Effects of Late Administration of Immunoglobulin on Experimental Atherosclerosis in Apolipoprotein E-Deficient Mice

Okabe, Taka-aki; Kishimoto, Chiharu; Shimada, Keisuke; Murayama, Toshinori; Yokode, Masayuki; Kita, Toru

doi:10.1253/circj.69.1543

Cited by 26 publications

(31 citation statements)

References 19 publications

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“…31,32 Accumulating data from both experimental studies and clinical trials suggest that ACE inhibitors may retard the development of atherosclerosis and its manifestations. 18,33,34 Based on the present findings, one might speculate that similar benefit could be attained by ACE inhibitors on C. pneumoniae-induced endothelial dysfunction and, perhaps, on the development of atherosclerosis with an infectious basis.…”

Section: Discussionsupporting

confidence: 60%

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Effects of Bradykinin on Aortic Endothelial Function in ApoE-Knockout Mice With Chronic Chlamydia Pneumoniae Infection

Liuba

Karnani

Pesonen

et al. 2007

Circ J

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Background Impaired muscarinic receptor-mediated vasodilation is an important feature of early atherosclerosis. Earlier studies on apolipoprotein E-knockout mice (apoE-KO) mice suggested adverse effects of Chlamydia pneumoniae infection on the endothelial vasomotor responses of aortas to the muscarinic agonist methacholine. Using additional aorta samples the present study investigated the responses to bradykinin. Methods and Results ApoE-KO mice were repeatedly inoculated with either Chlamydia pneumoniae (C. pneumoniae) or saline. At 2, 6, and 10 weeks after the first inoculation, precontracted aorta rings from both groups were exposed to bradykinin in the absence and presence of L-NAME and diclofenac. In noninfected animals, the vasomotor responses to bradykinin were similar at all timepoints (p>0.5). Compared with noninfected animals, the responses in infected animals tended to increase through the study period (p<0.05 at 10 weeks). Although diclofenac and L-NAME had no effect in noninfected mice, they inhibited the responses to bradykinin in infected mice at 6 and, more markedly, 10 weeks (p<0.05 for both). Conclusion Bradykinin stimulation of aorta endothelium from C. pneumoniae-infected apoE-KO animals appears to activate compensatory kinin receptor-related mechanisms that could involve nitric oxide and vasorelaxing prostanoids. Although the precise molecular mechanisms require further investigation, one could speculate that strategies increasing bradykinin availability might reverse the arterial dysfunction during chronic infectious disease. (Circ J 2007; 71: 1480 -1484

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Section: Discussionsupporting

confidence: 60%

“…The apoE-KO mouse develops atherosclerosis in a similar fashion to humans, 17 and has, therefore, been increasingly used in the past decade for studying the pathogenesis of atherosclerosis in relation to several pathological conditions, including infection. [18][19][20] …”

mentioning

confidence: 99%

Effects of Bradykinin on Aortic Endothelial Function in ApoE-Knockout Mice With Chronic Chlamydia Pneumoniae Infection

Liuba

Karnani

Pesonen

et al. 2007

Circ J

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“…All sections were immersed for 2 min in 60% isopropanol, stained for 15 min in a saturated oil red-O solution at 37°C, counterstained with hematoxylin, and then mounted under coverslips with glycerol gelatin. [13][14][15] …”

Section: Tissue Processingmentioning

confidence: 99%

Effects of MCI-186 (Edaravone), a Novel Free Radical Scavenger, Upon Experimental Atherosclerosis in Apolipoprotein E-Deficient Mice

Okabe

Kishimoto

Shimada

et al. 2006

Circ J

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“…Nicoletti et al found that injection with γ-globulin could inhibit the progression of atherosclerosis during the fatty streak phase and plaque phase in apoE knockout mice 31) . Another experimental study in Japan found that treatment with γ-globulin, even at a later stage of atherosclerosis, could suppress lesion development 32) . A basic science study found that γ-globulin, lipids and some cells can move from circulating blood into the arterial in cases and their corresponding controls.…”

Section: Synergistic Effect Of Albumin and Globulin On Chdmentioning

confidence: 99%

Synergistic Association of Serum Albumin and Globulin with Coronary Heart Disease

Wang

Liu

et al. 2012

JAT

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Aim: Serum albumin and globulin have important roles in atherosclerosis development; however, separate studies exploring the relationship between albumin or globulin and coronary heart disease (CHD) have been conducted. We explored whether there was a synergistic effect of albumin and globulin on the presence of CHD. Methods: A total of 395 patients aged 50-74 years with angiographically documented CHD were recruited, and 596 age-and sex-matched controls without CHD were randomly selected from the general population. The association of albumin and globulin with CHD was analyzed using conditional logistic regression after adjusting for traditional CHD risk factors. Results: Mean values of serum albumin and globulin were significantly lower in cases than in controls (p＜0.001). In the fully adjusted model, compared with participants whose albumin ( ≥ 47.3 g/L) and globulin ( ≥ 25.6 g/L) levels were both higher than the median levels in these participants, the odds ratio for CHD was 1.59 (p= 0.048) for participants with higher albumin ( ≥ 47

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Effects of Late Administration of Immunoglobulin on Experimental Atherosclerosis in Apolipoprotein E-Deficient Mice

Cited by 26 publications

References 19 publications

Effects of Bradykinin on Aortic Endothelial Function in ApoE-Knockout Mice With Chronic Chlamydia Pneumoniae Infection

Effects of Bradykinin on Aortic Endothelial Function in ApoE-Knockout Mice With Chronic Chlamydia Pneumoniae Infection

Effects of MCI-186 (Edaravone), a Novel Free Radical Scavenger, Upon Experimental Atherosclerosis in Apolipoprotein E-Deficient Mice

Synergistic Association of Serum Albumin and Globulin with Coronary Heart Disease

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