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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.
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