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Pressure stress reduces inducible NO synthase expression by interleukin-1β stimulation in cultured rat vascular smooth muscle cells.
Eur J Pharmacol 2014; 731:44-9EJ

Abstract

Elevated mechanical stress applied to vascular walls is well known to modulate vascular remodeling. We investigated the effect of pulsatile pressure stress on nitric oxide (NO) production and inducible NO synthase (iNOS) expression by interleukin-1β (IL-1β) stimulation in rat vascular smooth muscle cells (VSMCs). VSMCs were enzymatically isolated from aortic media of Wistar rats. Pulsatile pressure applied to VSMCs was repeatedly given between 80 and 160 mm Hg at a frequency of 4 cycles per min using an original apparatus. Protein expression and activation were evaluated by Western blot analysis. mRNA expression was evaluated by real-time reverse transcription-polymerase chain reaction. The pulsatile pressure reduced IL-1β-induced NO production, iNOS protein, and mRNA expression. The pressure also reduced GTP cyclohydrolase I mRNA expression. Furthermore, the pressure reduced phosphorylation of IL-1β-induced extracellular signal-regulated kinase (ERK), nuclear factor-κB (NF-κB) p65, and I-κBα. The pressure had no effect on I-κBβ degradation by IL-1β stimulation. The present study shows for the first time that pressure stress reduces IL-1β-induced iNOS expression via a mechanism involving the ERK-NF-κB signaling pathway.

Authors+Show Affiliations

Department of Pharmacological Sciences, School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido 061-0293, Japan. Electronic address: tmachida@hoku-iryo-u.ac.jp.Department of Pharmacological Sciences, School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido 061-0293, Japan.Department of Pharmacological Sciences, School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido 061-0293, Japan.Department of Pharmacological Sciences, School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido 061-0293, Japan.Department of Pharmacological Sciences, School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido 061-0293, Japan.Department of Pharmacological Sciences, School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido 061-0293, Japan.Department of Pharmacological Sciences, School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido 061-0293, Japan.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24632084

Citation

Machida, Takuji, et al. "Pressure Stress Reduces Inducible NO Synthase Expression By Interleukin-1β Stimulation in Cultured Rat Vascular Smooth Muscle Cells." European Journal of Pharmacology, vol. 731, 2014, pp. 44-9.
Machida T, Iizuka K, Shinohara K, et al. Pressure stress reduces inducible NO synthase expression by interleukin-1β stimulation in cultured rat vascular smooth muscle cells. Eur J Pharmacol. 2014;731:44-9.
Machida, T., Iizuka, K., Shinohara, K., Hatakeyama, N., Nakano, K., Kubo, Y., & Hirafuji, M. (2014). Pressure stress reduces inducible NO synthase expression by interleukin-1β stimulation in cultured rat vascular smooth muscle cells. European Journal of Pharmacology, 731, pp. 44-9. doi:10.1016/j.ejphar.2014.02.042.
Machida T, et al. Pressure Stress Reduces Inducible NO Synthase Expression By Interleukin-1β Stimulation in Cultured Rat Vascular Smooth Muscle Cells. Eur J Pharmacol. 2014 May 15;731:44-9. PubMed PMID: 24632084.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pressure stress reduces inducible NO synthase expression by interleukin-1β stimulation in cultured rat vascular smooth muscle cells. AU - Machida,Takuji, AU - Iizuka,Kenji, AU - Shinohara,Kosaku, AU - Hatakeyama,Nanae, AU - Nakano,Keita, AU - Kubo,Yuta, AU - Hirafuji,Masahiko, Y1 - 2014/03/13/ PY - 2013/08/28/received PY - 2014/02/07/revised PY - 2014/02/25/accepted PY - 2014/3/18/entrez PY - 2014/3/19/pubmed PY - 2014/12/15/medline KW - Extracellular signal-regulated kinase KW - Inducible nitric oxide synthase KW - Interleukin-1β KW - Nuclear factor-κB KW - Pulsatile pressure stress KW - Vascular smooth muscle cells SP - 44 EP - 9 JF - European journal of pharmacology JO - Eur. J. Pharmacol. VL - 731 N2 - Elevated mechanical stress applied to vascular walls is well known to modulate vascular remodeling. We investigated the effect of pulsatile pressure stress on nitric oxide (NO) production and inducible NO synthase (iNOS) expression by interleukin-1β (IL-1β) stimulation in rat vascular smooth muscle cells (VSMCs). VSMCs were enzymatically isolated from aortic media of Wistar rats. Pulsatile pressure applied to VSMCs was repeatedly given between 80 and 160 mm Hg at a frequency of 4 cycles per min using an original apparatus. Protein expression and activation were evaluated by Western blot analysis. mRNA expression was evaluated by real-time reverse transcription-polymerase chain reaction. The pulsatile pressure reduced IL-1β-induced NO production, iNOS protein, and mRNA expression. The pressure also reduced GTP cyclohydrolase I mRNA expression. Furthermore, the pressure reduced phosphorylation of IL-1β-induced extracellular signal-regulated kinase (ERK), nuclear factor-κB (NF-κB) p65, and I-κBα. The pressure had no effect on I-κBβ degradation by IL-1β stimulation. The present study shows for the first time that pressure stress reduces IL-1β-induced iNOS expression via a mechanism involving the ERK-NF-κB signaling pathway. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/24632084/Pressure_stress_reduces_inducible_NO_synthase_expression_by_interleukin_1β_stimulation_in_cultured_rat_vascular_smooth_muscle_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(14)00180-0 DB - PRIME DP - Unbound Medicine ER -