Upregulation of Cyclooxygenase-II Gene and PGE2 Production of Peritoneal Macrophages in Diabetic Rats1

Lo, Chang-fa

doi:10.1016/j.jss.2004.12.005

Cited by 20 publications

(8 citation statements)

References 29 publications

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“…from alloxan-treated animals presented impaired response to LPS, with altered cytokines and nitrite production. Increased glucose is described to be involved in some alterations of macrophages responses in diabetic animal models, including interleukin-12 expression (Wen et al, 2006) and upregulation of cyclooxygenase-II, leading to increased prostaglandin-E 2 production (Lo, 2005). Additionally, increased glucose is described to increase basal ROS production in macrophages (Guha et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Regulation of LPS stimulated ROS production in peritoneal macrophages from alloxan-induced diabetic rats: Involvement of high glucose and PPARγ

et al. 2007

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Section: Discussionmentioning

confidence: 99%

Regulation of LPS stimulated ROS production in peritoneal macrophages from alloxan-induced diabetic rats: Involvement of high glucose and PPARγ

et al. 2007

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“…In addition, hyperglycemia is proposed to modulate NO synthase activity and increase vasoconstrictor eicosanoid in endothelial cells through nonenzymatic glycation of serum albumin (2). Moreover, other evidence suggests that there is upregulation of cyclooxygenase-2 in diabetic humans and animals (7,23), which may contribute to the generation of vasoconstrictor metabolites from AA (31). However, more studies are needed to elucidate the link between chronic hyperglycemia and altered AA metabolism.…”

Section: Discussionmentioning

confidence: 99%

Chronic hyperglycemia impairs functional vasodilation via increasing thromboxane-receptor-mediated vasoconstriction

Xiang

Naik²,

Abram³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Individuals with hyperglycemia exhibit impaired exercise performance and functional vasodilatory response. Based on the importance of arachidonic acid (AA) metabolites in functional vasodilation and the increased thromboxane-to-prostacyclin ratio in diabetes, we hypothesized that chronic hyperglycemia in diabetes increases thromboxane-receptor (TP)-mediated vasoconstriction, resulting in an attenuated functional vasodilation. Three groups of lean Zucker rats (8 wk) were used to test the effects of chronic hyperglycemia on endothelial function: normal, streptozotocin (STZ; 70 mg/kg ip), and STZ + insulin (2 U/day). After 4 wk of treatment, spinotrapezius arcade arterioles were chosen for microcirculatory observation. Arteriolar diameter was measured following muscle stimulation and 10 microM AA application in the absence and presence of 1 microM SQ-29548 (TP antagonist). STZ rats exhibited significantly higher fasting glucose levels and attenuated functional and AA-induced dilation compared with normal animals. SQ-29548 improved the vasodilatory responses in STZ rats but had no effect in controls. Insulin treatment normalized both the glucose levels and the vasodilatory responses, and SQ-29548 treatment had no effect on functional or AA-mediated vasodilation in STZ + insulin animals. These results suggest that the impaired functional vasodilation in diabetic rats is due to hyperglycemia-mediated increases in TP-mediated vasoconstriction.

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“…In line with the finding that monocytes and macrophages take on a more inflammatory phenotype in the setting of diabetes [7–9], monocytes and macrophages from diabetic rodents and humans often exhibit increased C20:4 metabolism; indeed, overproduction of arachidonoyl-CoA, COX-2 and PGE 2 has been observed in monocytes and macrophages from rodent models of T1D and human subjects with T1D or T2D as compared to controls [3], [8], [16–17]. In one study on CD14 + monocytes from human subjects, COX-2 was found to be downregulated in subjects with juvenile onset T1D, but upregulated in subjects with adult onset T1D, latent autoimmune diabetes of the adult (LADA) or T2D, as compared to controls [8].…”

Section: Production Of Inflammatory Protein and Lipid Mediators In Inmentioning

confidence: 99%

Inflammation and diabetes-accelerated atherosclerosis: myeloid cell mediators

Kanter

Bornfeldt

2013

Trends in Endocrinology & Metabolism

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Monocytes and macrophages respond to and govern inflammation by producing a plethora of inflammatory modulators, including cytokines, chemokines and arachidonic acid (C20:4)-derived lipid mediators. One of the most prevalent inflammatory diseases is cardiovascular disease, caused by atherosclerosis, and accelerated by diabetes. Recent research has demonstrated that monocytes/macrophages from diabetic mice and humans with type 1 diabetes show upregulation of the enzyme, acyl-CoA synthetase 1 (ACSL1), which promotes C20:4 metabolism, and that ACSL1 inhibition selectively protects these cells from the inflammatory and pro-atherosclerotic effects of diabetes, in mice. Increased understanding of the role of ACSL1 and other culprits in monocytes/macrophages in inflammation and diabetes-accelerated atherosclerosis offers hope for new treatment strategies to combat diabetic vascular disease.

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Upregulation of Cyclooxygenase-II Gene and PGE2 Production of Peritoneal Macrophages in Diabetic Rats1

Cited by 20 publications

References 29 publications

Regulation of LPS stimulated ROS production in peritoneal macrophages from alloxan-induced diabetic rats: Involvement of high glucose and PPARγ

Regulation of LPS stimulated ROS production in peritoneal macrophages from alloxan-induced diabetic rats: Involvement of high glucose and PPARγ

Chronic hyperglycemia impairs functional vasodilation via increasing thromboxane-receptor-mediated vasoconstriction

Inflammation and diabetes-accelerated atherosclerosis: myeloid cell mediators

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