File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: Role of heat shock protein 65 kDa on vascular smooth muscle cell proliferation

TitleRole of heat shock protein 65 kDa on vascular smooth muscle cell proliferation
Authors
Issue Date1998
PublisherSpringer Netherlands.
Citation
The 1998 International Conference on Heat-Shock Proteins in Immune Response, Farmington, CT., 12-15 October 1998. In Cell Stress & Chaperones, v. 3 suppl 1, p. 23-24 How to Cite?
AbstractIntroduction. Proliferation of vascular smooth muscle cells (vSMC) is one of the most important pathological processes in atherosclerosis. Recently, heat-shock protein (Hsp65) has been implicated in the pathogenesis and propagation of this disease. The aim of this study was to examine the effect of Hsp65 on the proliferation of vSMCs. Materials/Methods. Male Dark Agouti rats were immunized with 200 gg of Hsp65 (n = 6) or saline control (n = 5) and then sacrificed at 10 weeks. The thoracic aortae were removed and from sections, vSMCs were grown using standard explant technique. Cells were grown to confluence using DMEM+ 10% fetal calf serum (FCS), trypsinized, plated into 96-well plates, and made quiescent. These were subsequently stimulated with FCS (0-20% concentration) over 24 and 48 h. Proliferation was determined by the uptake of 5-bromo-2' deoxyuridine using colorimetric ELISA. Results. At 24 h, there was no difference in proliferation in any of the groups. However, at 48 h, vSMC proliferation was significantly reduced in the rats immunized with Hsp65 compared to controls. Data are expressed as means?SEM (see Figure 1). Conclusions. These findings suggest that prior in vivo inoculation with Hsp65 subsequently inhibited smooth muscle cell proliferation in vitro. Therefore Hsp65 per se could not account for the proliferation of vSMC seen in atherosclerosis.
DescriptionStable URL: http://www.jstor.org/stable/3515900
Persistent Identifierhttp://hdl.handle.net/10722/148729
ISSN
2015 Impact Factor: 2.583
2015 SCImago Journal Rankings: 1.276

 

DC FieldValueLanguage
dc.contributor.authorShukla, N-
dc.contributor.authorChan, YC-
dc.contributor.authorIngledew, NB-
dc.contributor.authorOkonko, DO-
dc.contributor.authorBerwanger, CS-
dc.contributor.authorStanford, J-
dc.contributor.authorSingh, M-
dc.contributor.authorStansby, G-
dc.date.accessioned2012-05-30T01:48:31Z-
dc.date.available2012-05-30T01:48:31Z-
dc.date.issued1998-
dc.identifier.citationThe 1998 International Conference on Heat-Shock Proteins in Immune Response, Farmington, CT., 12-15 October 1998. In Cell Stress & Chaperones, v. 3 suppl 1, p. 23-24-
dc.identifier.issn1355-8145-
dc.identifier.urihttp://hdl.handle.net/10722/148729-
dc.descriptionStable URL: http://www.jstor.org/stable/3515900-
dc.description.abstractIntroduction. Proliferation of vascular smooth muscle cells (vSMC) is one of the most important pathological processes in atherosclerosis. Recently, heat-shock protein (Hsp65) has been implicated in the pathogenesis and propagation of this disease. The aim of this study was to examine the effect of Hsp65 on the proliferation of vSMCs. Materials/Methods. Male Dark Agouti rats were immunized with 200 gg of Hsp65 (n = 6) or saline control (n = 5) and then sacrificed at 10 weeks. The thoracic aortae were removed and from sections, vSMCs were grown using standard explant technique. Cells were grown to confluence using DMEM+ 10% fetal calf serum (FCS), trypsinized, plated into 96-well plates, and made quiescent. These were subsequently stimulated with FCS (0-20% concentration) over 24 and 48 h. Proliferation was determined by the uptake of 5-bromo-2' deoxyuridine using colorimetric ELISA. Results. At 24 h, there was no difference in proliferation in any of the groups. However, at 48 h, vSMC proliferation was significantly reduced in the rats immunized with Hsp65 compared to controls. Data are expressed as means?SEM (see Figure 1). Conclusions. These findings suggest that prior in vivo inoculation with Hsp65 subsequently inhibited smooth muscle cell proliferation in vitro. Therefore Hsp65 per se could not account for the proliferation of vSMC seen in atherosclerosis.-
dc.languageeng-
dc.publisherSpringer Netherlands.-
dc.relation.ispartofCell Stress & Chaperones-
dc.rightsThe original publication is available at www.springerlink.com-
dc.titleRole of heat shock protein 65 kDa on vascular smooth muscle cell proliferationen_US
dc.typeConference_Paperen_US
dc.identifier.emailChan, YC: ycchan88@hkucc.hku.hk-
dc.identifier.volume3-
dc.identifier.issuesuppl. 1-
dc.identifier.spage23-
dc.identifier.epage24-
dc.publisher.placeThe Netherlands-
dc.customcontrol.immutablesml 160630 amended-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats