Role of p38 MAP kinase signaling pathways in storage and voiding dysfunction in mice with spinal cord injury.
Role of p38 MAP kinase signaling pathways in storage and voiding dysfunction in mice with spinal cord injury.
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P38蛋白激酶信号通路在脊髓损伤小鼠储存和排尿功能障碍中的作用。
DOI：
10.1002/nau.24170
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发表时间：
2020-01
影响因子：
2
通讯作者：
Yoshimura N
中科院分区：
文献类型：
--
作者：
Shimizu N;Wada N;Shimizu T;Suzuki T;Kurobe M;Kanai AJ;de Groat WC;Hashimoto M;Hirayama A;Uemura H;Yoshimura N
To investigate the role of p38 MAP kinase in lower urinary tract dysfunction in mice with spinal cord injury (SCI). Cystometry and external urethral sphincter-electromyography were performed under an awake condition in 4-week SCI female mice. Two weeks after SCI, a catheter connected to an osmotic pump filled with a p38 mitogen-activated protein kinase (MAPK) inhibitor or artificial cerebrospinal fluid (CSF) was implanted into the intrathecal space of L6-S1 spinal cord for continuous intrathecal instillation at infusion rate of 0.51 μL/h for 2 weeks before the urodynamic study. L6 dorsal root ganglia were then removed from CSF and p38 MAPK inhibitor-treated SCI mice as well as from CSF-treated normal (spinal intact) mice to evaluate the levels of transient receptor potential cation channel subfamily V member 1 (TRPV1), tumor necrosis factor-α (TNF-α), and inducible nitric oxide synthase (iNOS) transcripts by real-time polymerase chain reaction. In p38 MAPK inhibitor-treated SCI mice, nonvoiding contractions during bladder filling, bladder capacity, and post-void residual volume were significantly reduced while micturition pressure and voiding efficiency were significantly increased in comparison to these measurements in CSF-treated SCI mice. The expression of TRPV1, TNF-α, and iNOS messenger RNA was increased in SCI mice compared with expression in spinal intact mice and significantly decreased after p38 MAPK inhibitor treatment. The p38 MAPK signaling pathway in bladder sensory neurons or in the spinal cord plays an important role in storage and voiding problems such as detrusor overactivity and inefficient voiding after SCI.
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影响因子：
6.6
作者：
Seki, S;Sasaki, K;Yoshimura, N
通讯作者：
Yoshimura, N
影响因子：
2.9
作者：
CHENG, CL;MA, CP;DEGROAT, WC
通讯作者：
DEGROAT, WC
影响因子：
2
作者：
Wada N;Shimizu T;Shimizu N;de Groat WC;Kanai AJ;Tyagi P;Kakizaki H;Yoshimura N
通讯作者：
Yoshimura N
影响因子：
3.3
作者：
Shimizu N;Doyal MF;Goins WF;Kadekawa K;Wada N;Kanai AJ;de Groat WC;Hirayama A;Uemura H;Glorioso JC;Yoshimura N
通讯作者：
Yoshimura N
影响因子：
2.9
作者：
Horiuchi, D;Ogata, T;Yamamoto, H
通讯作者：
Yamamoto, H