File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Programmed neuronal cell death induced by HIV-1 Tat and methamphetamine

TitleProgrammed neuronal cell death induced by HIV-1 Tat and methamphetamine
Authors
KeywordsApoptosis
Autophagy
HIV-1 tat
Methamphetamine
Programmed cell death
SH-SY5Y
Issue Date2011
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/1059-910X/
Citation
Microscopy Research and Technique , 2011, v. 74 n. 12, p. 1139-1144 How to Cite?
AbstractApoptosis and autophagy are the two major types of programmed cell death (PCD) in neurons. Homeostatic autophagy often precedes apoptosis, and when apoptosis is blocked, the failure to keep homeostasis will lead to necrosis instead. It has been reported that human immunodeficiency virus (HIV) infected methamphetamine (Meth) abusers represent greater neuropathological abnormalities than Meth abusers or HIV-positive non-Meth users. Recent publications suggest that Tat and Meth when administered together result in greater neuronal damage than when administered separately. However, the cellular events of the combined Tat-Meth effect have not yet been fully characterized. Therefore, we investigated the effects of Tat and/or Meth on apoptosis and autophagy to elucidate whether PCD was involved in Tat and/or Meth-induced neuronal damage. Annexin-V-FITC/PI staining assay was used to detect cellular apoptosis using a neuroblastoma cell line SH-SY5Y. Cellular ultrastructural changes were observed under transmission electron microscopy (TEM). Flow-cytometric data showed apoptosis following Meth treatment, and more extensive apoptosis with Tat + Meth treatment. The most important finding was that the autophagosome and/or multilamellar bodies (MLBs) were most pronounced with Tat + Meth treatment, were less so with Meth treatment, and infrequent with Tat treatment. This suggests the involvement of autophagy and apoptosis in Tat with Meth-elicited cell damage. However, the relation between apoptosis and autophagy remains unknown in this experiment. Further research is needed to analyze the relation among related molecules. A thorough understanding of this multifaceted relationship will be critical for the assessment of therapeutic modalities for patients with HIV with drug abuse.
Persistent Identifierhttp://hdl.handle.net/10722/135437
ISSN
2023 Impact Factor: 2.0
2023 SCImago Journal Rankings: 0.438
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Science Foundation of China (NSFC)30660202
Yunnan Provincial Department of Science Technology2006GH22
Funding Information:

Contract grant sponsor: National Natural Science Foundation of China (NSFC); Contract grant number: 30660202; Contract grant sponsor: Yunnan Provincial Department of Science & Technology; Contract grant number: 2006GH22

 

DC FieldValueLanguage
dc.contributor.authorLi, Qen_US
dc.contributor.authorLu, Gen_US
dc.contributor.authorKwong, WHen_US
dc.contributor.authorChoi, HLen_US
dc.contributor.authorZeng, Xen_US
dc.contributor.authorLi, Zen_US
dc.contributor.authorYew, DWen_US
dc.contributor.authorPoon, WSen_US
dc.date.accessioned2011-07-27T01:35:07Z-
dc.date.available2011-07-27T01:35:07Z-
dc.date.issued2011en_US
dc.identifier.citationMicroscopy Research and Technique , 2011, v. 74 n. 12, p. 1139-1144en_US
dc.identifier.issn1059-910X-
dc.identifier.urihttp://hdl.handle.net/10722/135437-
dc.description.abstractApoptosis and autophagy are the two major types of programmed cell death (PCD) in neurons. Homeostatic autophagy often precedes apoptosis, and when apoptosis is blocked, the failure to keep homeostasis will lead to necrosis instead. It has been reported that human immunodeficiency virus (HIV) infected methamphetamine (Meth) abusers represent greater neuropathological abnormalities than Meth abusers or HIV-positive non-Meth users. Recent publications suggest that Tat and Meth when administered together result in greater neuronal damage than when administered separately. However, the cellular events of the combined Tat-Meth effect have not yet been fully characterized. Therefore, we investigated the effects of Tat and/or Meth on apoptosis and autophagy to elucidate whether PCD was involved in Tat and/or Meth-induced neuronal damage. Annexin-V-FITC/PI staining assay was used to detect cellular apoptosis using a neuroblastoma cell line SH-SY5Y. Cellular ultrastructural changes were observed under transmission electron microscopy (TEM). Flow-cytometric data showed apoptosis following Meth treatment, and more extensive apoptosis with Tat + Meth treatment. The most important finding was that the autophagosome and/or multilamellar bodies (MLBs) were most pronounced with Tat + Meth treatment, were less so with Meth treatment, and infrequent with Tat treatment. This suggests the involvement of autophagy and apoptosis in Tat with Meth-elicited cell damage. However, the relation between apoptosis and autophagy remains unknown in this experiment. Further research is needed to analyze the relation among related molecules. A thorough understanding of this multifaceted relationship will be critical for the assessment of therapeutic modalities for patients with HIV with drug abuse.-
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/1059-910X/-
dc.relation.ispartofMicroscopy Research and Techniqueen_US
dc.rightsMicroscopy Research and Technique . Copyright © John Wiley & Sons, Inc.-
dc.subjectApoptosis-
dc.subjectAutophagy-
dc.subjectHIV-1 tat-
dc.subjectMethamphetamine-
dc.subjectProgrammed cell death-
dc.subjectSH-SY5Y-
dc.subject.meshApoptosis-
dc.subject.meshAutophagy-
dc.subject.meshMethamphetamine - toxicity-
dc.subject.meshNeurons - drug effects-
dc.subject.meshtat Gene Products, Human Immunodeficiency Virus - toxicity-
dc.titleProgrammed neuronal cell death induced by HIV-1 Tat and methamphetamineen_US
dc.typeArticleen_US
dc.identifier.emailLi, Q: liqi@hkucc.hku.hken_US
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/jemt.21006-
dc.identifier.pmid21563266-
dc.identifier.scopuseid_2-s2.0-81555214455-
dc.identifier.hkuros188274en_US
dc.identifier.volume74-
dc.identifier.issue12-
dc.identifier.spage1139-
dc.identifier.epage1144-
dc.identifier.isiWOS:000297859200011-
dc.publisher.placeUnited States-
dc.identifier.issnl1059-910X-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats