scholarly journals Role of p38 MAP kinase signaling pathways in storage and voiding dysfunction in mice with spinal cord injury

2019 ◽  
Vol 39 (1) ◽  
pp. 108-115
Author(s):  
Nobutaka Shimizu ◽  
Naoki Wada ◽  
Takahiro Shimizu ◽  
Takahisa Suzuki ◽  
Masahiro Kurobe ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Map Kinase ◽  
Signaling Pathways ◽  
Voiding Dysfunction ◽  
P38 Map Kinase ◽  
Kinase Signaling ◽  
Cord Injury ◽  
Map Kinase Signaling

Role of NF-κB and p38 MAP Kinase Signaling Pathways in the Lipopolysaccharide-Dependent Activation of Heme Oxygenase-1 Gene Expression

2004 ◽  
Vol 6 (5) ◽  
pp. 802-810 ◽  
Author(s):  
Nastiti Wijayanti ◽  
Sebastian Huber ◽  
Anatoly Samoylenko ◽  
Thomas Kietzmann ◽  
Stephan Immenschuh
Keyword(s):  
Gene Expression ◽  
Map Kinase ◽  
Signaling Pathways ◽  
Heme Oxygenase ◽  
P38 Map Kinase ◽  
Heme Oxygenase 1 ◽  
Kinase Signaling ◽  
Map Kinase Signaling

Role of NF-kB and p38 MAP Kinase Signaling Pathways in the Lipopolysaccharide-Dependent Activation of Heme Oxygenase-1 Gene Expression

2004 ◽  
Vol 6 (5) ◽  
pp. 802-810 ◽  
Author(s):  
Nastiti Wijayanti ◽  
Sebastian Huber ◽  
Anatoly Samoylenko ◽  
Thomas Kietzmann ◽  
Stephan Immenschuh
Keyword(s):  
Gene Expression ◽  
Map Kinase ◽  
Signaling Pathways ◽  
Heme Oxygenase ◽  
P38 Map Kinase ◽  
Heme Oxygenase 1 ◽  
Kinase Signaling ◽  
Map Kinase Signaling

Role of the p38 MAP-Kinase Signaling Pathway for Cx32 and Claudin-1 in the Rat Liver

2003 ◽  
Vol 10 (4-6) ◽  
pp. 437-443 ◽  
Author(s):  
Takashi Kojima ◽  
Toshinobu Yamamoto ◽  
Masaki Murata ◽  
Mengdong Lan ◽  
Ken-ichi Takano ◽  
...  
Keyword(s):  
Map Kinase ◽  
Signaling Pathway ◽  
Rat Liver ◽  
P38 Map Kinase ◽  
Kinase Signaling ◽  
Map Kinase Signaling ◽  
Kinase Signaling Pathway ◽  
Map Kinase Signaling Pathway

scholarly journals PD55-05 THERAPEUTIC EFFECTS OF P38 MAP KINASE INHIBITOR ON BLADDER DYSFUNCTION IN MICE WITH SPINAL CORD INJURY (SCI)

2018 ◽  
Vol 199 (4S) ◽  
Author(s):  
Nobutaka Shimizu ◽  
Takahisa Suzuki ◽  
Ei-ichiro Takaoka ◽  
Joombeom Kwon ◽  
Naoki Wada ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Map Kinase ◽  
Bladder Dysfunction ◽  
Kinase Inhibitor ◽  
P38 Map Kinase ◽  
Therapeutic Effects ◽  
Cord Injury

Mechanical strain regulates syndecan-4 expression and shedding in smooth muscle cells through differential activation of MAP kinase signaling pathways

2007 ◽  
Vol 292 (1) ◽  
pp. C517-C525 ◽  
Author(s):  
Matheau A. Julien ◽  
Peiyi Wang ◽  
Carolyn A. Haller ◽  
Jing Wen ◽  
Elliot L. Chaikof
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Map Kinase ◽  
Signaling Pathways ◽  
Map Kinases ◽  
Muscle Cells ◽  
Kinase Signaling ◽  
Fold Reduction ◽  
Map Kinase Signaling

Syndecan-4 (S4) belongs to a family of transmembrane proteoglycans, acts as a coreceptor for growth factor binding as well as cell-matrix and cell-cell interactions, and is induced in neointimal smooth muscle cells (SMCs) after balloon catheter injury. We investigated S4 expression in SMCs in response to several force profiles and the role of MAP kinase signaling pathways in regulating these responses. S4 mRNA expression increased in response to 5% and 10% cyclic strain (4 h: 200 ± 34% and 182 ± 17%, respectively; P < 0.05) before returning to basal levels by 24 h. Notably, the SMC mechanosensor mechanism was reset after an initial 24-h “preconditioning” period, as evident by an increase in S4 gene expression following a change in cyclic stress from 10% to 20% (28 h: 181 ± 1%; P < 0.05). Mechanical stress induced a late decrease in cell-associated S4 protein levels (24 h: 70 ± 6%; P < 0.05), with an associated increase in S4 shedding (24 h: 537 ± 109%; P < 0.05). To examine the role of MAP kinases, cells were treated with U-0126 (ERK1/2 inhibitor), SB-203580 (p38 inhibitor), or JNKI I (JNK/SAPK inhibitor). Late reduction in cell-associated S4 levels was attributed to ERK1/2 and p38 signaling. In contrast, accelerated S4 shedding required both ERK1/2 (5-fold reduction in accelerated shedding; P < 0.05) and JNK/SAPK (4-fold reduction; P < 0.05) signaling. Given the varied functions of S4, stress-induced effects on SMC S4 expression and shedding may represent an additional component of the proinflammatory, growth-stimulating pathways that are activated in response to changes in the mechanical microenvironment of the vascular wall.

Probiotic Lactobacillus casei activates innate immunity via NF-κB and p38 MAP kinase signaling pathways

2006 ◽  
Vol 8 (4) ◽  
pp. 994-1005 ◽  
Author(s):  
Yun-Gi Kim ◽  
Toshihisa Ohta ◽  
Takuya Takahashi ◽  
Akira Kushiro ◽  
Koji Nomoto ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Map Kinase ◽  
Signaling Pathways ◽  
Lactobacillus Casei ◽  
P38 Map Kinase ◽  
Kinase Signaling ◽  
Probiotic Lactobacillus ◽  
Map Kinase Signaling

scholarly journals Involvement of Ca2+-activated K+ channel 3.1 in hypoxia-induced pulmonary arterial hypertension and therapeutic effects of TRAM-34 in rats

2017 ◽  
Vol 37 (4) ◽  
Author(s):  
Shujin Guo ◽  
Yongchun Shen ◽  
Guangming He ◽  
Tao Wang ◽  
Dan Xu ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Map Kinase ◽  
Signaling Pathways ◽  
Vascular Remodeling ◽  
Primary Cultures ◽  
P38 Map Kinase ◽  
Therapeutic Effects ◽  
Mrna Levels ◽  
Kinase Signaling ◽  
Map Kinase Signaling

Pulmonary artery hypertension (PAH) is an incurable disease associated with the proliferation of pulmonary artery smooth muscle cells (PASMCs) and vascular remodeling. The present study examined whether TRAM-34, a highly selective blocker of calcium-activated potassium channel 3.1 (Kca3.1), can help prevent such hypertension by reducing proliferation in PASMCs. Rats were exposed to hypoxia (10% O2) for 3 weeks and treated daily with TRAM-34 intraperitoneally from the first day of hypoxia. Animals were killed and examined for vascular hypertrophy, Kca3.1 expression, and downstream signaling pathways. In addition, primary cultures of rat PASMCs were exposed to hypoxia (3% O2) or normoxia (21% O2) for 24 h in the presence of TRAM-34 or siRNA against Kca3.1. Activation of cell signaling pathways was examined using Western blot analysis. In animal experiments, hypoxia triggered significant medial hypertrophy of pulmonary arterioles and right ventricular hypertrophy, and it significantly increased pulmonary artery pressure, Kca3.1 mRNA levels and ERK/p38 MAP kinase signaling. These effects were attenuated in the presence of TRAM-34. In cell culture experiments, blocking Kca3.1 using TRAM-34 or siRNA inhibited hypoxia-induced ERK/p38 signaling. Kca3.1 may play a role in the development of PAH by activating ERK/p38 MAP kinase signaling, which may then contribute to hypoxia-induced pulmonary vascular remodeling. TRAM-34 may protect against hypoxia-induced PAH.

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