High hydrostatic pressure causes stress response in many types of mammalian cells. We have previously shown that an accumulation of heat shock protein 70 (Hsp70) in a chondrocytic cell line occurred without an activation of the gene itself. Stabilization of the hsp70 mRNA was shown to be the reason for the Hsp70 stress response in the pressurized cells. Since accumulation of Hsp70 in pressurized cells indicated that high hydrostatic pressure induces a stress response without heat shock transcription factor activation, we decided to investigate the activation of two other stress-associated transcription factors, activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB). Induction of Hsp70 in immortalized and primary chondrocytes, murine Neuro-2a neuroblastoma and HeLa cervical carcinoma cell lines was investigated at both mRNA and protein levels. In immortalized chondrocytes and HeLa cells, hsp70 mRNA levels were clearly elevated after 6 hours of the onset of 30 MPa continuous hydrostatic pressure, while in primary chondrocytes and Neuro-2a cells (the cells known to be stress-sensitive) no induction was observed. Surprisingly, neither heat shock nor high hydrostatic pressure could induce the hsp70 mRNA in Neuro-2a cells, although an activation of heat shock transcription factor could be observed in heat-shocked cells. No activation of the AP-1 and NF-kappaB binding to their target DNA sequences could be shown in the immortalized chondrocytes.