title: [Study on the influence of hypoxia induced microtubule damage on the opening of mitochondrial permeable transition pore of cardiac myocytes in rat].
abstract: OBJECTIVE
  To investigate the influence of hypoxia induced microtubule damage on the opening of mitochondrial permeable transition pore (MPTP)of cardiac myocytes and on the decrease of respiratory function in rat.
  
  
  METHODS
  Primary cultured myocardial cells from 30 neonatal rats were randomized as normoxic group (A), hypoxia group (B), normoxia with microtubule destabilizing agent group (C, with treatment of 8 micromol/L colchicines for 30 minutes before normoxia), and hypoxia with microtubule stabilizing agent group (D, with treatment of 10 micromol/L taxol for 30 minutes before hypoxia). beta-tubulin immunofluorescence ,the opening of mitochondria permeability transition pore, and the mitochondrial inner membrane potential were detected at 0.5, 1, 3, 6 and 12 post-treatment hours (PTH), and the mitochondrial respiratory function was determined by MTT method. The changes in these indices were also determined in A group at the corresponding time-points.
  
  
  RESULTS
  Obvious damage of polymerized microtubule, opening of MPTP, mitochondrial inner membrane potential loss and decrease of myocardial respiratory activity were observed in both group B and C at 0.5 PTH, and they became more and more serious afterwards. However, the changes in the above indices in D group were much better than those in B group (P < 0.05 or 0.01), and no difference was found between D (92.8 +/- 4.0)% and C [(100.0 +/- 0.0) %, P > 0.05] groups.
  
  
  CONCLUSIONS
  Hypoxia played a role in the myocardial microtubule damage as well as in the opening of MPTP. Moreover, hypoxia could also impair the mitochondrial respiratory function. Microtubule destabilizing agent could reproduce well the process of hypoxia induced microtubule damage, while the stabilizing agent exerted protective effect by improving the transition of mitochondrial permeability and the mitochondria respiratory function.
authors.affiliation: Institute of Burn Research, Southwest Hospital, State Key Laboratory of Trauma, Burns and Combined Injury, The Third Military Medical University, Chongqing 400038, PR China.
authors.forename: Ji
authors.initials: J
authors.lastname: Zheng
authors.forename: Ya-dong
authors.initials: YD
authors.lastname: Fang
authors.forename: Miao
authors.initials: M
authors.lastname: Teng
authors.forename: Yong-ming
authors.initials: YM
authors.lastname: Dang
authors.forename: Yong
authors.initials: Y
authors.lastname: Kuang
authors.forename: Hong
authors.initials: H
authors.lastname: Yan
authors.forename: Dong-xia
authors.initials: DX
authors.lastname: Zhang
authors.forename: Hua-pei
authors.initials: HP
authors.lastname: Song
authors.forename: Qiong
authors.initials: Q
authors.lastname: Zhang
authors.forename: Yue-sheng
authors.initials: YS
authors.lastname: Huang
mesh_terms: D000818:Animals; D015687:Cell Hypoxia; D002478:Cells, Cultured; D000860:Hypoxia / Q000378:metabolism* / Q000473:pathology; D053078:Membrane Potential, Mitochondrial; D008870:Microtubules / Q000473:pathology*; D008929:Mitochondria, Heart / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley