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E-Prostanoid Receptor Distribution in Airway Smooth Muscle Cells of a Rat Model of Asthma

Received: 3 November 2014     Accepted: 13 November 2014     Published: 23 November 2014
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Abstract

Airway remodeling is a main pathological characteristic of asthma, and strongly associated with migration and proliferation of airway smooth muscle cells. E-prostanoid (EP) receptor can regulate airway remodeling. This study established a rat model of asthma and evaluated EP changes in airway smooth muscle cells under the asthmatic state so as to provide theoretical evidence for developing EP drugs to treat airway remodeling in asthma. A total of 20 clean Sprague-Dawley rats were randomly assigned to asthma group and control group. 28 days later, they were sacrificed for histological examination. Airway smooth muscle cells were isolated, cultured and measured using quantitative fluorescent PCR. Histopathological examination revealed that rat models of asthma were in accordance with the manifestations of asthmatic airway remodeling. After reverse transcription, real-time quantitative fluorescent PCR was performed using miRNA Q-PCR diagnostic kit. GAPDH was considered the internal reference. Relative expressions of E-prostanoid 1–4 (EP1–4) (2-△△Ct) in the control and asthma groups were respectively as follows: EP1: 4.35±0.18, 6.55±1.21; EP2: 3.64±0.12, 1.35±1.06; EP3: 4.59±1.14, 5.89±1.74; EP4: 2.89±1.85, 1.69±0.44. EP2/4 significantly decreased, but EP1 significantly increased in the asthma group (P < 0.01). These results suggested that the reduced EP2/4 and increased EP1 expressions in airway smooth muscle cells of rat models of asthma were probably important factors for asthmatic airway remodeling.

Published in American Journal of Clinical and Experimental Medicine (Volume 2, Issue 6)
DOI 10.11648/j.ajcem.20140206.17
Page(s) 156-160
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2014. Published by Science Publishing Group

Keywords

Asthma, Airway Smooth Muscle Cells, Prostaglandin E Receptor

References
[1] Huber HL, Koessler KK.The pathololgy of bronchial asthma. Arch Intern Med, 1922, 30:689 -760.
[2] Busse W, Banks-Schlegel S, Noel P, etal. NHLBI Working Group. Future research directions in asthma: an NHLBI Working Group report. Am J Respir Crit Care Med. 2004 15,170(6):683-90.
[3] Balzary RW, Cocks TM. Lipopolysaccharide induces epithelium- and prostaglandin E2-dependent relaxation of mouse isolated trachea through activation of COX-1 and COX-2. J Pharmacol Exp Ther. 2006, 317: 806-812.
[4] Hartney JM, Coggins KG, Tilley SL, etal.Prostaglandin E2 protects lower airways against bronchoconstriction. Am J Physiol Lung Cell Mol Physiol. 2006,290(1):L105-13.
[5] Xie M, Liu XS, Xu YJ, etal. Role of the extracellular signal-regulated kinase 1/2 signaling pathway in regulating the secretion of bronchial smooth muscle cells in a rat model of chronic asthma. Chin Med J (Engl). 2008 ,121(1):73-7.
[6] Belvisi MG, Saunders MA, Haddad E, etal. Induction of cyclo-oxygenase-2 by cytokines in human cultured airway smooth muscle cells: novel inflammatory role of this cell type. Br. J. Pharmacol.1997, 120:910–916.
[7] Roscioni SS, Dekkers BG, Prins AG, etal.cAMP inhibits modulation of airway smooth muscle phenotype via the exchange protein activated by cAMP (Epac) and protein kinase A.Br J Pharmacol. 2010 Aug 26. doi: 10.1111/j.1476-5381.2010.01011.x. [Epub ahead of print]
[8] Lundequist A, Nallamshetty SN, Xing W,etal.Prostaglandin E(2) exerts homeostatic regulation of pulmonary vascular remodeling in allergic airway inflammation.J Immunol. 2010, 184:433-41.
[9] Sachem J, Dahlén SE, Delin I, etal. PGE2 maintains the tone of the guinea pig trachea through a balance between activation of contractile EP1 receptors and relaxant EP2 receptors. Br J Pharmacol. 2013, 168:794-806.
[10] Tilley SL, Hartney JM, Erikson CJ, et al. Receptors and pathways mediating the effects of prostaglandin E2 on airway tone. Am J Physiol Lung Cell Mol Physiol. 2003, 284: L599-606.
[11] Fortner CN, Breyer RM , Paul RJ. EP2 receptors mediate airway relaxation to substance P, ATP, and PGE2. Am J Physiol Lung Cell Mol Physiol. 2001, 281: L469-474.
[12] Aso H, Ito S, Mori A, etal.Differential regulation of airway smooth muscle cell migration by E-prostanoid receptor subtypes. Am J Respir Cell Mol Biol. 2013, 48:322-9.
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    Yanfeng Ying, Ye Hu, Haohao Chen, Pingguang Tu. (2014). E-Prostanoid Receptor Distribution in Airway Smooth Muscle Cells of a Rat Model of Asthma. American Journal of Clinical and Experimental Medicine, 2(6), 156-160. https://doi.org/10.11648/j.ajcem.20140206.17

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    ACS Style

    Yanfeng Ying; Ye Hu; Haohao Chen; Pingguang Tu. E-Prostanoid Receptor Distribution in Airway Smooth Muscle Cells of a Rat Model of Asthma. Am. J. Clin. Exp. Med. 2014, 2(6), 156-160. doi: 10.11648/j.ajcem.20140206.17

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    AMA Style

    Yanfeng Ying, Ye Hu, Haohao Chen, Pingguang Tu. E-Prostanoid Receptor Distribution in Airway Smooth Muscle Cells of a Rat Model of Asthma. Am J Clin Exp Med. 2014;2(6):156-160. doi: 10.11648/j.ajcem.20140206.17

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  • @article{10.11648/j.ajcem.20140206.17,
      author = {Yanfeng Ying and Ye Hu and Haohao Chen and Pingguang Tu},
      title = {E-Prostanoid Receptor Distribution in Airway Smooth Muscle Cells of a Rat Model of Asthma},
      journal = {American Journal of Clinical and Experimental Medicine},
      volume = {2},
      number = {6},
      pages = {156-160},
      doi = {10.11648/j.ajcem.20140206.17},
      url = {https://doi.org/10.11648/j.ajcem.20140206.17},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20140206.17},
      abstract = {Airway remodeling is a main pathological characteristic of asthma, and strongly associated with migration and proliferation of airway smooth muscle cells. E-prostanoid (EP) receptor can regulate airway remodeling. This study established a rat model of asthma and evaluated EP changes in airway smooth muscle cells under the asthmatic state so as to provide theoretical evidence for developing EP drugs to treat airway remodeling in asthma. A total of 20 clean Sprague-Dawley rats were randomly assigned to asthma group and control group. 28 days later, they were sacrificed for histological examination. Airway smooth muscle cells were isolated, cultured and measured using quantitative fluorescent PCR. Histopathological examination revealed that rat models of asthma were in accordance with the manifestations of asthmatic airway remodeling. After reverse transcription, real-time quantitative fluorescent PCR was performed using miRNA Q-PCR diagnostic kit. GAPDH was considered the internal reference. Relative expressions of E-prostanoid 1–4 (EP1–4) (2-△△Ct) in the control and asthma groups were respectively as follows: EP1: 4.35±0.18, 6.55±1.21; EP2: 3.64±0.12, 1.35±1.06; EP3: 4.59±1.14, 5.89±1.74; EP4: 2.89±1.85, 1.69±0.44. EP2/4 significantly decreased, but EP1 significantly increased in the asthma group (P < 0.01). These results suggested that the reduced EP2/4 and increased EP1 expressions in airway smooth muscle cells of rat models of asthma were probably important factors for asthmatic airway remodeling.},
     year = {2014}
    }
    

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  • TY  - JOUR
    T1  - E-Prostanoid Receptor Distribution in Airway Smooth Muscle Cells of a Rat Model of Asthma
    AU  - Yanfeng Ying
    AU  - Ye Hu
    AU  - Haohao Chen
    AU  - Pingguang Tu
    Y1  - 2014/11/23
    PY  - 2014
    N1  - https://doi.org/10.11648/j.ajcem.20140206.17
    DO  - 10.11648/j.ajcem.20140206.17
    T2  - American Journal of Clinical and Experimental Medicine
    JF  - American Journal of Clinical and Experimental Medicine
    JO  - American Journal of Clinical and Experimental Medicine
    SP  - 156
    EP  - 160
    PB  - Science Publishing Group
    SN  - 2330-8133
    UR  - https://doi.org/10.11648/j.ajcem.20140206.17
    AB  - Airway remodeling is a main pathological characteristic of asthma, and strongly associated with migration and proliferation of airway smooth muscle cells. E-prostanoid (EP) receptor can regulate airway remodeling. This study established a rat model of asthma and evaluated EP changes in airway smooth muscle cells under the asthmatic state so as to provide theoretical evidence for developing EP drugs to treat airway remodeling in asthma. A total of 20 clean Sprague-Dawley rats were randomly assigned to asthma group and control group. 28 days later, they were sacrificed for histological examination. Airway smooth muscle cells were isolated, cultured and measured using quantitative fluorescent PCR. Histopathological examination revealed that rat models of asthma were in accordance with the manifestations of asthmatic airway remodeling. After reverse transcription, real-time quantitative fluorescent PCR was performed using miRNA Q-PCR diagnostic kit. GAPDH was considered the internal reference. Relative expressions of E-prostanoid 1–4 (EP1–4) (2-△△Ct) in the control and asthma groups were respectively as follows: EP1: 4.35±0.18, 6.55±1.21; EP2: 3.64±0.12, 1.35±1.06; EP3: 4.59±1.14, 5.89±1.74; EP4: 2.89±1.85, 1.69±0.44. EP2/4 significantly decreased, but EP1 significantly increased in the asthma group (P < 0.01). These results suggested that the reduced EP2/4 and increased EP1 expressions in airway smooth muscle cells of rat models of asthma were probably important factors for asthmatic airway remodeling.
    VL  - 2
    IS  - 6
    ER  - 

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Author Information
  • No. 1188, Wuzhou Street, Jinhua City, Zhejiang Province, China Jinhua Polytechnic

  • No. 1188, Wuzhou Street, Jinhua City, Zhejiang Province, China Jinhua Polytechnic

  • No. 1188, Wuzhou Street, Jinhua City, Zhejiang Province, China Jinhua Polytechnic

  • No. 1188, Wuzhou Street, Jinhua City, Zhejiang Province, China Jinhua Polytechnic

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