Minimally modified low-density lipoprotein upregulates mouse mesenteric arterial 5-HT1B receptor in vivo via activation of the JAK2/STAT3 pathway

兴奋剂 内科学 受体 内分泌学 下调和上调 车站3 信号转导 低密度脂蛋白受体 受体表达 生物 化学 医学 脂蛋白 细胞生物学 胆固醇 生物化学 基因
作者
Hongxia Tang,Jie Lin,Cang‐Bao Xu,Gen Chen,Yajie Liao,Ning-Ren Lei,Jie Li
出处
期刊:Microvascular Research [Elsevier BV]
卷期号:139: 104260-104260
标识
DOI:10.1016/j.mvr.2021.104260
摘要

To explore whether minimally modified low-density lipoprotein (mmLDL) upregulates mesenteric arterial 5-hydroxytryptamine 1B (5-HT1B) receptor expression by activating the JAK2/STAT3 signaling pathway.Mice were randomly divided into the following groups: the normal saline (NS), LDL, mmLDL, mmLDL+galiellactone (GL, a JAK2/STAT3 pathway inhibitor), and mmLDL+DMSO groups. The dose-response curve of mesenteric arterial ring constriction after administration of 5-carboxamidotryptamine (5-CT), an agonist of 5-HT1B, was recorded with a microvascular tensiometer. JAK2, p-JAK2, STAT3, p-STAT3, and 5-HT1B receptor protein expression levels were determined by Western blotting. 5-HT1B receptor mRNA levels were measured by RT-PCR. 5-HT1B receptor protein expression was determined by immunofluorescence.Injection of mmLDL into the tail vein significantly increased the contractile dose-response curve after 5-CT stimulation, as the Emax was 82.15 ± 6.15% in the NS group and 171.88 ± 5.78% in the mmLDL group (P < 0.01); significantly elevated 5-HT1B receptor mRNA and protein expression levels; and significantly increased p-JAK2 and p-STAT3 protein expression levels. After intraperitoneal injection of GL, the vasoconstrictive response was significantly reduced compared with that in the mmLDL group, as the Emax was decreased to 97.14 ± 1.20% (P < 0.01); 5-HT1B receptor mRNA and protein expression levels were significantly reduced; STAT3 phosphorylation and p-JAK2 and p-STAT3 protein expression were not significantly changed; and 5-HT1B receptor expression was altered via inhibition of p-STAT3 binding to DNA, which suppressed transcription.mmLDL can upregulate 5-HT1B receptor expression in mouse mesenteric arteries by activating the JAK2/STAT3 signaling pathway.
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
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

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
2秒前
3秒前
晗月完成签到,获得积分10
3秒前
情怀应助如意枫叶采纳,获得10
4秒前
量子星尘发布了新的文献求助10
6秒前
Akim应助SS采纳,获得10
7秒前
张雷应助清新的夜蕾采纳,获得20
7秒前
chennn发布了新的文献求助10
7秒前
罗一完成签到,获得积分10
9秒前
11秒前
丘比特应助wu采纳,获得10
14秒前
俏皮芷蕊发布了新的文献求助30
14秒前
称心的菲鹰完成签到,获得积分10
15秒前
碧蓝问安发布了新的文献求助10
16秒前
16秒前
打打应助ZZZ采纳,获得10
18秒前
22秒前
呆萌板凳发布了新的文献求助10
22秒前
hp关闭了hp文献求助
23秒前
24秒前
都选C完成签到,获得积分10
25秒前
壮观以松完成签到,获得积分10
25秒前
Liufgui应助郭小宝采纳,获得20
25秒前
heli完成签到,获得积分10
27秒前
如意枫叶发布了新的文献求助10
28秒前
都选C发布了新的文献求助10
29秒前
英俊的铭应助淡烟流水采纳,获得10
30秒前
30秒前
Miracle完成签到,获得积分10
32秒前
36秒前
wu发布了新的文献求助10
36秒前
忧心的听双完成签到,获得积分10
36秒前
Timon完成签到,获得积分10
37秒前
深情安青应助Miracle采纳,获得10
38秒前
李健应助猪猪hero采纳,获得10
38秒前
kingwill应助Harlotte采纳,获得60
38秒前
张雯思发布了新的文献求助10
39秒前
西瓜刀发布了新的文献求助10
39秒前
寒冷的发箍完成签到,获得积分10
41秒前
41秒前
高分求助中
A new approach to the extrapolation of accelerated life test data 1000
ACSM’s Guidelines for Exercise Testing and Prescription, 12th edition 500
‘Unruly’ Children: Historical Fieldnotes and Learning Morality in a Taiwan Village (New Departures in Anthropology) 400
Indomethacinのヒトにおける経皮吸収 400
Phylogenetic study of the order Polydesmida (Myriapoda: Diplopoda) 370
基于可调谐半导体激光吸收光谱技术泄漏气体检测系统的研究 350
Robot-supported joining of reinforcement textiles with one-sided sewing heads 320
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 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 3989242
求助须知:如何正确求助?哪些是违规求助? 3531393
关于积分的说明 11253753
捐赠科研通 3270010
什么是DOI,文献DOI怎么找? 1804868
邀请新用户注册赠送积分活动 882084
科研通“疑难数据库(出版商)”最低求助积分说明 809136