Thromb Haemost 1996; 75(02): 352-358
DOI: 10.1055/s-0038-1650273
Original Article
Schattauer GmbH Stuttgart

Effect of Heat Shock on the Expression of Urokinase-Type Plasminogen Activator Receptor in Human Umbilical Vein Endothelial Cells

Hideharu Fukao
1   The department of Physiology, Kinki University School of Medicine, Osaka-sayama, Japan
,
Yasuhiro Hagiya
1   The department of Physiology, Kinki University School of Medicine, Osaka-sayama, Japan
,
Shigeru Ueshima
1   The department of Physiology, Kinki University School of Medicine, Osaka-sayama, Japan
,
Kiyotaka Okada
1   The department of Physiology, Kinki University School of Medicine, Osaka-sayama, Japan
,
Tomaoki Takaishi
1   The department of Physiology, Kinki University School of Medicine, Osaka-sayama, Japan
,
Sellichi Izaki
2   Saitama Medical Center, Saitama Medical School, Kawagoe, Japan
,
Osamu Matsuo
1   The department of Physiology, Kinki University School of Medicine, Osaka-sayama, Japan
› Author Affiliations
Further Information

Publication History

Received: 31 January 1995

Accepted after resubmission06 November 1995

Publication Date:
31 August 2018 (online)

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Summary

We investigated the effect of heat shock on the fibrinolytic potential of human umbilical vein endothelial cells (HUVECs) in culture. When cultured at 43° C, the mRNA for heat shock protein 70 (HSP70) was dramatically induced within 120 min with a maximal induction of more than 90-fold compared with that in HUVECs cultured at 37° C. The level of urokinase-type plasminogen activator (u-PA) receptor (u-PAR) mRNA increased up to 2.2-fold in response to heat shock, which was associated with the increased u-PA binding and cell-surface u-PA activity determined by adding exogenous u-PA to acid-treated HUVECs. The increased u-PAR mRNA returned to normal level when HUVECs were further incubated at 37° C for 180 min, and this decline was not affected in the presence of actinomycin D. Though the secreted antigens for tissue-type plasminogen activator (t-PA) and type 1 plasminogen activator inhibitor (PAI-1) in the conditioned medium (CM) of HUVECs were simultaneously increased at 43° C during this period, the increase in the levels of t-PA (about 26.6-fold at 120 min) was greater than that of PAI-1 (1.8-fold at 120 min). The fibrinolytic activity of CM obtained from HUVECs at 43° C was significantly enhanced up to 3-fold, indicating that heat shock induced hyperfibrinolytic states in HUVECs. The secretion of u-PA into CM was also enhanced by heat shock. These results suggested that human endothelial cells respond to hyperthermia by inducing HSP70 followed by hyperfibrinolytic states with the enhanced expression of u-PAR as well as that of t-PA and u-PA.

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