Heat stress lipids and schizophrenia.
The neurodevelopmental hypothesis of schizophrenia implicates abnormal or disrupted neural growth during embryogenesis. It is postulated here that stress-inducing agents acting upon a compromised cellular system resulting from abnormal plasma membrane lipids could effect the neuronal abnormalities observed in schizophrenia. The heat stress response is induced by exposure to hyperthermia as well as a variety of other agents. The response to these agents includes the cessation of most transcriptional and translational activities, accompanied by the induction of a highly specific set of proteins. A concomitant reduction in metabolic activity including cell cycle delays is also observed. Much of the enormous literature on the heat stress response concentrates on protein and DNA interactions, especially with regard to transcriptional control. However, a variety of lipids are intrinsically involved in the heat stress response. This paper will provide a brief introduction to the heat shock proteins and will explore the roles that lipids play in the heat shock response.
Faculty of Science and Technology, Griffith University, Nathan, Australia.
P R
PR
Bates
A
A
Hawkins
S P
SP
Mahadik
J J
JJ
McGrath
D006360:Heat-Shock Proteins / Q000378:metabolism; D018869:Heat-Shock Response / Q000502:physiology*; D006801:Humans; D050356:Lipid Metabolism; D009420:Nervous System / Q000196:embryology; D009421:Nervous System Malformations; D012559:Schizophrenia / Q000378:metabolism*; D013696:Temperature; D013997:Time Factors
D006360:Heat-Shock Proteins