title: [Effect of hydrostatic pressure on intracellular free calcium concentration and transient receptor potential vanilloid expression in human bladder smooth muscle cells].
abstract: OBJECTIVE
  To explore the effect of hydrostatic pressure on intracellular free calcium concentration ([Ca2+]i) and the gene expression of transient receptor potential vanilloid (TRPV) in cultured human bladder smooth muscle cells (hb-SMCs), and to preliminarily probe into the possible molecular mechanism of hb-SMCs proliferation stimulated by hydrostatic pressure.
  
  
  METHODS
  The passage 6-7 hb-SMCs were loaded with Ca2+ indicator Fluo-3/AM. When the hb-SMCs were under 0 cm H2O (1cm H2O = 0.098 kPa) (group A) or 200 cm H2O hydrostatic pressure for 30 minutes (group B) and then removing the 200 cm H2O hydrostatic pressure (group C), the [Ca2+]i was measured respectively by inverted laser scanning confocal microscope. When the hb-SMCs were given the 200 cm H2O hydrostatic pressure for 0 hour, 2 hours, 6 hours, 12 hours, and 24 hours, the mRNA expressions of TRPV1, TRPV2, and TRPV4 were detected by RT-PCR technique.
  
  
  RESULTS
  The [Ca2+]i of group A, group B, and group C were (100.808 +/- 1.724), (122.008 +/- 1.575), and (99.918 +/- 0.887) U, respectively; group B was significantly higher than groups A and C (P < 0.001). The [Ca2+]i of group C decreased to the base line level of group A after removing the pressure (t = 0.919, P = 0.394). The TRPV1, TRPV2, and TRPV4 genes expressed in hb-SMCs under 200 cm H2O hydrostatic pressure at 0 hour, 2 hours, 6 hours, 12 hours, and 24 hours, but the expressions had no obvious changes with time. There was no significant difference in the expressions of TRPV1, TRPV2, and TRPV4 among 3 groups (P > 0.05).
  
  
  CONCLUSIONS
  The [Ca2+]i of hb-SMCs increases significantly under high hydrostatic pressure. As possible genes in stretch-activated cation channel, the TRPV1, TRPV2, and TRPV4 express in hb-SMCs under 200 cm H2O hydrostatic pressure. It is possible that the mechanical pressure regulates the [Ca2+]i of hb-SMCs by opening the stretch-activated cation channel rather than up-regulating its expression.
authors.affiliation: Department of Urology, Ministry of Health, West China Hospital, Sichuan University, Chengdu Sichuan, 610041, P.R. China.
authors.forename: Zhenwei
authors.initials: Z
authors.lastname: Han
authors.forename: Kunjie
authors.initials: K
authors.lastname: Wang
authors.forename: Lin
authors.initials: L
authors.lastname: Chen
authors.forename: Tangqiang
authors.initials: T
authors.lastname: Wei
authors.forename: Deyi
authors.initials: D
authors.lastname: Luo
authors.forename: Shengfu
authors.initials: S
authors.lastname: Li
mesh_terms: D002118:Calcium / Q000378:metabolism*; D049109:Cell Proliferation; D002478:Cells, Cultured; D006801:Humans; D006874:Hydrostatic Pressure; D007477:Ions / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013314:Stress, Mechanical; D050052:TRPC Cation Channels / Q000378:metabolism; D050916:TRPV Cation Channels / Q000235:genetics / Q000378:metabolism*; D001743:Urinary Bladder / Q000166:cytology* / Q000378:metabolism
chemical_list: D007477:Ions; D012333:RNA, Messenger; D050052:TRPC Cation Channels; D050916:TRPV Cation Channels; D002118:Calcium