Arachidonate is a potent modulator of human heat shock gene transcription.

Abstract

Cell and tissue injury activate the inflammatory response through the action(s) of arachidonic acid and its metabolites, leading to the expression of acute-phase proteins and inflammatory cytokines. At the molecular level, little is known how arachidonic acid regulates the inflammatory response. As inflammation is also associated with local increase in tiue temperatures, we eamned whether aridonic acid was directly involved in the heat shock response. Transcriptional Run-On Assays. In vitro nuclear run-on analysis was done as described (25 Abbreviations: HSE, heat shock element; HSF, heat shock factor.

Heat Shock and Caloric Restriction Have a Synergistic Effect on the Heat Shock Response in a sir2.1-dependent Manner in Caenorhabditis elegans

“…For example, the non-steroidal anti-inflammatory drug indomethacin can cooperate with a mild heat stress to induce increased levels of chaperone gene expression over treatment with just heat alone (52). Other small molecules shown to work synergistically with HS include the inflammatory pathway intermediate arachidonic acid, the hydroxylamine derivative bimoclomal, and the triterpenoid celastrol (35,53,54). We now add CR as another HSR activator that can synergize with HS.…”

Characterization of Hypothermia-induced Cellular Stress Response in Mouse Tissues

“…Our results suggest a mechanism that may explain these beneficial effects of hypothermia. Several pharmacological agents have been identified that induce the heat shock response (23)(24)(25)(26)(27), and several reagents have been identified which lower body temperature, such as lipopolysaccharide (28), cyclooxygenase inhibitors (28), and 8-hydroxy-2-(di-n-propyl)aminotetralin, a serotonin 1A receptor agonist (29). Based on our findings, these types of pharmacological agents may provide useful tools for medical applications.…”

Hyperthermia in the febrile range induces HSP72 expression proportional to exposure temperature but not to HSF-1 DNA-binding activity in human lung epithelial A549 cells

“…For example, lymphoid tissues, including spleen, exhibit a low thermal threshold for induction of heat shock protein expression (Gothard et al 2003;Ostberg et al 2002), which appears to derive from T lymphocyte rather than B lymphocyte behavior (Gothard et al 2003). Furthermore, the thermal threshold for induction of HSF-1 activation and HSP expression may be modified by exposure to certain agents, such as arachidonic acid (Jurivich et al 1994) and type I interferons (Morange et al 1986). Collectively, these studies suggest that regulation of the HS response is complex and may be modified by multiple factors in addition to the magnitude of hyperthermia to which the organism is exposed.…”