Glucocorticoids induce beta(2)-adrenergic receptor function in human nasal mucosa
Glucocorticoids induce beta(2)-adrenergic receptor function in human nasal mucosa
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DOI：
10.1164/ajrccm.155.2.9032216
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发表时间：
1997-02-01
影响因子：
24.7
通讯作者：
Troost, T
中科院分区：
文献类型：
--
作者：
Baraniuk, JN;Ali, M;Troost, T
假设糖皮质激素诱导β（2）-肾上腺素能受体（β（2）-R）及其功能。本文研究了地塞米松（DEX）和二丙酸倍氯米松（BDP）在体外和体内诱导人鼻粘膜β（2）-R信使RNA（mRNA）和功能的能力。在该组织中，沙丁胺醇在体内或体外均不会刺激胞吐作用（Mullol和同事，1992）。因此，糖皮质激素诱导β（2）-R介导的腺体再胞吐作用被认为是一个明确的结果指标。人鼻粘膜在有和没有1 μ M DEX的情况下培养3天，然后用培养基或100 μ M沙丁胺醇攻击。收集培养物上清液用于测量胞吐的腺产物。提取外植体mRNA进行逆转录-聚合酶链反应（RT-PCR），并进行β（2）-R mRNA的原位杂交。在体内，正常受试者在沙丁胺醇鼻激发前接受生理盐水或BDP 3d。在鼻分泌物中测量胞吐产物的浓度。从鼻上皮刮屑中提取RNA进行RT-PCR，在体外，DEX处理诱导白蛋白醇介导的腺胞吐（p
Glucocorticoids are hypothesized to induce beta(2)-adrenergic receptors (beta(2)-R) and their functions. The ability of dexamethasone (DEX) in vitro and beclomethasone dipropionate (BDP) in vivo to induce beta(2)-R messenger RNA (mRNA) and function was investigated in human nasal mucosa. In this tissue, albuterol does not stimulate exocytosis either in vivo or in vitro (Mullol and coworkers, 1992). Therefore, induction of beta(2)-R-mediated glandula rexocytosis by glucocorticoids was proposed as an unambiguous outcome measure. Human nasal mucosa was cultured for 3 d with and without 1 mu M DEX, then challenged with media or 100 mu M albuterol. Culture supernatants were collected for measurement of exocytosed glandular products. Explant mRNA was extracted for reverse transcriptase-polymerase chain reaction (RT-PCR), and in situ hybridization of beta(2)-R mRNA performed. In vivo, normal subjects received saline or BDP for 3 d before albuterol nasal provocation. Concentrations of exocytosed products were measured in nasal secretions. RNA was extracted from nasal epithelial scrapings for RT-PCR, fn vitro, DEX treatment induced albuterol-mediated glandular exocytosis (p