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Grant: Discovery Grants Program - Individual

Université du Québec à Montréal

$40,000.00

Cellular and molecular studies of adaptive survival responses: thermotolerance induced at 40C

EF 2015-16

Résumé
Stress response pathways allow cells to sense and respond to adverse environmental changes. Exposure to sub-lethal doses of different stresses (e.g. reactive oxygen species (ROS), heat shock, radiation) can lead to adaptive responses that allow cells and organisms to continue normal function in the face of an adverse stimulus. Adaptive responses appear to be mediated by a core group of powerful anti-apoptotic genes (e.g. Hsps, antioxidants) that protect against diverse toxic stresses and enable the cell to survive. The adaptive response could counteract stress-induced damage to lipids, proteins and DNA, and/or increase tolerance to such damage. If the adaptive response cannot protect the cell, then the damaged cell will be eliminated by apoptosis. During recent years, we have studied the adaptive response induced at a mild fever range temperature (40C), and its cytoprotective effect against toxic stresses (e.g. heat shock, ROS). However, the cellular and molecular basis of this adaptive response is not clearly understood. The long-term goals of our research program are to determine the cellular and molecular basis of the adaptive survival response of thermotolerance induced at a low, non-lethal temperature of 40C. Our Hypothesis is: Preconditioning of cells by non-lethal heat stress at 40C is an adaptive response that likely involves induction of multiple defenses to protect cells against adverse effects of different stresses. To achieve these goals, we will focus on the following Short-term objectives: 1.To investigate the role of ROS in the induction thermotolerance at 40C; 2.To determine whether thermal adaption (40C) alters the threshold between induction of autophagy and apoptosis by stress (ROS and heat shock); 3. To determine changes in gene expression during development of thermal adaption at 40C. A search for the cellular and molecular basis of death/survival pathways induced by different stresses could provide the basis for understanding environmental health problems, providing more sensitive biomarkers for toxicological risk assessment, and utilizing the healing capacity of adaptive responses to protect against deleterious effects of toxic and environmental stresses in humans and other living species.
Programme
Discovery Grants Program - Individual
Emplacement
Quebec, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
NSERC's Awards Data

Tel que publié

Application id
36725-2011
Name nom
AverillBates, Diana
Department département
Sciences biologiques
Organization id
57
Institution établissement
Université du Québec à Montréal
Province en
Québec
Province fr
Québec
Country en
CANADA
Country fr
CANADA
Fiscal year exercice financier
2015
Competition year année de concours
2011
Award amount
40000
Program id
RGPIN
Program name en
Discovery Grants Program - Individual
Program name fr
Programme de subventions à la découverte - individuelles
Group en
Discovery grants programs
Group fr
Programmes de subventions à la découverte
Committee code
1501
Committee name en
Genes, Cells and Molecules
Committee name fr
Gènes, cellules et molécules
Area of application code
1201
Area of application group en
Advancement of knowledge
Area of application group fr
Avancement des connaissances
Area of application en
Life sciences (including biotechnology)
Area of application fr
Sciences de la vie (y compris biotechnologie)
Research subject code
5100
Research subject group en
Cell biology
Research subject group fr
Biologie cellulaire
Research subject en
Cell biology
Research subject fr
Biologie cellulaire
Partie
5
Nb partie
6
Application title
Cellular and molecular studies of adaptive survival responses: thermotolerance induced at 40C
Keyword
NSERC
Application summary
Stress response pathways allow cells to sense and respond to adverse environmental changes. Exposure to sub-lethal doses of different stresses (e.g. reactive oxygen species (ROS), heat shock, radiation) can lead to adaptive responses that allow cells and organisms to continue normal function in the face of an adverse stimulus. Adaptive responses appear to be mediated by a core group of powerful anti-apoptotic genes (e.g. Hsps, antioxidants) that protect against diverse toxic stresses and enable the cell to survive. The adaptive response could counteract stress-induced damage to lipids, proteins and DNA, and/or increase tolerance to such damage. If the adaptive response cannot protect the cell, then the damaged cell will be eliminated by apoptosis. During recent years, we have studied the adaptive response induced at a mild fever range temperature (40C), and its cytoprotective effect against toxic stresses (e.g. heat shock, ROS). However, the cellular and molecular basis of this adaptive response is not clearly understood. The long-term goals of our research program are to determine the cellular and molecular basis of the adaptive survival response of thermotolerance induced at a low, non-lethal temperature of 40C. Our Hypothesis is: Preconditioning of cells by non-lethal heat stress at 40C is an adaptive response that likely involves induction of multiple defenses to protect cells against adverse effects of different stresses. To achieve these goals, we will focus on the following Short-term objectives: 1.To investigate the role of ROS in the induction thermotolerance at 40C; 2.To determine whether thermal adaption (40C) alters the threshold between induction of autophagy and apoptosis by stress (ROS and heat shock); 3. To determine changes in gene expression during development of thermal adaption at 40C. A search for the cellular and molecular basis of death/survival pathways induced by different stresses could provide the basis for understanding environmental health problems, providing more sensitive biomarkers for toxicological risk assessment, and utilizing the healing capacity of adaptive responses to protect against deleterious effects of toxic and environmental stresses in humans and other living species.