File Download

There are no files associated with this item.

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

Conference Paper: Dexmedetomidine suppresses gap junctional intercellular communication and attenuates the sensitivity of gliocytoma to temozolomid

TitleDexmedetomidine suppresses gap junctional intercellular communication and attenuates the sensitivity of gliocytoma to temozolomid
Authors
Issue Date2014
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Experimental Biology (EB), San Diego, California, USA, 26-30 April 2014. In The FASEB Journal, 2014, v. 28 n. Suppl. 1, p. abstract no. LB642 How to Cite?
AbstractDexmedetomidine(DEX), an alpha-2 adrenergic agonist which can affect cell-to-cell gap junctions(GJ), is used as an adjuvant analgesic and sedatives in patients with cancer pain, especially in neural cancer patients who concomitantly receiving chemotherapy. GJ may increase the sensitivity of tumor cells to chemotherapeutic agents (Oncol Rep. 2014;31:540-550). It is unknown whether or not DEX may affect the sensitivity of gliocytoma (U87 cell, which richly expresses the GJ protein Connexin43) to temozolomide (TEM, an anticancer agent for gliocytoma) and if DEX exerts its effect via affecting GJ. U87 cells were treated with TEM, respectively at high density (which form GJ) or low density (without GJ formation), for 1 hour in the absence or presence of 3 hours DEX pretreatment prior to applying TEM. TEM toxicity (i.e., reduction of clonogenic cell survival), was assayed by “Standard Clony-forming assay” and GJ function was examined by “Parachute' dye-coupling assay. TEM toxicity was greater at high density than at low density cells (P<0.01), while either oleamide (a GJ inhibitor) or Cx43 siRNA reduced TEM toxicity. Similarly, DEX reduced GJ function and compromised TEM treatment effects, manifested as increases in clonogenic cell survivals at high but not at low cell density. We concluded that DEX reduced TEM cytotoxicity through inhibiting GJ function in gliocytoma.
DescriptionConference Theme: Transforming the Future through Science
Session: Pharmacology and Experimental Therapeutics - Toxicology
Persistent Identifierhttp://hdl.handle.net/10722/204768
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorWang, Len_US
dc.contributor.authorZhang, S-
dc.contributor.authorHuang, H-
dc.contributor.authorXia, W-
dc.contributor.authorXia, Z-
dc.date.accessioned2014-09-20T00:39:20Z-
dc.date.available2014-09-20T00:39:20Z-
dc.date.issued2014en_US
dc.identifier.citationExperimental Biology (EB), San Diego, California, USA, 26-30 April 2014. In The FASEB Journal, 2014, v. 28 n. Suppl. 1, p. abstract no. LB642en_US
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/204768-
dc.descriptionConference Theme: Transforming the Future through Science-
dc.descriptionSession: Pharmacology and Experimental Therapeutics - Toxicology-
dc.description.abstractDexmedetomidine(DEX), an alpha-2 adrenergic agonist which can affect cell-to-cell gap junctions(GJ), is used as an adjuvant analgesic and sedatives in patients with cancer pain, especially in neural cancer patients who concomitantly receiving chemotherapy. GJ may increase the sensitivity of tumor cells to chemotherapeutic agents (Oncol Rep. 2014;31:540-550). It is unknown whether or not DEX may affect the sensitivity of gliocytoma (U87 cell, which richly expresses the GJ protein Connexin43) to temozolomide (TEM, an anticancer agent for gliocytoma) and if DEX exerts its effect via affecting GJ. U87 cells were treated with TEM, respectively at high density (which form GJ) or low density (without GJ formation), for 1 hour in the absence or presence of 3 hours DEX pretreatment prior to applying TEM. TEM toxicity (i.e., reduction of clonogenic cell survival), was assayed by “Standard Clony-forming assay” and GJ function was examined by “Parachute' dye-coupling assay. TEM toxicity was greater at high density than at low density cells (P<0.01), while either oleamide (a GJ inhibitor) or Cx43 siRNA reduced TEM toxicity. Similarly, DEX reduced GJ function and compromised TEM treatment effects, manifested as increases in clonogenic cell survivals at high but not at low cell density. We concluded that DEX reduced TEM cytotoxicity through inhibiting GJ function in gliocytoma.-
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journalen_US
dc.titleDexmedetomidine suppresses gap junctional intercellular communication and attenuates the sensitivity of gliocytoma to temozolomiden_US
dc.typeConference_Paperen_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.identifier.hkuros235645en_US
dc.identifier.volume28en_US
dc.identifier.issueSuppl. 1en_US
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats