title: [Effect of siRNA silencing the role of JNK gene in excessive endoplasmic reticulum stress on lung ischemia/reperfusion injury].
abstract: OBJECTIVE
  To investigate the effect of siRNA silencing the role of C-Jun N-terminal Kinase (JNK) gene in excessive endoplasmic reticulum stress on lung ischemia/reperfusion injury.
  
  
  METHODS
  Mouse model of pulmonary ischemia reperfusion injury (PIRI) in situ was established with unilateral lung in vivo. Seventy experimental mice were randomly allocated into seven groups (n = 10): Sham group (Sham group), ischemia reperfusion group (I/R), PBS+ Lipofectamine2000TM transfection reagent group (I/R + PBS+ Lipo group), negative control group (I/R+ SCR group), JNK-siRNA group (I/R + siRNA(JNK1), siRNA(JNK2), siRNA(JNK3)). Mice were euthanized after experimental time out, and left lung tissue was extracted. Wet/dry lung weight ratio (W/D) and total lung water content (TLW) were tested. Light microscope, alveolar damage quantitative evaluation index (IQA) and electron microscope were observed. The expression levels of JNK and glucose regulatex protein(GRP78) were detected by RT-PCR and Western blot. Apoptosis of lung tissue was determined by TUNEL.
  
  
  RESULTS
  Compared with Sham group, all indicators above of I/R + PBS + Lipo group and I/R + SCR group were significantly increased (P < 0.01), and compared with I/R group, those indicators of the three groups all had no notable difference; those indicators were not statistically different between I/R + PBS + Lipo group and I/R + SCR group, and compared to the three groups, the above indicators in JNK-siRNA group were lower (P < 0.05, P < 0.01) except that the expression levels of GRP78 was not statistically different.
  
  
  CONCLUSIONS
  I/R induces excessive ERS in lung tissue, in which JNK pathway participates in apoptosis, leading to lung tissue injury.
authors.forename: Mao-Lin
authors.initials: ML
authors.lastname: Hao
authors.forename: Shan
authors.initials: S
authors.lastname: Zhao
authors.forename: Hai-E
authors.initials: HE
authors.lastname: Chen
authors.forename: Dan
authors.initials: D
authors.lastname: Chen
authors.forename: Dong
authors.initials: D
authors.lastname: Song
authors.forename: Jin-Bo
authors.initials: JB
authors.lastname: He
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.forename: Wan-Tie
authors.initials: WT
authors.lastname: Wang
mesh_terms: D000818:Animals; D017209:Apoptosis; D000091342:Endoplasmic Reticulum Chaperone BiP; D059865:Endoplasmic Reticulum Stress; D006360:Heat-Shock Proteins / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000235:genetics*; D008168:Lung / Q000503:physiopathology*; D055370:Lung Injury / Q000235:genetics*; D020935:MAP Kinase Signaling System; D051379:Mice; D034741:RNA, Small Interfering; D015427:Reperfusion Injury / Q000235:genetics*
chemical_list: D000091342:Endoplasmic Reticulum Chaperone BiP; D006360:Heat-Shock Proteins; C000717248:Hspa5 protein, mouse; D034741:RNA, Small Interfering; D048031:JNK Mitogen-Activated Protein Kinases