已入深夜,您辛苦了!由于当前在线用户较少,发布求助请尽量完整地填写文献信息,科研通机器人24小时在线,伴您度过漫漫科研夜!祝你早点完成任务,早点休息,好梦!

The role of protease‐activated receptors PAR‐1 and PAR‐2 in the repair of 16HBE 14o−epithelial cell monolayersin vitro

蛋白酵素 受体 丝氨酸蛋白酶 纤维蛋白 分子生物学 化学 蛋白酶激活受体2 蛋白酶 中和抗体 凝结 体外 细胞培养 细胞生物学 生物 抗体 生物化学 免疫学 内科学 医学 酶联受体 遗传学
作者
D. Ewen,Siân Clarke,James R. Smith,Christopher L. Berger,Gary Salmon,Michael A. Trevethick,Janis K. Shute
出处
期刊:Clinical & Experimental Allergy [Wiley]
卷期号:40 (3): 435-449 被引量:9
标识
DOI:10.1111/j.1365-2222.2010.03453.x
摘要

Summary Background We recently reported that repair following mechanical wounding of epithelial cell layers in vitro is dependent on fibrin formation and the activity of locally expressed coagulation cascade proteins. Serine proteases of the coagulation cascade are an important group of protease‐activated receptor (PAR) activators and PAR‐1 to 4 are expressed by the normal bronchial epithelium. Objective We tested the hypothesis that activation of PAR‐1 and PAR‐2 by coagulation cascade proteases stimulates epithelial repair via effects on fibrin formation. Methods Using mechanically wounded 16HBE 14o − epithelial cell layers in culture, we investigated the effect of PAR‐1 and PAR‐2 agonist peptides, control partially scrambled peptides and PAR‐neutralizing antibodies on the rate of repair and fibrin formation. Coagulation factors in culture supernatants were measured by immunoblot. RT‐PCR was used to investigate PAR‐1, PAR‐2 and PGE2 receptor (EP‐1 to EP‐4) expression in this model and qRT‐PCR to quantify responses to wounding. Additionally, we investigated the effect of exogenously added factor Xa (FXa) and neutrophil elastase and the influence of PGE2 and indomethacin on the repair response. Results PAR‐1 and PAR‐2 peptide agonists stimulated the rate of repair and enhanced the formation of a fibrin provisional matrix to support the repair process. Conversely, PAR‐neutralizing antibodies inhibited repair. Under serum‐free culture conditions, 16HBE 14o − cells expressed EP‐2 and EP‐3, but not EP‐1 or EP‐4, receptors. Wounding induced an increased expression of EP‐3 but did not alter EP‐2, PAR‐1 or PAR‐2 expression. In the absence of PAR agonists, there was no evidence for a role for PGE2 in fibrin formation or the repair process. Indomethacin attenuated fibrin formation in wounded cultures only in the presence of the PAR‐2 peptide. FXa stimulated epithelial repair while neutrophil elastase reduced the levels of coagulation factors and inhibited repair. Conclusion Locally expressed serine proteases of the coagulation cascade activate PAR‐1 and PAR‐2 to enhance fibrin formation and bronchial epithelial repair. Cite this as : D. Ewen, S.L. Clarke, J.R. Smith, C. Berger, G. Salmon, M. Trevethick and J.K. Shute, Clinical & Experimental Allergy , 2010 (40) 435–449.
最长约 10秒,即可获得该文献文件

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
nanmu完成签到,获得积分10
1秒前
LNdOjk完成签到,获得积分10
2秒前
顾矜应助悦悦采纳,获得10
2秒前
香蕉觅云应助悦悦采纳,获得10
2秒前
搜集达人应助悦悦采纳,获得10
2秒前
隐形曼青应助悦悦采纳,获得10
3秒前
深情安青应助ifast采纳,获得10
3秒前
传奇3应助悦悦采纳,获得10
3秒前
深情安青应助悦悦采纳,获得10
3秒前
上官若男应助悦悦采纳,获得10
3秒前
西吴完成签到 ,获得积分0
3秒前
华仔应助悦悦采纳,获得10
3秒前
深情安青应助悦悦采纳,获得10
3秒前
充电宝应助悦悦采纳,获得10
4秒前
舟舟完成签到 ,获得积分10
5秒前
绝世冰淇淋完成签到 ,获得积分10
6秒前
友人应助王禹恒采纳,获得10
8秒前
Akim应助王禹恒采纳,获得10
8秒前
Jasper应助Wu采纳,获得10
9秒前
Hedy发布了新的文献求助30
9秒前
香蕉觅云应助ifast采纳,获得10
10秒前
du完成签到 ,获得积分10
15秒前
科研通AI6.1应助suda采纳,获得10
18秒前
allover完成签到,获得积分10
21秒前
科研通AI6.2应助shio采纳,获得10
22秒前
Lilies完成签到,获得积分10
27秒前
务实的海之完成签到,获得积分20
28秒前
司忆完成签到 ,获得积分10
29秒前
32秒前
隐形曼青应助ezekiet采纳,获得10
34秒前
tjnksy完成签到,获得积分10
34秒前
叶云夕完成签到,获得积分10
35秒前
一只不受管束的小狸Miao完成签到 ,获得积分10
36秒前
ifast发布了新的文献求助10
36秒前
小蘑菇应助大气冰旋采纳,获得10
39秒前
Artin完成签到,获得积分10
39秒前
jjjdj完成签到,获得积分10
43秒前
45秒前
49秒前
50秒前
高分求助中
Ideology and Meaning-Making under the Putin Regime 750
Prompt Engineering for Clinicians: Harnessing AI in Everyday Medical Practice 600
Handbook of Luminescence Dating 500
Safety Pharmacology 500
《KNN基无铅压电陶瓷电学性能优化与物理机理研究》 500
Introduction to Industrial/Organizational Psychology 400
Advances in Design and Control Robust Adaptive Control: Deadzone-Adapted Disturbance Suppression 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 计算机科学 化学工程 生物化学 物理 内科学 复合材料 催化作用 光电子学 物理化学 电极 细胞生物学 基因 遗传学
热门帖子
关注 科研通微信公众号,转发送积分 6926360
求助须知:如何正确求助?哪些是违规求助? 8615126
关于积分的说明 18276313
捐赠科研通 6346311
什么是DOI,文献DOI怎么找? 3072002
关于科研通互助平台的介绍 2104913
邀请新用户注册赠送积分活动 2049150