Involvement of CGRP, Substance P and Blood Circulation in Aggravating Mechanism of Absolute Ethanol-Induced Antral Lesions by Capsaicin Treatment in Rats

Yamaguchi, Yu; Kitagawa, Satomi; Imaizumi, Noriko; Kunitomo, Masaru; Fujiwara, Motohatsu

doi:10.1254/jjp.61.291

Cited by 6 publications

(6 citation statements)

References 57 publications

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“…43,44 Interestingly, strain MRL/lpr mice exhibit about half the LCAT activity of strain ICR mice. 13 The QTL on Chr 8 also leads to significantly increased V/LDL cholesterol and UC levels ( Figure 4B), consistent with the hypothesis that LCAT deficiency in MRL/lpr mouse underlies the Chr 8 QTL in this cross. Northern analyses using age controlled female mice fed the chow diet showed no significant difference in LCAT mRNA levels between MRL/lpr and BALB/cJ mice (data not shown).…”

Section: Discussionsupporting

confidence: 84%

“…12 The observation that MRL/n mice, lacking the lpr mutation, exhibited very different lipoprotein profiles compared with MRL/lpr mice suggested that the unusual lipoprotein profiles were related to autoimmunity. 13,14 Previous studies have also shown that MRL/lpr mice, a model for systemic lupus erythematosus (SLE), develop severe coronary lipid lesions and increased myocardial infarction when fed an atherogenic, high fat diet. 13,14 This suggests that the autoimmune background may contribute to the abnormal lipoprotein metabolism and CAD seen in the MRL mice.…”

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confidence: 99%

“…13,14 Previous studies have also shown that MRL/lpr mice, a model for systemic lupus erythematosus (SLE), develop severe coronary lipid lesions and increased myocardial infarction when fed an atherogenic, high fat diet. 13,14 This suggests that the autoimmune background may contribute to the abnormal lipoprotein metabolism and CAD seen in the MRL mice. In an attempt to dissect these interactions, we examined the genetic determinants of lipoprotein metabolism and atherogenesis in the MRL strain.…”

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confidence: 99%

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Quantitative Trait Locus Analysis of Plasma Lipoprotein Levels in an Autoimmune Mouse Model

Johnson

Lusis

1999

ATVB

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Abstract-The autoimmune MRL/lpr mouse strain, a model for systemic lupus erythematosus, exhibited an unusual plasma lipoprotein profile, suggesting a possible interaction of autoimmune disease and lipoprotein metabolism.In an effort to examine the genetic basis of such interactions, and to study their relationship to atherogenesis, we performed a quantitative trait locus analysis using a total of 272 (MRL/lprϫBALB/cJ) second generation (F2) intercross mice. These mice were examined for levels of total plasma cholesterol, HDL cholesterol, VLDL and LDL cholesterol, unesterified cholesterol, autoantibodies, and aortic fatty streak lesions. Key Words: linkage analysis Ⅲ antibodies, antinuclear Ⅲ genes Ⅲ lupus erythematosus, systemic Ⅲ HDL P lasma lipoprotein levels are an important determinant of atherosclerosis, the major cause of coronary artery disease (CAD) and stroke. High levels of LDL and VLDL are strongly associated with increased incidence of CAD, whereas HDL has a protective effect. 1-4 Although a number of mendelian disorders contributing to lipoprotein metabolism, such as those of the LDL receptor in familial hypercholesterolemia and cholesterol ester transfer protein deficiency in hyperalphalipoproteinemia, have been elucidated, 1,5,6 they explain only a small fraction of the population variance of plasma lipoprotein levels. As yet, relatively little is known of the genetic factors contributing to common, complex genetic variations. Studies of such variations in humans are complicated by dietary influences and genetic heterogeneity. Animal models have significant advantages for the analysis of complex traits 7-11 ; in particular, planned breeding can be performed and the environment can be controlled. The mouse, the most useful mammal for genetic studies, has been developed as a model for the analysis of lipoprotein metabolism and other traits relevant to atherosclerosis. In previous studies in our laboratory, we have identified several quantitative-trait loci (QTL) for lipoprotein metabolism in mice, and some of the underlying genes were elucidated using a positional candidate gene strategy. 10,11

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Section: Discussionsupporting

confidence: 84%

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confidence: 99%

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confidence: 99%

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Quantitative Trait Locus Analysis of Plasma Lipoprotein Levels in an Autoimmune Mouse Model

Johnson

Lusis

1999

ATVB

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“…Serum levels of total cholesterol, LDL-C and HDL-C were higher in both immunized and NI mice fed an HD than those fed a standard diet starting from the day of the CIA boost. Immunized mice fed a HD showed high serum cholesterol but significantly lower serum TG, a phenomenon already described in inflammatory models [35]. Interestingly, in mice lacking the liver-X-receptor (LXR) fed a high-cholesterol diet, serum TG are dramatically reduced because of hepatic accumulation of cholesteryl esters that compete with TG for incorporation into very low-density lipoproteins (VLDL) [36].…”

Section: Discussionmentioning

confidence: 86%

Aortic VCAM‐1: an early marker of vascular inflammation in collagen‐induced arthritis

Denys

Clavel

Lemeiter

et al. 2016

J Cellular Molecular Medi

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Cardiovascular disease (CVD) is a major cause of morbidity and mortality in rheumatoid arthritis (RA). There are limited experimental data on vascular involvement in arthritis models. To study the link between CVD and inflammation in RA, we developed a model of vascular dysfunction and articular inflammation by collagen‐induced arthritis (CIA) in C57Bl/6 (B6) mice. We studied the expression of vascular inflammatory markers in CIA with and without concomitant hyperlipidic diet (HD). Collagen‐induced arthritis was induced with intradermal injection of chicken type‐II collagen followed by a boost 21 days later. Mice with and without CIA were fed a standard diet or an HD for 12 weeks starting from the day of the boost. Arthritis severity was evaluated with a validated clinical score. Aortic mRNA levels of vascular cell adhesion molecule‐1 (VCAM‐1), inducible nitric oxide synthase (iNOS) and interleukin‐17 were analysed by quantitative RT‐PCR. Vascular cell adhesion molecule‐1 localization in the aortic sinus was determined by immunohistochemistry. Atherosclerotic plaque presence was assessed in aortas. Collagen‐induced arthritis was associated with increased expression of VCAM‐1, independent of diet. VCAM‐1 overexpression was detectable as early as 4 weeks after collagen immunization and persisted after 15 weeks. The HD induced atheroma plaque formation and aortic iNOS expression regardless of CIA. Concomitant CIA and HD had no additive effect on atheroma or VCAM‐1 or iNOS expression. CIA and an HD diet induced a distinct and independent expression of large‐vessel inflammation markers in B6 mice. This model may be relevant for the study of CVD in RA.

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“…The topographical distribution map will facilitate the study of the functions of SP‐IR axons in the different regions of the stomach. It has been shown that capsaicin‐sensitive afferent axons (SP‐ and CGRP‐containing axons) may be either protective or harmful to the stomach during injuries and diseases (Gazzieri et al., 2007; Harrison & Geppetti, 2001; Larauche et al., 2004; Pongor et al., 2011; Uchida et al., 1993). The detailed analysis of SP‐IR axons in different regions provides a foundation for a quantitative assessment of the changes of SP‐axons in response to noxious stimuli during injuries and in pathological conditions.…”

Section: Discussionmentioning

confidence: 99%

Topographical organization and morphology of substance P (SP)‐immunoreactive axons in the whole stomach of mice

Mistareehi

Madas

et al. 2022

J of Comparative Neurology

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Nociceptive afferents innervate the stomach and send signals centrally to the brain and locally to stomach tissues. Nociceptive afferents can be detected with a variety of different markers. In particular, substance P (SP) is a neuropeptide and is one of the most commonly used markers for nociceptive nerves in the somatic and visceral organs. However, the topographical distribution and morphological structure of SPimmunoreactive (SP-IR) axons and terminals in the whole stomach have not yet been fully determined. In this study, we labeled SP-IR axons and terminals in flat mounts of the ventral and dorsal halves of the stomach of mice. Flat-mount stomachs, including the longitudinal and circular muscular layers and the myenteric ganglionic plexus, were processed with SP primary antibody followed by fluorescent secondary antibody and then scanned using confocal microscopy. We found that (1) SP-IR axons and terminals formed an extensive network of fibers in the muscular layers and within the ganglia of the myenteric plexus of the whole stomach. (2) Many axons that ran in parallel with the long axes of the longitudinal and circular muscles were also immunoreactive for the vesicular acetylcholine transporter (VAChT). (3) SP-IR axons formed very dense terminal varicosities encircling individual neurons in the myenteric plexus; many of these were VAChT immunoreactive. (4) The regional density of SP-IR axons and terminals in the muscle and myenteric plexus varied in the following order from high to low: antrum-pylorus, corpus, fundus, and cardia. (5) In only the longitudinal and circular muscles, the regional density of SP-IR axon innervation from high to low were: antrumpylorus, corpus, cardia, and fundus. ( 6) The innervation patterns of SP-IR axons and terminals in the ventral and dorsal stomach were comparable. Collectively, our data provide for the first time a map of the distribution and morphology of SP-IR axons and terminals in the whole stomach with single-cell/axon/synapse resolution. This work will establish an anatomical foundation for functional mapping of the SP-IR axon innervation of the stomach and its pathological remodeling in gastrointestinal diseases.

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Involvement of CGRP, Substance P and Blood Circulation in Aggravating Mechanism of Absolute Ethanol-Induced Antral Lesions by Capsaicin Treatment in Rats

Cited by 6 publications

References 57 publications

Quantitative Trait Locus Analysis of Plasma Lipoprotein Levels in an Autoimmune Mouse Model

Quantitative Trait Locus Analysis of Plasma Lipoprotein Levels in an Autoimmune Mouse Model

Aortic VCAM‐1: an early marker of vascular inflammation in collagen‐induced arthritis

Topographical organization and morphology of substance P (SP)‐immunoreactive axons in the whole stomach of mice

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