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Conference Paper: Cytoplasmic signaling involved in sonoporation-induced apoptosis andmitosis repression of myeloid leukemia cells

TitleCytoplasmic signaling involved in sonoporation-induced apoptosis andmitosis repression of myeloid leukemia cells
Authors
Keywordsapoptosis
cytoplasmmic signals
mitosis
sonoporation
Issue Date2010
PublisherIEEE.
Citation
The 2010 IEEE International Ultrasonics Symposium, San Diego, CA., 11-14 October 2010. In Proceedings of IEEE IUS, 2010, p. 1771-1774 How to Cite?
AbstractSonoporation is known to be a transient phenomenon that may disrupt thehomeostasis of living cells. In this work, we showed that sonoporation may beartime-lapse impact on cellular viability through up-regulation of cytoplasmicsignaling proteins related to apoptosis and cell-cycle arrest. Our experimentswere done on HL-60 leukemia cells (10 6 cells/ml), and sonoporationwas induced via the use of 1% v/v microbubbles and 1-min. pulsed ultrasoundexposure (0.5MPa peak negative pressure, 1MHz center frequency, 10% duty cycle,1 kHz pulse repetition frequency). The transient nature of sonoporation in thesecells was confirmed by performing scanning electron microscopy on selected cellsamples that were fixed respectively after a few seconds into the ultrasoundexposure and one minute after the end of exposure. Cytoplasmic signaling changesof these cells were studied at four post-sonoporation time points (4h, 8h, 12h,24h) using western blot analysis. Five signaling proteins related to apoptosisand mitosis were analyzed in this work: 1) PARP (for DNA repair); 2)cleaved-PARP (fragments due to cleavage by pro-apoptotic caspase proteins); 3)Bcl-2 (inhibitor for mitochrondrial release of pro-apoptotic molecules); 4) Bax(complement of Bcl-2); 5) Cdc-2 (regulator for cell mitosis). Three key resultswere found from the cytoplasmic signaling analysis. First, PARP levels werereduced over the monitoring period whilst cleaved-PARP had increased inexpression, and in turn they indicate that the cells' anti-apoptotic responseswere dampened following sonoporation and pro-apoptotic caspase proteins werelikely activated. Second, drop in Bcl-2 and rise in Bax were observed, and thesesuggest that the mitochondrion was involved in apoptotic signal transductioninside sonoporated cells. Third, Cdc-2 was seen to decrease, implying thatmitosis was repressed in sonoporated cells. © 2010 IEEE.
Persistent Identifierhttp://hdl.handle.net/10722/129732
ISBN
ISSN
References

 

DC FieldValueLanguage
dc.contributor.authorZhong, Wen_HK
dc.contributor.authorSit, WHen_HK
dc.contributor.authorWan, JMFen_HK
dc.contributor.authorYu, ACHen_HK
dc.date.accessioned2010-12-23T08:41:21Z-
dc.date.available2010-12-23T08:41:21Z-
dc.date.issued2010en_HK
dc.identifier.citationThe 2010 IEEE International Ultrasonics Symposium, San Diego, CA., 11-14 October 2010. In Proceedings of IEEE IUS, 2010, p. 1771-1774en_HK
dc.identifier.isbn978-1-4577-0380-5-
dc.identifier.issn1051-0117en_HK
dc.identifier.urihttp://hdl.handle.net/10722/129732-
dc.description.abstractSonoporation is known to be a transient phenomenon that may disrupt thehomeostasis of living cells. In this work, we showed that sonoporation may beartime-lapse impact on cellular viability through up-regulation of cytoplasmicsignaling proteins related to apoptosis and cell-cycle arrest. Our experimentswere done on HL-60 leukemia cells (10 6 cells/ml), and sonoporationwas induced via the use of 1% v/v microbubbles and 1-min. pulsed ultrasoundexposure (0.5MPa peak negative pressure, 1MHz center frequency, 10% duty cycle,1 kHz pulse repetition frequency). The transient nature of sonoporation in thesecells was confirmed by performing scanning electron microscopy on selected cellsamples that were fixed respectively after a few seconds into the ultrasoundexposure and one minute after the end of exposure. Cytoplasmic signaling changesof these cells were studied at four post-sonoporation time points (4h, 8h, 12h,24h) using western blot analysis. Five signaling proteins related to apoptosisand mitosis were analyzed in this work: 1) PARP (for DNA repair); 2)cleaved-PARP (fragments due to cleavage by pro-apoptotic caspase proteins); 3)Bcl-2 (inhibitor for mitochrondrial release of pro-apoptotic molecules); 4) Bax(complement of Bcl-2); 5) Cdc-2 (regulator for cell mitosis). Three key resultswere found from the cytoplasmic signaling analysis. First, PARP levels werereduced over the monitoring period whilst cleaved-PARP had increased inexpression, and in turn they indicate that the cells' anti-apoptotic responseswere dampened following sonoporation and pro-apoptotic caspase proteins werelikely activated. Second, drop in Bcl-2 and rise in Bax were observed, and thesesuggest that the mitochondrion was involved in apoptotic signal transductioninside sonoporated cells. Third, Cdc-2 was seen to decrease, implying thatmitosis was repressed in sonoporated cells. © 2010 IEEE.en_HK
dc.languageengen_US
dc.publisherIEEE.-
dc.relation.ispartofProceedings - IEEE Ultrasonics Symposiumen_HK
dc.rightsIEEE International Ultrasonics Symposium Proceedings. Copyright © IEEE.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rights©2010 IEEE. Personal use of this material is permitted. However, permission to reprint/republish this material for advertising or promotional purposes or for creating new collective works for resale or redistribution to servers or lists, or to reuse any copyrighted component of this work in other works must be obtained from the IEEE.-
dc.subjectapoptosisen_HK
dc.subjectcytoplasmmic signalsen_HK
dc.subjectmitosisen_HK
dc.subjectsonoporationen_HK
dc.titleCytoplasmic signaling involved in sonoporation-induced apoptosis andmitosis repression of myeloid leukemia cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailWan, JMF: jmfwan@hku.hken_HK
dc.identifier.emailYu, ACH: alfred.yu@hku.hken_HK
dc.identifier.authorityWan, JMF=rp00798en_HK
dc.identifier.authorityYu, ACH=rp00657en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1109/ULTSYM.2010.5935545en_HK
dc.identifier.scopuseid_2-s2.0-80054062664en_HK
dc.identifier.hkuros176825en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80054062664&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.spage1771en_HK
dc.identifier.epage1774en_HK
dc.publisher.placeUnited Statesen_HK
dc.description.otherThe 2010 IEEE International Ultrasonics Symposium, San Diego, CA., 11-14 October 2010. In Proceedings of IEEE IUS, 2010, p. 1771-1774-
dc.identifier.scopusauthoridZhong, W=46761637400en_HK
dc.identifier.scopusauthoridSit, WH=8528923000en_HK
dc.identifier.scopusauthoridWan, JMF=8930305000en_HK
dc.identifier.scopusauthoridYu, ACH=8699317700en_HK

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