Local Heat Shock Priming Promotes Recanalization of Thromboembolized Microvasculature by Upregulation of Plasminogen Activators

Rücker, Martin; Schäfer, T.; Scheuer, Cláudia; Harder, Yves; Vollmar, Brigitte; Menger, Michael D.

doi:10.1161/01.atv.0000223144.65958.c3

Cited by 12 publications

(12 citation statements)

References 40 publications

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“…Uchiyama et al (30) described that adenovirus vectormediated overexpression of HSF1 gene reduced PAI-1 expression in arterial EC; however, their results were not verified using a gene knockdown approach or knockout animal model. The results of the present study support the report from Rücker et al (22). HSF1-mediated stress response is considered as an important chain reaction for a self-defense mechanism of the body.…”

Section: Discussionsupporting

confidence: 92%

“…Results from previous studies on the relationship between PAI-1 and heat shock response or its mediators were controversial. Rücker et al (22) reported that local heat shock increased PAI-1 expression in arterioles from rat skeletal muscle. Uchiyama et al (30) described that adenovirus vectormediated overexpression of HSF1 gene reduced PAI-1 expression in arterial EC; however, their results were not verified using a gene knockdown approach or knockout animal model.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Involvement of NADPH oxidase in oxidized LDL-induced upregulation of heat shock factor-1 and plasminogen activator inhibitor-1 in vascular endothelial cells

Zhao¹,

Ma²,

Xie³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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. 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 (H2O2) and the expression of NOX2, HSF1, and PAI-1 in EC. Treatment with H2O2 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.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Involvement of NADPH oxidase in oxidized LDL-induced upregulation of heat shock factor-1 and plasminogen activator inhibitor-1 in vascular endothelial cells

Zhao¹,

Ma²,

Xie³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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“…As reported, these changes were related to mammary function and include 1) inhibited milk secretion by upregulating an endogenous milk enzymatic system (Rucker et al 2006, Silanikove et al 2009), 2) disrupted tight junction of mammary gland epithelial cells, increased casein degradation and decreased the protein synthesis (Stelwagen et al 1998, Silanikove et al 2000, Shamay et al 2003, and 3) disrupted cytoskeletal components and inhibited cell cycle of BMECs (Collier et al 2006, Du et al 2008. In this study, we also found that these genes, SERPINE, PLAU, and PLAUR, coding an endogenous milk enzymatic system were upregulated; some genes, such as RICTOR, PIK3 and ELF2, involving in mTOR signaling pathway of mediated protein synthesis were down-regulated (Table S1).…”

Section: Discussionmentioning

confidence: 84%

The global effect of heat on gene expression in cultured bovine mammary epithelial cells

Sun

et al. 2015

Cell Stress and Chaperones

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Heat stress (HS) in hot climates is a major cause that strongly negatively affects milk yield in dairy cattle, leading to immeasurable economic loss. The heat stress response of bovine mammary epithelial cells (BMECs) is one component of the acute systemic response to HS. Gene networks of BMECs respond to environmental heat loads with both intra-and extracellular signals that coordinate cellular and whole-animal metabolism. Our experimental objective was to characterize the direct effects of heat stress on the cultured bovine mammary epithelial cells by microarray analyses. The data identified 2716 differentially expressed genes in 43,000 transcripts which were changed significantly between heat-stressed and normal bovine mammary epithelial cells (fold change ≥2, P≤0.001). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that these differentially expressed genes are involved in different pathways that regulate cytoskeleton, cell cycle, and stress response processes. Our study provides an overview of gene expression profile and the interaction between gene expression and heat stress, which will lead to further understanding of the potential effects of heat stress on bovine mammary glands.

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“…During certain stresses, including wounding or bleeding, the increased generation of PAI-1 from endothelial cells may play a protective role through maintaining fibrin clots or the integrity of the extracellular matrix. Rü cker et al (41) demonstrated that heat shock increased the expression of PAI-1 in vascular tissue of rat muscle. Uchiyama et al (42) reported that adenovirus vector-mediated overexpression of HSF1 gene reduced PAI-1 expression in cultured arterial endothelial cells, but the finding was not verified using any gene knockdown approach.…”

Section: Hsf1 In Glycated Ldl-induced Pai-1mentioning

confidence: 99%

Involvement of Heat Shock Factor-1 in Glycated LDL–Induced Upregulation of Plasminogen Activator Inhibitor-1 in Vascular Endothelial Cells

Zhao

Shen²

2007

Diabetes

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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 ( T he incidence of diabetes in North America has rapidly increased during the last three decades, and the trend is expected to continue (1). The most common cause of death in diabetic patients is coronary artery disease (CAD). Acute coronary syndrome is often associated with thrombosis at the lesions of atherosclerotic plaques (2,3). Thrombogenesis depends on an imbalance between coagulation and fibrinolysis in local blood circulation. Attenuated fibrinolytic activity has been detected in peripheral circulation of type 1 or type 2 diabetic patients (4,5). Plasminogen activator inhibitor-1 (PAI-1) is the major physiological inhibitor for fibrinolysis, which modulates the activity of tissue and urokinase plasminogen activators on the formation of plasmin. PAI-1 is also implicated in inflammation, endothelial dysfunction, and extracellular matrix remodeling (6). An elevated level of PAI-1 in plasma has been considered as a nontraditional risk factor for CAD and a marker of endothelial dysfunction (7).Hyperglycemia and dyslipoproteinemia are two major biochemical markers of diabetes. Elevated LDL is a classical risk factor for atherosclerotic cardiovascular disease. LDL clearance via the LDL receptor is attenuated by glycation (8). Elevated levels of small, dense LDL and glycated LDL were frequently detected in diabetic patients (9 -11). Previous studies in our laboratory demonstrated that glycated LDL increased the production of PAI-1 in cultured venous or arterial endothelial cells. LDL isolated from diabetic patients or glycated LDL modified in vitro enhanced the activity of PAI-1 promoter in endothelial cells (12)(13)(14)(15). Glycated LDL stimulated the generation of reactive oxygen species (ROS) and decreased the abundance of reduced glutathione in endothelial cells (16). The findings imply that glycated LDL may induce oxidative stress in vasculature. Heat shock, mechanical shear, or oxidative stress induces stress responses in cells, which are mediated by heat shock proteins (Hsps). The transcription of Hsp is mediated by heat shock factor (HSF) (17). HSF1 is the most widely distributed form of HSF in human body (18 -20). The activation of HSF1 is detected during embryo growth (21) or in diet-induced atherosclerotic animal models (22). The levels of Hsp-70 were increased in the peripheral circulation of diabetic patients with ketoacidosis (23). Neither the impact of ...

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Local Heat Shock Priming Promotes Recanalization of Thromboembolized Microvasculature by Upregulation of Plasminogen Activators

Cited by 12 publications

References 40 publications

Involvement of NADPH oxidase in oxidized LDL-induced upregulation of heat shock factor-1 and plasminogen activator inhibitor-1 in vascular endothelial cells

Involvement of NADPH oxidase in oxidized LDL-induced upregulation of heat shock factor-1 and plasminogen activator inhibitor-1 in vascular endothelial cells

The global effect of heat on gene expression in cultured bovine mammary epithelial cells

Involvement of Heat Shock Factor-1 in Glycated LDL–Induced Upregulation of Plasminogen Activator Inhibitor-1 in Vascular Endothelial Cells

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