Activation of GPR39 with the agonist TC-G 1008 ameliorates ox-LDL-induced attachment of monocytes to endothelial cells
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Keywords:
Proinflammatory cytokine
Endothelial Activation
Endothelial Dysfunction
VCAM-1
Monocyte
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The dual radiolabeled mAb technique was used to quantify the constitutive and induced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in the microvasculature of different organs of the mouse. The constitutive expression of both adhesion molecules varied significantly between tissues, with ICAM-1 levels consistently higher than VCAM-1 in all tissues studied. Following systemic administration of endotoxin (LPS), an increased surface expression of both adhesion molecules occurred in most organs, with the largest increases for ICAM-1 (2 to 3x increase) noted in the heart, small intestine, and brain, while heart and small intestine exhibited the largest increases in LPS-induced VCAM-1 expression (2 to 5x increase). These responses occurred in the face of an unaltered expression of platelet endothelial cell adhesion molecule-1 (PECAM-1) in all tissues. TNF-alpha also elicited an increased expression of both adhesion molecules, with initial increases noted at 2 to 5 h, peak levels at 5 to 9 h, and a sustained elevation above baseline at 24 h. The TNF-alpha-induced increases in both ICAM-1 and VCAM-1 were dose dependent, with significant up-regulation noted at 5 microg/kg and maximal increases occurring at 10 to 25 microg/kg. These studies indicate that while there are significant quantitative differences in constitutive and induced expression of murine ICAM-1 and VCAM-1, the kinetics and dose-response characteristics of the two adhesion molecules to TNF-alpha are qualitatively similar.
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E-selectin
P-selectin
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Intercellular adhesion molecules 1(ICAM-1) and vascular cell adhesion molecule 1(VCAM-1) play important roles in the inflammatory process of cerebral ischemic injury.The expression of ICAM-1 and VCAM-1 increases following cerebral ischemia;ICAM-1 and VCAM-1 promote ischemic inflammation through mediating leukocytes adhesion to the endothelial cells and eventually migration into brain tissue;the inhibition of the overexpression and effect of ICAM-1 and VCAM-1 can reduce cerebral ischemic injury.
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目的：检测细胞间黏附分子-1（ICAM-1）和血管细胞黏附分子-1（VCAM-1）在结直肠癌（CRC）组织和外周血中的表达，探讨 ICAM-1和 VCAM-1在 CRC 发生、转移中的作用和临床意义。方法应用免疫组织化学法（SP 法）测定78例 CRC 原发病灶及癌旁正常组织、42例结直肠腺瘤组织中ICAM-1和 VCAM-1的表达，用 ELISA 法检测78例 CRC 患者和40例健康者血清 ICAM-1和 VCAM-1的含量。结果CRC 原发病灶组织中 ICAM-1和 VCAM-1的表达明显高于结直肠腺瘤组织和癌旁正常组织，差异有统计学意义（P ＜0．01）；CRC 组血清 ICAM-1和 VCAM-1含量明显高于正常对照组（P ＜0．01）；组织中 ICAM-1和 VCAM-1的表达与性别、年龄、肿瘤部位及组织学分型无关（P ＞0．05），但与淋巴结转移及 Dukes 分期有相关性（P ＜0．01）。结论 ICAM-1和 VCAM-1在 CRC 原发病灶组织和外周血中均呈高表达，且随着肿瘤浸润转移的发展而增加，其可能对肿瘤的进展、恶性程度的判断及发生机制具有重要意义。
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Abstract Activated endothelium releases the soluble adhesion molecules vascular cell adhesion molecule‐1 (sVCAM‐1) and intercellular adhesion molecule‐1 (sICAM‐1). Measurement of fluid‐phase adhesion molecules is therefore used to quantify endothelial activation, but it is unclear which is the better marker. The aims of the study were to compare the relationships between mRNA, surface and total expression and released VCAM‐1 and ICAM‐1 in endothelial cell cultures during activation, and to compare human umbilical vein endothelial cells (HUVEC) with the microvascular cell line HMEC‐1. sVCAM‐1 better represented mRNA and surface expression changes in HUVEC undergoing endotoxin stimulation than did sICAM‐1. Very little VCAM‐1 was released from endotoxin‐stimulated HMEC‐1, and sICAM‐1 seemed a better activation marker for these cells. During incubation of HUVEC in media with glucose concentrations of 5.6, 10.6 or 20.6 m m , VCAM‐1 was released to the media in a dose‐dependent way without changes in surface expression. ICAM‐1 was not influenced by the glucose concentration. There are situations when VCAM‐1 concentrations in the media do not mirror the surface expression on HUVEC in culture, indicating that measurements of soluble adhesion molecules may not necessarily be representative of the conditions on the cell surface. Endothelium from different locations showed varying responses with respect to VCAM‐1 and ICAM‐1 liberation upon endotoxin stimulation. Thus, both sVCAM‐1 and sICAM‐1 should be quantified in clinical studies of endothelial activation until their characteristics are better clarified.
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Endothelial Activation
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Intercellular adhesion molecules 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCM-l) play important roles in the inflammatory process of cerebral ischemic injury. The expression of ICAM-l and VCAM-1 increases following cerebral ischemia; ICAM1 and VCAM-l promote ischemic inflammation through mediating leukocytes adhesion to the endothelial cells and eventually migration into brain tissue; the inhibition of the overexpression and effect of ICAM-l and VCAM-l can reduce cerebral ischemic injury.
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مقدمه: تمرین شنا و مصرف سیر می توانند از عوامل پیشگیری کننده از بیماری عروق کرونر باشد. بنابراین، هدف این پژوهش تاثیر هشت هفته تمرین شنا و مصرف سیر بر مقادیر intercellular cell adhesion molecule (ICAM) و vascular cell adhesion molecule (VCAM) سرمی در موش های نر چاق است. روش بررسی: در این مطالعه تجربی، 28 سر موش صحرایی نر نژاد ویستار (میانگین وزن۹/۵ ±۲۸۱ گرم) به طور تصادفی به چهار گروه (کنترل، مکمل سیر ، تمرین شنا، تمرین شنا + مکمل سیر) تقسیم شدند. سپس گروه های تمرین به مدت 8 هفته و هر هفته 3 جلسه تحت تاثیر تمرین و گروه های دریافت کننده مکمل و تمرین+ مکمل، روزانه یک میلی لیتر عصاره محلول سیر به ازای هر کیلوگرم وزن بدن دریافت کردند. داده ها با استفاده از نرم افزار آماري SPSS v 16و روش آماری تحلیل واریانس یک طرفه و سطح معنی داری (۰۵/۰ ≥ P) ارزیابی شد. نتایج: یافته های پژوهش نشان داد هشت هفته تمرین و مصرف سیر بر مقادیرICAM موشها کاهش معنیداری داشت (05/0 >P). با این حال بر مقادیر VCAMموش ها نر چاق تاثیر معنیداری نداشت (05/0<P). نتیجهگیری: به نظر میرسد ترکیب دو عامل تمرین شنا و مصرف مکمل عصاره سیر یا تمرین ورزشی به تنهایی، به کاهش سطوح مولکول های چسبان می انجامد و استفاده از آن توصیه می شود. هرچند به منظور مشخص شدن تاثیر آن به یژوهش های بیشتری در نمونه های انسانی نیازمندیم.
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Intercellular adhesion molecule
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