" uniqKey="Kim J" first="Ji Young" last="Kim">Ji Young Kim</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Park, Soo Young" sort="Park, Soo Young" uniqKey="Park S" first="Soo Young" last="Park">Soo Young Park</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Lyoo, Hey Rhyoung" sort="Lyoo, Hey Rhyoung" uniqKey="Lyoo H" first="Hey Rhyoung" last="Lyoo">Hey Rhyoung Lyoo</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Koo, Eung Seo" sort="Koo, Eung Seo" uniqKey="Koo E" first="Eung Seo" last="Koo">Eung Seo Koo</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Kim, Man Su" sort="Kim, Man Su" uniqKey="Kim M" first="Man Su" last="Kim">Man Su Kim</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Jeong, Yong Seok" sort="Jeong, Yong Seok" uniqKey="Jeong Y" first="Yong Seok" last="Jeong">Yong Seok Jeong</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">25557483</idno><idno type="pmc">7090764</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7090764</idno><idno type="RBID">PMC:7090764</idno><idno type="doi">10.1007/s12275-015-4661-z</idno><date when="2015">2015</date><idno type="wicri:Area/Pmc/Corpus">000278</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000278</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Extended stability of cyclin D1 contributes to limited cell cycle arrest at G1-phase in BHK-21 cells with Japanese encephalitis virus persistent infection</title><author><name sortKey="Kim, Ji Young" sort="Kim, Ji Young" uniqKey="Kim J" first="Ji Young" last="Kim">Ji Young Kim</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Park, Soo Young" sort="Park, Soo Young" uniqKey="Park S" first="Soo Young" last="Park">Soo Young Park</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Lyoo, Hey Rhyoung" sort="Lyoo, Hey Rhyoung" uniqKey="Lyoo H" first="Hey Rhyoung" last="Lyoo">Hey Rhyoung Lyoo</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Koo, Eung Seo" sort="Koo, Eung Seo" uniqKey="Koo E" first="Eung Seo" last="Koo">Eung Seo Koo</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Kim, Man Su" sort="Kim, Man Su" uniqKey="Kim M" first="Man Su" last="Kim">Man Su Kim</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Jeong, Yong Seok" sort="Jeong, Yong Seok" uniqKey="Jeong Y" first="Yong Seok" last="Jeong">Yong Seok Jeong</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Microbiology (Seoul, Korea)</title><idno type="ISSN">1225-8873</idno><idno type="eISSN">1976-3794</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>There is increasing evidence that many RNA viruses manipulate cell cycle control to achieve favorable cellular environments for their efficient replication during infection. Although virus-induced G0/G1 arrest often delays early apoptosis temporarily, a prolonged replication of the infected virus leads host cells to eventual death. In contrast, most mammalian cells with RNA virus persistent infection often escape cytolysis in the presence of productive viral replication. In this study, we demonstrated that the extended endurance of cyclin D1 was clearly associated with the suppression of glycogen synthase kinase-3ß (GSK-3ß) expression in BHK-21 cells that are persistently infected with Japanese encephalitis virus (JEV). The G0/G1 arrest of these cells turned much loose compared to the normal BHK-21 cells with JEV acute infection. After cycloheximide treatment, cyclin D1 in the persistently infected cells lasted several hours longer than those in acutely infected cells. Furthermore, both p21<sup>Cip1</sup> and p27<sup>Kip1</sup>, positive regulators for cyclin D1 accumulation in the nucleus, were suppressed in their expression, which contrasts with those in JEV acute infection. Inhibition of the GSK-3ß by lithium chloride treatment rescued a significant number of cells from cytolysis in JEV acute infection, which coincided with the levels of cyclin D1 that escaped from proteolysis. Therefore, the limitation of G1/S arrest in the BHK-21 cells with JEV persistent infection is associated with the suppression of GSK-3ß expression, resulting in the extended duration of cyclin D1.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Alt, J R" uniqKey="Alt J">J.R. Alt</name></author><author><name sortKey="Gladden, A B" uniqKey="Gladden A">A.B. Gladden</name></author><author><name sortKey="Diehl, J A" uniqKey="Diehl J">J.A. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">J Microbiol</journal-id><journal-id journal-id-type="iso-abbrev">J. Microbiol</journal-id><journal-title-group><journal-title>Journal of Microbiology (Seoul, Korea)</journal-title></journal-title-group><issn pub-type="ppub">1225-8873</issn><issn pub-type="epub">1976-3794</issn><publisher><publisher-name>The Microbiological Society of Korea</publisher-name><publisher-loc>Heidelberg</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">25557483</article-id><article-id pub-id-type="pmc">7090764</article-id><article-id pub-id-type="publisher-id">4661</article-id><article-id pub-id-type="doi">10.1007/s12275-015-4661-z</article-id><article-categories><subj-group subj-group-type="heading"><subject>Virology</subject></subj-group></article-categories><title-group><article-title>Extended stability of cyclin D1 contributes to limited cell cycle arrest at G1-phase in BHK-21 cells with Japanese encephalitis virus persistent infection</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Kim</surname><given-names>Ji Young</given-names></name><xref ref-type="aff" rid="Aff1"></xref></contrib><contrib contrib-type="author"><name><surname>Park</surname><given-names>Soo Young</given-names></name><xref ref-type="aff" rid="Aff1"></xref></contrib><contrib contrib-type="author"><name><surname>Lyoo</surname><given-names>Hey Rhyoung</given-names></name><xref ref-type="aff" rid="Aff1"></xref></contrib><contrib contrib-type="author"><name><surname>Koo</surname><given-names>Eung Seo</given-names></name><xref ref-type="aff" rid="Aff1"></xref></contrib><contrib contrib-type="author"><name><surname>Kim</surname><given-names>Man Su</given-names></name><xref ref-type="aff" rid="Aff1"></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Jeong</surname><given-names>Yong Seok</given-names></name><address><phone>+82-2-961-0829</phone><fax>+82-2-961-0244</fax><email>ysjeong@khu.ac.kr</email></address><xref ref-type="aff" rid="Aff1"></xref></contrib><aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.289247.2</institution-id><institution-id institution-id-type="ISNI">0000000121717818</institution-id><institution>Department of Biology and Research Institute of Basic Sciences,</institution><institution>Kyung Hee University,</institution></institution-wrap>Seoul, 130-701 Republic of Korea</aff></contrib-group><pub-date pub-type="epub"><day>4</day><month>1</month><year>2015</year></pub-date><pub-date pub-type="ppub"><year>2015</year></pub-date><volume>53</volume><issue>1</issue><fpage>77</fpage><lpage>83</lpage><history><date date-type="received"><day>20</day><month>11</month><year>2014</year></date><date date-type="rev-recd"><day>1</day><month>12</month><year>2014</year></date><date date-type="accepted"><day>1</day><month>12</month><year>2014</year></date></history><permissions><copyright-statement>© The Microbiological Society of Korea and Springer-Verlag Berlin Heidelberg 2015</copyright-statement><license><license-p>This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.</license-p></license></permissions><abstract id="Abs1"><p>There is increasing evidence that many RNA viruses manipulate cell cycle control to achieve favorable cellular environments for their efficient replication during infection. Although virus-induced G0/G1 arrest often delays early apoptosis temporarily, a prolonged replication of the infected virus leads host cells to eventual death. In contrast, most mammalian cells with RNA virus persistent infection often escape cytolysis in the presence of productive viral replication. In this study, we demonstrated that the extended endurance of cyclin D1 was clearly associated with the suppression of glycogen synthase kinase-3ß (GSK-3ß) expression in BHK-21 cells that are persistently infected with Japanese encephalitis virus (JEV). The G0/G1 arrest of these cells turned much loose compared to the normal BHK-21 cells with JEV acute infection. After cycloheximide treatment, cyclin D1 in the persistently infected cells lasted several hours longer than those in acutely infected cells. Furthermore, both p21<sup>Cip1</sup> and p27<sup>Kip1</sup>, positive regulators for cyclin D1 accumulation in the nucleus, were suppressed in their expression, which contrasts with those in JEV acute infection. Inhibition of the GSK-3ß by lithium chloride treatment rescued a significant number of cells from cytolysis in JEV acute infection, which coincided with the levels of cyclin D1 that escaped from proteolysis. Therefore, the limitation of G1/S arrest in the BHK-21 cells with JEV persistent infection is associated with the suppression of GSK-3ß expression, resulting in the extended duration of cyclin D1.</p></abstract><kwd-group xml:lang="en"><title>Keywords</title><kwd>Japanese encephalitis virus</kwd><kwd>persistent infection</kwd><kwd>cell cycle</kwd><kwd>cyclin D1</kwd><kwd>GSK-3ß</kwd></kwd-group><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© The Microbiological Society of Korea and Springer-Verlag Berlin Heidelberg 2015</meta-value></custom-meta></custom-meta-group></article-meta></front><back><ref-list id="Bib1"><title>References</title><ref id="CR1"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Alt</surname><given-names>J.R.</given-names></name><name><surname>Gladden</surname><given-names>A.B.</given-names></name><name><surname>Diehl</surname><given-names>J.A.</given-names></name></person-group><article-title>p21 (Cip1) promotes cyclin D1 nuclear accumulation via direct inhibition of nuclear export</article-title><source>J. 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