Ln. Song, EFFECTS OF HEAT-SHOCK ON GLUCOCORTICOID RECEPTOR, Science in China. Series B, Chemistry, life sciences & earth sciences, 37(5), 1994, pp. 557-562
The changes of glucocorticoid receptor (GR) during the heat shock resp
onse have been studied using a human osteosarcoma cell line (HOS-8603)
as the model. The expression of the heat shock protein 70 (hsp70) mRN
A in HOS-8603 cells has been enhanced markedly after a heat treatment
at 43-degrees-C for 30 min. A mild thermal pretreatment (42-degrees-C
for 1 h) protects the HOS-8603 cells against a subsequent heat challen
ge (46-degrees-C). This induced thermotolerance is reflected by the in
crease of cell viability of HOS-8603 cells. The GR binding activity in
HOS-8603 cells decreased rapidly after the heat treatment at 43-degre
es-C; only 42.61% of controls were detected 60 min after the heat trea
tment. However, there was no significant change in the dissociation co
nstant value (K(d)). These results indicate that the heat shock induce
not only the heat shock mRNA expression, but also the rapid reduction
in GR binding activity, suggesting that there might be a functional r
elationship between GR action and the heat shock response.