Intestinal metaplasia of human stomach displays distinct patterns of mucin (MUC1, MUC2, MUC5AC, and MUC6) expression.

粘蛋白 肠化生 粘蛋白2 MUC1号 化生 杯状细胞 生物 病理 肠粘膜 医学 上皮 内科学 基因表达 基因 生物化学
作者
Celso A. Reis,Leonor David,P Corréa,Fátima Carneiro,Carme de Bolós,E Garcia,Ulla Mandel,Henrik Clausen,Manuel Sobrinho‐Simões
出处
期刊:PubMed 卷期号:59 (5): 1003-7 被引量:361
链接
标识
摘要

Intestinal metaplasia is a well-established premalignant condition of the stomach that is characterized by mucin carbohydrate modifications defined by histochemical methods. The purpose of the present study was to see whether the expression of mucin core proteins was modified in the different types of intestinal metaplasia and to evaluate the putative usefulness of mucins as "molecular markers" in this setting. We used a panel of monoclonal antibodies with well-defined specificities to MUC1, MUC2, MUC5AC, and MUC6 to characterize the expression pattern of mucins. In contrast to normal gastric mucosa, the complete form or type I intestinal metaplasia (n = 20) displayed little or no expression of MUC1, MUC5AC, or MUC6 in the metaplastic cells and strong expression of the intestinal mucin MUC2 in the goblet cells of all cases. The incomplete forms of intestinal metaplasia, type II (n = 25) and type III (n = 16), expressed MUC1 and MUC5AC in every case, both in goblet and in columnar cells. MUC6 was also expressed in 16 cases of type II intestinal metaplasia and in 11 cases of type III intestinal metaplasia. The intestinal mucin MUC2 was expressed in every case of incomplete intestinal metaplasia, mostly in goblet cells. The mucin expression profile in the different types of intestinal metaplasia allows the identification of two patterns: one defined by decreased levels of expression of "gastric" mucins (MUC1, MUC5AC, and MUC6) and expression of MUC2 intestinal mucin, which corresponds to type I intestinal metaplasia, and the other defined by coexpression of "gastric mucins" (MUC1, MUC5AC, and MUC6) together with the MUC2 mucin, encompassing types II and III intestinal metaplasia. Our results challenge the classical sequential pathway of intestinal metaplasia (from type I to type III via a type II intermediate step).

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
慕青应助秭归子归采纳,获得10
2秒前
吼吼吼吼发布了新的文献求助50
2秒前
科目三应助tengfei采纳,获得10
4秒前
梅子完成签到 ,获得积分10
4秒前
桐桐应助shilifengcheng采纳,获得10
4秒前
8秒前
吼吼吼吼完成签到,获得积分10
9秒前
脑洞疼应助DoctorG采纳,获得30
11秒前
12秒前
白白完成签到,获得积分10
13秒前
15秒前
冰魂应助过昼采纳,获得10
15秒前
jjwen发布了新的文献求助10
15秒前
科研通AI2S应助机灵哲瀚采纳,获得10
16秒前
tengfei发布了新的文献求助10
18秒前
秭归子归发布了新的文献求助10
19秒前
脑洞疼应助家立诚采纳,获得10
21秒前
斯文败类应助斑其采纳,获得10
22秒前
24秒前
25秒前
落寞的又菡完成签到,获得积分10
28秒前
30秒前
DoctorG发布了新的文献求助30
31秒前
上官若男应助jjwen采纳,获得10
32秒前
33秒前
lixm完成签到,获得积分10
34秒前
35秒前
科研通AI2S应助DoctorG采纳,获得30
36秒前
家立诚发布了新的文献求助10
36秒前
快去爬山完成签到 ,获得积分10
37秒前
lixm发布了新的文献求助10
39秒前
司徒不正发布了新的文献求助10
40秒前
yym发布了新的文献求助10
45秒前
科研通AI5应助雾野采纳,获得10
47秒前
NexusExplorer应助BBking采纳,获得50
51秒前
54秒前
54秒前
56秒前
57秒前
BBking发布了新的文献求助50
1分钟前
高分求助中
【此为提示信息,请勿应助】请按要求发布求助,避免被关 20000
ISCN 2024 – An International System for Human Cytogenomic Nomenclature (2024) 3000
Continuum Thermodynamics and Material Modelling 2000
Encyclopedia of Geology (2nd Edition) 2000
105th Edition CRC Handbook of Chemistry and Physics 1600
Maneuvering of a Damaged Navy Combatant 650
China—Art—Modernity: A Critical Introduction to Chinese Visual Expression from the Beginning of the Twentieth Century to the Present Day 360
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 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3777008
求助须知:如何正确求助?哪些是违规求助? 3322389
关于积分的说明 10210090
捐赠科研通 3037746
什么是DOI,文献DOI怎么找? 1666872
邀请新用户注册赠送积分活动 797711
科研通“疑难数据库(出版商)”最低求助积分说明 758040