赖氨酸氧化酶样1基因的缺失导致大鼠弹性蛋白纤维合成受损和尿道关闭效率低下。

IF 1.3 4区 医学 Q4 MEDICINE, RESEARCH & EXPERIMENTAL Biomedical Research-tokyo Pub Date : 2021-01-01 DOI:10.2220/biomedres.42.23
Katsumi Kadekawa, Saori Nishijima, Katsuhiko Noguchi, Shiho Okitsu, Kennosuke Karube, Seiji Matsumoto, Hideyuki Yamamoto, Kimio Sugaya
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引用次数: 0

摘要

我们在缺乏赖氨酸氧化酶样蛋白1 (Loxl1)的大鼠模型中研究了膀胱和尿道功能。雌性Loxl1-/-或年龄匹配野生型(WT)大鼠进行漏点压力测试、膀胱术、下尿路组织病理学分析和离体逼尿肌条对乙醇和电场刺激的收缩反应。与WT大鼠相比,Loxl1-/-大鼠皮肤松弛度和冗余度增加,膀胱术中收缩间隔和空量减少,漏点压力降低,肠系膜、膀胱、尿道和阴道的弹性纤维变薄,逼尿肌条对乙醇的收缩反应变小。由此可见,Loxl1-/-大鼠尿道粘膜下弹性蛋白合成受损导致尿道静息闭锁压力降低,逼尿肌胆碱能收缩反应减弱可能与膀胱活动有关。
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Deletion of the lysyl oxidase-like 1 gene induces impaired elastin fiber synthesis and inefficient urethral closure in rats.

We investigated the bladder and urethral function in a rat model lacking the protein lysyl oxidase-like 1 (Loxl1). Female nulliparous rats of Loxl1-/- or age-matched wild type (WT) rats had leak-point pressure testing, cystometry, histopathological analyses of lower urinary tract, and contractile response of isolated detrusor strips to carbachol and electric field stimulation. The Loxl1-/- rats showed increased looseness and redundancy of the skin, the decreased intercontraction interval and voided volume in cystometry, the lower leak-point pressure, thinner elastic fibers of the mesentery, bladder, urethra and vagina, and smaller contractile response of detrusor strips to carbachol when compared to the WT rats. Thus, the insufficient hydrostatic mechanism of urethra via submucosal impaired elastin synthesis might reduce the resting urethral closure pressure and the diminished cholinergic contractile response of detrusor smooth muscle might be involved in bladder activity in the Loxl1-/- rats.

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来源期刊
Biomedical Research-tokyo
Biomedical Research-tokyo 医学-医学:研究与实验
CiteScore
2.40
自引率
0.00%
发文量
19
审稿时长
>12 weeks
期刊介绍: Biomedical Research is peer-reviewed International Research Journal . It was first launched in 1990 as a biannual English Journal and later became triannual. From 2008 it is published in Jan-Apr/ May-Aug/ Sep-Dec..
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