tailieunhanh - Báo cáo khoa học: The hyperfluidization of mammalian cell membranes acts as a signal to initiate the heat shock protein response

The concentrations of two structurally distinct membrane fluidizers, the local anesthetic benzyl alcohol (BA) and heptanol (HE), were used at con-centrations so that their addition to K562 cells caused identical increases in the level of plasma membrane fluidity as tested by 1,6-diphenyl-1,3,5-hexa-triene (DPH) anisotropy. | ềFEBS Journal The hyperfluidization of mammalian cell membranes acts as a signal to initiate the heat shock protein response Gabor Balogh1 Ibolya Horvath1 Eniko Nagy1 Zsofia Hoyk2 Sandor Benko3 Olivier Bensaude4 and László Vigh1 1 Institute of Biochemistry BiologicalResearch Centre Hungarian Academy of Sciences Szeged Hungary 2 Institute of Biophysics BiologicalResearch Centre Hungarian Academy of Sciences Szeged Hungary 3 Outpatient MedicalCentre Municipality of Szeged Hungary 4 Departement de Genetique Moleculaire Ecole Normale Superieure Paris France Keywords local anesthetics molecular chaperones membrane fluidity membrane microdomains stress proteins Correspondence L. Vigh Institute of Biochemistry Biological Research Centre Hungarian Academy of Sciences Szeged POB 521 H-6701 Hungary Tel Fax 36 62 432048 E-mail vigh@ Received 18 July 2005 revised 27 September 2005 accepted 3 October 2005 doi The concentrations of two structurally distinct membrane fluidizers the local anesthetic benzyl alcohol BA and heptanol HE were used at concentrations so that their addition to K562 cells caused identical increases in the level of plasma membrane fluidity as tested by 1 6-diphenyl-1 3 5-hexa-triene DPH anisotropy. The level of membrane fluidization induced by the chemical agents on isolated membranes at such concentrations corresponded to the membrane fluidity increase seen during a thermal shift up to 42 C. The formation of isofluid membrane states in response to the administration of BA or HE resulted in almost identical downshifts in the temperature thresholds of the heat shock response accompanied by increases in the expression of genes for stress proteins such as heat shock protein HSP -70 at the physiological temperature. Similarly to thermal stress the exposure of the cells to these membrane fluidizers elicited nearly identical increases of cytosolic Ca2 concentration in both Ca2 -containing and Ca2 -free media and also closely