EFFECT OF Β2-Adrenoceptor ACTIVATION AND ANGIOTENSIN II ON TUMOUR NECROSIS FACTOR AND INTERLEUKIN 6 GENE TRANSCRIPTION IN THE RAT RENAL RESIDENT MACROPHAGE CELLS

Nakamura, Akio; Johns, Edward J.; Imaizumi, Akira; Yanagawa, Yukishige; Kohsaka, Takao

doi:10.1006/cyto.1999.0488

Cited by 58 publications

(34 citation statements)

References 19 publications

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“…Moriyama et al (10) and our own study (11) documented that Ang II caused IL-6 release and gene expression in cultured mesangial cells and in renal resident macrophage cells. Kaneto et al (12) demonstrated that the elevation in TNF-a mRNA levels after ureteral obstruction was decreased following Ang II inhibition, which suggested that Ang II was involved in the increased expression of TNF-a mRNA in the obstructed kidney (12).…”

mentioning

confidence: 54%

Suppression of Endotoxin-Induced Renal Tumor Necrosis Factor-α and Interleukin-6 mRNA by Renin-Angiotensin System Inhibitors

Niimi

Yanagawa

2002

Japanese Journal of Pharmacology

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ABSTRACT-The present study was designed to clarify the role of angiotensin II (Ang II) in modulating renal tumor necrosis factor (TNF)-a and interleukin-6 (IL-6) production and to investigate the effect of one dose of Ang II inhibitor on cytokines production following lipopolysaccharide (LPS) to cause endotoxemia. Two studies were performed: 1) Ang II was infused intravenously at a rate of 0.2 mg/kg per minute for 4 h in rats and then kidneys were collected to assay TNF-a and IL-6 mRNA levels; 2) Four-week-old Wistar rats pre-treated with angiotensin-converting enzyme inhibitor, enalapril, or type I Ang II-receptor antagonist, TCV-116, were injected with LPS (0.1, 0.5, 1.0 mg, i.p.), and then 2 or 4 h later, kidneys were collected to assay TNF-a, IL-6, renin and angiotensinogen mRNA levels. After a 4-h intravenous infusion of Ang II, renal TNF-a or IL-6 mRNA level significantly increased 1.9-fold or 2.1-fold (each P<0.05) to the control level, respectively. LPS stimulated TNF-a, IL-6 and angiotensinogen mRNA levels in the kidney but in rats given enalapril or TCV-116, LPS-induced IL-6 and TNF-a mRNA levels were completely suppressed (each P<0.05). This suggests that a single dose of renin-angiotensin system inhibitor suppressed renal IL-6 and TNF-a production and may prevent cytokine-induced renal damage during endotoxemia.

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mentioning

confidence: 54%

Suppression of Endotoxin-Induced Renal Tumor Necrosis Factor-α and Interleukin-6 mRNA by Renin-Angiotensin System Inhibitors

Niimi

Yanagawa

2002

Japanese Journal of Pharmacology

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“…Furthermore, Kowala et al (17) reported activated macrophages increase the gene expression and protein of ACE. When candesartan block angiotensin II type 1 (AT1) receptors in macrophages, the activation of macrophages via stimulation of AT1 receptors may be reduced (18,19), resulting in a decrease of aortic ACE activity in the present study. In cultured vascular smooth muscle cells, angiotensin II promotes not only the cell growth but also ACE expression via stimulation of AT1 receptors (20)(21)(22).…”

Section: Fig 2 Time Course Of Plasma Cholesterol Levels In Monkeys mentioning

confidence: 68%

Comparative Effects of Candesartan and Amlodipine in a Monkey Atherosclerotic Model

et al. 2004

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Angiotensin II receptor blockers could prevent the development of atherosclerosis beyond reducing blood pressure in monkeys fed a high-cholesterol diet. However, it has been unclear whether hypotensive effects improve atherosclerosis in primates. We investigated whether antihypertensive agents, an angiotensin II receptor antagonist, candesartan, and a calcium channel blocker, amlodipine, prevent areas of atherosclerotic lesions in the aorta of monkeys fed a high-cholesterol diet. Seventeen male monkeys fed a high-cholesterol diet for 6 months were grouped as follows: a high-cholesterol diet group (n 5), a candesartan-treated group Angiotensin II has been shown to be a potent vasoconstrictor, and it also promotes vascular proliferation via induction of several growth factors and cytokines (4, 5). We previously reported that ACE activity in atherosclerotic lesions in monkeys fed a high-cholesterol diet was increased significantly compared with that in normal lesions (6,7). In this atherosclerotic model, an ACE inhibitor or an angiotensin II receptor blocker (ARB) significantly reduced the progression of atherosclerosis beyond reduction of blood pressure and plasma cholesterol levels (6-8). The mechanism of angiotensin II in the development of atherosclerosis is thought to be various angiotensin II-induced actions such as the induction of growth factors, inflammatory cytokines, adhesion

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“…Delayed-type hypersensitivity (DTH) was elicited 1 wk after the last immunization by injecting a hind footpad with TAA-pulsed eEC incubated with or without adrenergic antagonists. Specifically, 5 ϫ 10 5 CAF 1 eEC were incubated at 37°C with 10 Ϫ8 M EPI or NE for 3 h. In some experiments the ␤ 2 -blocker ICI 118,551 (30,31) or the ␣-blocker phentolamine at 10 Ϫ8 M was added as well. Cells were then washed and 5 ϫ 10 6 cells/ml were pulsed with soluble TAA for 3 h. eEC were washed four times in PBS to remove catecholamines, unbound TAA, and medium, before injection of 7.5 ϫ 10 5 cells in 50 l PBS into the right hind footpad of each of five CAF 1 mice.…”

Section: Immunization Of Mice and Elicitation Of Dthmentioning

confidence: 99%

Catecholamines Inhibit the Antigen-Presenting Capability of Epidermal Langerhans Cells

Seiffert¹,

Hosoi²,

Torii³

et al. 2002

The Journal of Immunology

120

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The sympathetic nervous system modulates immune function at a number of levels. Within the epidermis, APCs (Langerhans cells (LC)) are frequently anatomically associated with peripheral nerves. Furthermore, some neuropeptides have been shown to regulate LC Ag-presenting function. We explored the expression of adrenergic receptors (AR) in murine LC and assessed their functional role on Ag presentation and modulation of cutaneous immune responses. Both purified LC and the LC-like cell lines XS52-4D and XS106 expressed mRNA for the ARs α1A and β2. XS106 cells and purified LC also expressed β1-AR mRNA. Treatment of murine epidermal cell preparations with epinephrine (EPI) or norepinephrine inhibited Ag presentation in vitro. Furthermore, pretreatment of epidermal cells with EPI or norepinephrine in vitro suppressed the ability of these cells to present Ag for elicitation of delayed-type hypersensitivity in previously immunized mice. This effect was blocked by use of the β2-adrenergic antagonist ICI 118,551 but not by the α-antagonist phentolamine. Local intradermal injection of EPI inhibited the induction of contact hypersensitivity to epicutaneously administered haptens. Surprisingly, injection of EPI at a distant site also suppressed induction of contact hypersensitivity. Thus, catecholamines may have both local and systemic effects. We conclude that specific ARs are expressed on LC and that signaling through these receptors can decrease epidermal immune reactions.

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EFFECT OF Β2-Adrenoceptor ACTIVATION AND ANGIOTENSIN II ON TUMOUR NECROSIS FACTOR AND INTERLEUKIN 6 GENE TRANSCRIPTION IN THE RAT RENAL RESIDENT MACROPHAGE CELLS

Cited by 58 publications

References 19 publications

Suppression of Endotoxin-Induced Renal Tumor Necrosis Factor-α and Interleukin-6 mRNA by Renin-Angiotensin System Inhibitors

Suppression of Endotoxin-Induced Renal Tumor Necrosis Factor-α and Interleukin-6 mRNA by Renin-Angiotensin System Inhibitors

Comparative Effects of Candesartan and Amlodipine in a Monkey Atherosclerotic Model

Catecholamines Inhibit the Antigen-Presenting Capability of Epidermal Langerhans Cells

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