title: Effect of TRPV1 channel on the proliferation and apoptosis in asthmatic rat airway smooth muscle cells.
abstract: BACKGROUND
  Hyperplasia of airway smooth muscle cells (ASMC) is a major contributor to airway remodeling in asthma. Transient receptor potential vanilloid 1 (TRPV1) is an important channel to mediate Ca(2+) influx. This study explores the expression of TRPV1 channel and its effect on the proliferation and apoptosis in rat ASMC, in order to find a new target to treat airway remodeling in asthma.
  
  
  METHODS
  Rats were sensitized and challenged with ovalbumin to replicate asthmatic models. Proliferating cell nuclear antigen (PCNA) was detected by immunohistochemistry. Reverse transcriptase-polymerase chain reaction, immunocytochemistry, and Western blot were used to detect the mRNA and protein expression of TRPV1 channel. Intracellular calcium ([Ca(2+)]i) was detected using confocal fluorescence Ca(2+) imaging. [(3)H] thymidine incorporation and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay were used to observe the DNA synthesis and proliferation. TUNEL assay was used to detect the apoptosis of ASMC.
  
  
  RESULTS
  (1) The expression of PCNA was significantly increased in intact asthmatic rat ASMC. (2) The expression of TRPV1 channel was significantly increased in asthmatic rat ASMC. (3) [Ca(2+)]i in ASMC of the asthmatic group was significantly increased. After treatment with TRPV1 agonist capsaicin (CAP), [Ca(2+)]i was further increased, whereas [Ca(2+)]i was decreased after administration of TRPV1 antagonist capsazepine (CPZ) in ASMC of the asthmatic group. (4) The DNA synthesis and absorbance of MTT were significantly increased, while apoptosis was significantly decreased in asthmatic ASMC. CAP further enhanced proliferation and decreased apoptosis. CPZ significantly inhibited the effect of CAP in asthmatic ASMC.
  
  
  CONCLUSIONS
  TRPV1 channel was involved in the regulation of proliferation and apoptosis in asthmatic ASMC.
authors.affiliation: Department of Respiratory and Critical Care Medicine, Zhengzhou University People's Hospital, Zhengzhou, Henan, China.
authors.forename: Limin
authors.initials: L
authors.lastname: Zhao
authors.forename: Xiaoyu
authors.initials: X
authors.lastname: Zhang
authors.forename: Hongyan
authors.initials: H
authors.lastname: Kuang
authors.forename: Jizhen
authors.initials: J
authors.lastname: Wu
authors.forename: Yali
authors.initials: Y
authors.lastname: Guo
authors.forename: Lijun
authors.initials: L
authors.lastname: Ma
mesh_terms: D056151:Airway Remodeling / Q000502:physiology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D001249:Asthma / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism; D002211:Capsaicin / Q000031:analogs & derivatives / Q000494:pharmacology; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D004195:Disease Models, Animal; D006965:Hyperplasia; D008297:Male; D032389:Myocytes, Smooth Muscle / Q000187:drug effects / Q000473:pathology*; D010047:Ovalbumin / Q000009:adverse effects; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012137:Respiratory System / Q000473:pathology*; D050916:TRPV Cation Channels / Q000819:agonists / Q000037:antagonists & inhibitors / Q000502:physiology*
chemical_list: D018809:Proliferating Cell Nuclear Antigen; D050916:TRPV Cation Channels; C493922:Trpv1 protein, rat; D010047:Ovalbumin; C071423:capsazepine; D002211:Capsaicin; D002118:Calcium