Expression profile of active genes in mouse lymph node high endothelial cells

高内皮静脉 生物 分子生物学 单元格排序 川地31 内皮干细胞 互补DNA 趋化因子 细胞粘附分子 基因 细胞生物学 流式细胞术 淋巴细胞 血管生成 受体 免疫学 遗传学 体外
作者
Dai Izawa,Takashi Tanaka,Koichi Saito,Hitoshoi Ogihara,Tateo Usui,Shoko Kawamoto,Kouki Matsubara,Kousaku Okubo,M Miyasaka
出处
期刊:International Immunology [Oxford University Press]
卷期号:11 (12): 1989-1998 被引量:55
标识
DOI:10.1093/intimm/11.12.1989
摘要

High endothelial venules (HEV) allow rapid and selective lymphocyte trafficking from the blood into secondary lymphoid tissues. Here we report the expression profile of active genes in mouse high endothelial cells (HEC). HEC were first purified from mouse lymph nodes (LN) by magnetic cell sorting with MECA-79 mAb and a 3′-directed cDNA library that faithfully represents the composition of mRNA was constructed. A total of 1495 cDNA sequences were obtained from randomly selected clones. Based on their sequence identity, they were grouped into 754 different species [gene signatures (GS)] of which 335 GS were identified in GenBank. Among the previously identified genes, expression of several endothelial cell surface molecules including endoglin and ICAM-1 was detected in HEC. Comparison of the gene expression profile with that of purified CD31+ flat endothelial cells identified several molecules, such as KC chemokine and Duffy antigen/receptor for chemokines, that are known to be selectively expressed in activated endothelial cells or post-capillary venules. Interestingly, mac25/TAF, which is known to be expressed specifically in tumor vessels and implicated in the regulation of cell adhesion, was highly and selectively expressed in HEC in mouse LN, suggesting that it may participate in regulating HEC-specific functions. Comparison with the expression profiles obtained from 35 different cell types showed at least 22 GS that were apparently specific to HEC. Our results illustrate the expression differences between HEC and CD31+ flat endothelial cells, and will be useful for the identification and characterization of genes specific for HEC.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
科研通AI6.1应助yehe采纳,获得10
刚刚
Pam发布了新的文献求助20
2秒前
GQC发布了新的文献求助10
2秒前
小蓝完成签到 ,获得积分10
3秒前
3秒前
所所应助雾让空山采纳,获得10
3秒前
小佳完成签到,获得积分10
4秒前
华仔应助xx采纳,获得10
4秒前
4秒前
小果冻啊噗啊噗关注了科研通微信公众号
4秒前
猪猪hero发布了新的文献求助10
5秒前
Ava应助豆豆豆豆采纳,获得10
5秒前
6秒前
Tengchao发布了新的文献求助10
6秒前
6秒前
6秒前
7秒前
7秒前
英姑应助kgf采纳,获得10
7秒前
故事的小红花完成签到,获得积分10
7秒前
Lucas应助蘑菇蘑菇采纳,获得10
8秒前
8秒前
8秒前
8秒前
9秒前
goldNAN发布了新的文献求助10
10秒前
一一发布了新的文献求助10
10秒前
稳重冰之完成签到,获得积分10
10秒前
li完成签到,获得积分10
10秒前
10秒前
11秒前
iwhisper发布了新的文献求助10
12秒前
12秒前
iwhisper发布了新的文献求助10
12秒前
苹果发布了新的文献求助10
13秒前
13秒前
11发布了新的文献求助10
13秒前
13秒前
iwhisper发布了新的文献求助10
14秒前
14秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Modern Epidemiology, Fourth Edition 5000
Handbook of pharmaceutical excipients, Ninth edition 5000
Kinesiophobia : a new view of chronic pain behavior 5000
Molecular Biology of Cancer: Mechanisms, Targets, and Therapeutics 3000
Digital Twins of Advanced Materials Processing 2000
Weaponeering, Fourth Edition – Two Volume SET 2000
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 纳米技术 化学工程 生物化学 物理 计算机科学 内科学 复合材料 催化作用 物理化学 光电子学 电极 冶金 细胞生物学 基因
热门帖子
关注 科研通微信公众号,转发送积分 6019600
求助须知:如何正确求助?哪些是违规求助? 7614266
关于积分的说明 16162653
捐赠科研通 5167378
什么是DOI,文献DOI怎么找? 2765636
邀请新用户注册赠送积分活动 1747492
关于科研通互助平台的介绍 1635652