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Involvement of NADPH oxidase in oxidized LDL-induced upregulation of heat shock factor-1 and plasminogen activator inhibitor-1 in vascular endothelial cells.
Am J Physiol Endocrinol Metab. 2009 Jul; 297(1):E104-11.AJ

Abstract

Plasminogen activator inhibitor-1 (PAI-1) is implicated in thrombogenesis, inflammation, and extracellular matrix remodeling. Previous studies indicated that oxidized low-density lipoprotein (LDL) stimulated the generation of PAI-1 in vascular endothelial cells (EC). The present study demonstrated that LDL oxidized by copper, iron, or 3-morpholinosydnonimine increased the expression of NADPH oxidase (NOX) 2, PAI-1, and heat shock factor-1 (HSF1) in human umbilical vein EC or coronary artery EC compared with LDL or vehicle. Diphenyleneiodonium, a NOX inhibitor, prevented the increases of the expression of HSF1 and PAI-1 in EC induced by oxidized LDLs. Small-interference RNA (siRNA) for p22(phox), an essential subunit of NOX, prevented oxidized LDL-induced expression of NOX2, HSF1, and PAI-1 in EC. HSF1 siRNA inhibited oxidized LDL-induced expression of PAI-1 and HSF1, but not NOX2, in EC. The binding of HSF1 to PAI-1 promoter and the activity of PAI-1 promoter in EC were enhanced by oxidized LDL. Butylated hydroxytulene, a potent antioxidant, inhibited oxidized LDL-induced release of hydrogen peroxide (H(2)O(2)) and the expression of NOX2, HSF1, and PAI-1 in EC. Treatment with H(2)O(2) increased the abundance of NOX2, HSF1, and PAI-1 in EC. The results of the present study indicate that oxidized LDL-induced expression of NOX may lead to the elevated release of reactive oxygen species, the activation of HSF1, and the enhancement of the transcription of PAI-1 gene in cultured vascular EC.

Authors+Show Affiliations

Diabetes Research Group, University of Manitoba, 835-715 McDermot Ave., Winnipeg, Manitoba R3E 3P4, Canada.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

19401454

Citation

Zhao, Ruozhi, et al. "Involvement of NADPH Oxidase in Oxidized LDL-induced Upregulation of Heat Shock Factor-1 and Plasminogen Activator Inhibitor-1 in Vascular Endothelial Cells." American Journal of Physiology. Endocrinology and Metabolism, vol. 297, no. 1, 2009, pp. E104-11.
Zhao R, Ma X, Xie X, et al. Involvement of NADPH oxidase in oxidized LDL-induced upregulation of heat shock factor-1 and plasminogen activator inhibitor-1 in vascular endothelial cells. Am J Physiol Endocrinol Metab. 2009;297(1):E104-11.
Zhao, R., Ma, X., Xie, X., & Shen, G. X. (2009). Involvement of NADPH oxidase in oxidized LDL-induced upregulation of heat shock factor-1 and plasminogen activator inhibitor-1 in vascular endothelial cells. American Journal of Physiology. Endocrinology and Metabolism, 297(1), E104-11. https://doi.org/10.1152/ajpendo.91023.2008
Zhao R, et al. Involvement of NADPH Oxidase in Oxidized LDL-induced Upregulation of Heat Shock Factor-1 and Plasminogen Activator Inhibitor-1 in Vascular Endothelial Cells. Am J Physiol Endocrinol Metab. 2009;297(1):E104-11. PubMed PMID: 19401454.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of NADPH oxidase in oxidized LDL-induced upregulation of heat shock factor-1 and plasminogen activator inhibitor-1 in vascular endothelial cells. AU - Zhao,Ruozhi, AU - Ma,Xiuli, AU - Xie,Xueping, AU - Shen,Garry X, Y1 - 2009/04/28/ PY - 2009/4/30/entrez PY - 2009/4/30/pubmed PY - 2009/8/11/medline SP - E104 EP - 11 JF - American journal of physiology. Endocrinology and metabolism JO - Am J Physiol Endocrinol Metab VL - 297 IS - 1 N2 - Plasminogen activator inhibitor-1 (PAI-1) is implicated in thrombogenesis, inflammation, and extracellular matrix remodeling. Previous studies indicated that oxidized low-density lipoprotein (LDL) stimulated the generation of PAI-1 in vascular endothelial cells (EC). The present study demonstrated that LDL oxidized by copper, iron, or 3-morpholinosydnonimine increased the expression of NADPH oxidase (NOX) 2, PAI-1, and heat shock factor-1 (HSF1) in human umbilical vein EC or coronary artery EC compared with LDL or vehicle. Diphenyleneiodonium, a NOX inhibitor, prevented the increases of the expression of HSF1 and PAI-1 in EC induced by oxidized LDLs. Small-interference RNA (siRNA) for p22(phox), an essential subunit of NOX, prevented oxidized LDL-induced expression of NOX2, HSF1, and PAI-1 in EC. HSF1 siRNA inhibited oxidized LDL-induced expression of PAI-1 and HSF1, but not NOX2, in EC. The binding of HSF1 to PAI-1 promoter and the activity of PAI-1 promoter in EC were enhanced by oxidized LDL. Butylated hydroxytulene, a potent antioxidant, inhibited oxidized LDL-induced release of hydrogen peroxide (H(2)O(2)) and the expression of NOX2, HSF1, and PAI-1 in EC. Treatment with H(2)O(2) increased the abundance of NOX2, HSF1, and PAI-1 in EC. The results of the present study indicate that oxidized LDL-induced expression of NOX may lead to the elevated release of reactive oxygen species, the activation of HSF1, and the enhancement of the transcription of PAI-1 gene in cultured vascular EC. SN - 1522-1555 UR - https://www.unboundmedicine.com/medline/citation/19401454/Involvement_of_NADPH_oxidase_in_oxidized_LDL_induced_upregulation_of_heat_shock_factor_1_and_plasminogen_activator_inhibitor_1_in_vascular_endothelial_cells_ L2 - https://journals.physiology.org/doi/10.1152/ajpendo.91023.2008?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -