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Involvement of heat shock factor-1 in glycated LDL-induced upregulation of plasminogen activator inhibitor-1 in vascular endothelial cells.
Diabetes. 2007 May; 56(5):1436-44.D

Abstract

Coronary artery disease is the predominant cause of death in diabetic patients. Plasminogen activator inhibitor-1 (PAI-1) is the major physiological inhibitor of plasminogen activators. Heat shock protein (Hsp) was upregulated in uncontrolled diabetic patients. Our previous studies demonstrated that glycated LDL stimulated the generation of PAI-1 from vascular endothelial cells. The present study examined the effect of glycated LDL on the expression of heat shock factor-1 (HSF1), a physiological transcription factor of Hsp, and the involvement of HSF-1 in glycated LDL-induced production of PAI-1 in cultured human umbilical vein endothelial cells (HUVECs) and coronary artery endothelial cells (HCAECs). Treatment with glycated LDL increased the expression of HSF1 and Hsp-70 compared with LDL in subconfluent HCAECs or HUVECs, and that was associated with an increase of PAI-1 expression. The transfection of HSF1 gene enhanced the expression of PAI-1 in endothelial cells. Small interference RNA against HSF1 prevented glycated LDL-induced upregulation of PAI-1 in HCAECs or HUVECs. Glycated LDL increased the binding of a nuclear protein to the PAI-1 promoter. The nuclear protein-DNA complex was supershifted by HSF1 antibody. The presence of an antioxidant, butylated hydroxytulene, during the glycation of LDL prevented glycated LDL-induced increases of the expression of HSF1 or PAI-1 in endothelial cells. The results suggest that HSF-1 is involved in glycated LDL-induced upregulation of PAI-1 in subconfluent vascular endothelial cells through the binding of HSF1 to PAI-1 promoter. Glyco-oxidation may contribute to glycated LDL-induced expression of HSF1 and PAI-1 in endothelial cells.

Authors+Show Affiliations

Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17259369

Citation

Zhao, Ruozhi, and Garry X. Shen. "Involvement of Heat Shock Factor-1 in Glycated LDL-induced Upregulation of Plasminogen Activator Inhibitor-1 in Vascular Endothelial Cells." Diabetes, vol. 56, no. 5, 2007, pp. 1436-44.
Zhao R, Shen GX. Involvement of heat shock factor-1 in glycated LDL-induced upregulation of plasminogen activator inhibitor-1 in vascular endothelial cells. Diabetes. 2007;56(5):1436-44.
Zhao, R., & Shen, G. X. (2007). Involvement of heat shock factor-1 in glycated LDL-induced upregulation of plasminogen activator inhibitor-1 in vascular endothelial cells. Diabetes, 56(5), 1436-44.
Zhao R, Shen GX. Involvement of Heat Shock Factor-1 in Glycated LDL-induced Upregulation of Plasminogen Activator Inhibitor-1 in Vascular Endothelial Cells. Diabetes. 2007;56(5):1436-44. PubMed PMID: 17259369.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of heat shock factor-1 in glycated LDL-induced upregulation of plasminogen activator inhibitor-1 in vascular endothelial cells. AU - Zhao,Ruozhi, AU - Shen,Garry X, Y1 - 2007/01/26/ PY - 2007/1/30/pubmed PY - 2007/6/20/medline PY - 2007/1/30/entrez SP - 1436 EP - 44 JF - Diabetes JO - Diabetes VL - 56 IS - 5 N2 - Coronary artery disease is the predominant cause of death in diabetic patients. Plasminogen activator inhibitor-1 (PAI-1) is the major physiological inhibitor of plasminogen activators. Heat shock protein (Hsp) was upregulated in uncontrolled diabetic patients. Our previous studies demonstrated that glycated LDL stimulated the generation of PAI-1 from vascular endothelial cells. The present study examined the effect of glycated LDL on the expression of heat shock factor-1 (HSF1), a physiological transcription factor of Hsp, and the involvement of HSF-1 in glycated LDL-induced production of PAI-1 in cultured human umbilical vein endothelial cells (HUVECs) and coronary artery endothelial cells (HCAECs). Treatment with glycated LDL increased the expression of HSF1 and Hsp-70 compared with LDL in subconfluent HCAECs or HUVECs, and that was associated with an increase of PAI-1 expression. The transfection of HSF1 gene enhanced the expression of PAI-1 in endothelial cells. Small interference RNA against HSF1 prevented glycated LDL-induced upregulation of PAI-1 in HCAECs or HUVECs. Glycated LDL increased the binding of a nuclear protein to the PAI-1 promoter. The nuclear protein-DNA complex was supershifted by HSF1 antibody. The presence of an antioxidant, butylated hydroxytulene, during the glycation of LDL prevented glycated LDL-induced increases of the expression of HSF1 or PAI-1 in endothelial cells. The results suggest that HSF-1 is involved in glycated LDL-induced upregulation of PAI-1 in subconfluent vascular endothelial cells through the binding of HSF1 to PAI-1 promoter. Glyco-oxidation may contribute to glycated LDL-induced expression of HSF1 and PAI-1 in endothelial cells. SN - 1939-327X UR - https://www.unboundmedicine.com/medline/citation/17259369/Involvement_of_heat_shock_factor_1_in_glycated_LDL_induced_upregulation_of_plasminogen_activator_inhibitor_1_in_vascular_endothelial_cells_ L2 - https://diabetes.diabetesjournals.org/lookup/pmidlookup?view=long&pmid=17259369 DB - PRIME DP - Unbound Medicine ER -