Plasma membranes as heat stress sensors: From lipid-controlled molecular switches to therapeutic applications

The classic heat shock (stress) response (HSR) was originally attributed to protein denaturation. However, heat shock protein (Hsp) induction occurs in many circumstances where no protein denaturation is observed. Recently considerable evidence has been accumulated to the favor of the “Membrane Sens...

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Published in:	Biochimica et biophysica acta Vol. 1838; no. 6; pp. 1594 - 1618
Main Authors:	Török, Zsolt, Crul, Tim, Maresca, Bruno, Schütz, Gerhard J., Viana, Felix, Dindia, Laura, Piotto, Stefano, Brameshuber, Mario, Balogh, Gábor, Péter, Mária, Porta, Amalia, Trapani, Alfonso, Gombos, Imre, Glatz, Attila, Gungor, Burcin, Peksel, Begüm, Vigh, László, Csoboz, Bálint, Horváth, Ibolya, Vijayan, Mathilakath M., Hooper, Phillip L., Harwood, John L.
Format:	Journal Article
Language:	English
Published:	Netherlands Elsevier B.V 01-06-2014
Subjects:	Animals Cell Membrane - metabolism Cell-to-cell heterogeneity Heat shock response Heat-Shock Proteins - metabolism Heat-Shock Response - physiology Humans Lipid raft Lipidomics Membrane lipid therapy Membrane Lipids - metabolism Neurodegenerative Diseases - metabolism Neurodegenerative Diseases - therapy Stress hormone TRP channel APAP Cell-to-cell heterogeneity GPI SGT SPC Membrane lipid therapy CHO Cdase MPS POPE MBCD TRP PI3K GSK3 MD POPC Ld mTOR DMPC CHOL AA Lipid raft Lo aSMase HSP HSR PKA PhA PLA2 Heat shock response PKC Lipidomics MAPK ERK1/2 Stress hormone CRA PIP3 GlcCer LPA DPH LPC PIP2 BA PLC PLD BM PHB NPN EGFR LPS TIRF SFA GFP UFA TRP channel GFR S1P NADA HSF1 SK1 FRET SM YFP MALDI DAG GR IP3 PI4P CaMKII GCS LB TOCCSL ATP HNE
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Summary:	The classic heat shock (stress) response (HSR) was originally attributed to protein denaturation. However, heat shock protein (Hsp) induction occurs in many circumstances where no protein denaturation is observed. Recently considerable evidence has been accumulated to the favor of the “Membrane Sensor Hypothesis” which predicts that the level of Hsps can be changed as a result of alterations to the plasma membrane. This is especially pertinent to mild heat shock, such as occurs in fever. In this condition the sensitivity of many transient receptor potential (TRP) channels is particularly notable. Small temperature stresses can modulate TRP gating significantly and this is influenced by lipids. In addition, stress hormones often modify plasma membrane structure and function and thus initiate a cascade of events, which may affect HSR. The major transactivator heat shock factor-1 integrates the signals originating from the plasma membrane and orchestrates the expression of individual heat shock genes. We describe how these observations can be tested at the molecular level, for example, with the use of membrane perturbers and through computational calculations. An important fact which now starts to be addressed is that membranes are not homogeneous nor do all cells react identically. Lipidomics and cell profiling are beginning to address the above two points. Finally, we observe that a deregulated HSR is found in a large number of important diseases where more detailed knowledge of the molecular mechanisms involved may offer timely opportunities for clinical interventions and new, innovative drug treatments. This article is part of a Special Issue entitled: Membrane Structure and Function: Relevance in the Cell's Physiology, Pathology and Therapy. [Display omitted] •Mild heat stress (within typical fever ranges) is sensed by rearrangement of plasma membrane nanoplatforms.•Cell profiling, lipidomics and computer modeling are tools to study membrane events•HSF1 integrates stress signals that originate from the plasma membrane•Membrane lipid therapy offers a timely and important application of agents that can modify stress responses
ISSN:	0005-2736 0006-3002 1879-2642
DOI:	10.1016/j.bbamem.2013.12.015