title: Expression of selected genes in preterm premature rupture of fetal membranes.
abstract: OBJECTIVE
  To analyse the expression of 15 genes encoding receptors and enzymes associated with the molecular mechanism of the tocolytic drugs atosiban (oxytocin receptor antagonist), nifedipine (calcium channel blocker) and celecoxib (selective cyclo-oxygenase-2 inhibitor) in preterm labor patients with premature rupture of fetal membranes in relation to symptoms of intrauterine infection and preterm labor risk factors.
  
  
  METHODS
  Experimental molecular study.
  
  
  METHODS
  Tertiary obstetric care center.
  
  
  METHODS
  Myometrial samples were obtained during cesarean sections from 35 patients who delivered preterm with unverified symptoms of intrauterine infection, 35 patients who delivered preterm without symptoms of intrauterine infection and 90 women who delivered at term.
  
  
  METHODS
  The Micro Fluidic Profiling Card analytic system was used to evaluate mRNA expression of the genes of interest.
  
  
  METHODS
  The relative quantification values for mRNA expression.
  
  
  RESULTS
  The median oxytocin receptor and cyclo-oxygenase-2 mRNA expression in preterm patients with clinical symptoms of intrauterine infection was significantly higher than in preterm patients without symptoms. The median mRNA expression of β(1) , β(3) and β(4) subunits of the L-type calcium channel and prostaglandin E(2) receptor was significantly higher in preterm patients compared with term patients.
  
  
  CONCLUSIONS
  The mRNA expression of hormones, enzymes and their receptors associated with tocolytic actions can differ in various clinical conditions. The expression of these genes is regulated at different levels and can be modified by inflammatory factors, which affect their functions.
authors.affiliation: Department of Perinatology, Medical University of Białystok, Białystok, Poland. pawel.kuc@umwb.edu.pl
authors.forename: Paweł
authors.initials: P
authors.lastname: Kuć
authors.forename: Piotr
authors.initials: P
authors.lastname: Laudański
authors.forename: Oksana
authors.initials: O
authors.lastname: Kowalczuk
authors.forename: Lech
authors.initials: L
authors.lastname: Chyczewski
authors.forename: Tadeusz
authors.initials: T
authors.lastname: Laudański
mesh_terms: D000328:Adult; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000235:genetics / Q000378:metabolism*; D000068579:Celecoxib; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000235:genetics / Q000378:metabolism*; D004716:Endometritis / Q000382:microbiology; D005260:Female; D005322:Premature Rupture of Fetal Membranes / Q000378:metabolism*; D020869:Gene Expression Profiling; D018507:Gene Expression Regulation, Developmental; D006801:Humans; D009543:Nifedipine / Q000494:pharmacology; D007752:Obstetric Labor, Premature / Q000188:drug therapy* / Q000378:metabolism*; D010120:Oxytocics / Q000494:pharmacology; D011247:Pregnancy; D011262:Pregnancy Trimester, Second; D011263:Pregnancy Trimester, Third; D047928:Premature Birth / Q000188:drug therapy / Q000378:metabolism; D011720:Pyrazoles / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D013449:Sulfonamides / Q000494:pharmacology; D047929:Term Birth / Q000378:metabolism; D015149:Tocolytic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D014668:Vasotocin / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D052246:Cyclooxygenase 2 Inhibitors; D010120:Oxytocics; D011720:Pyrazoles; D012333:RNA, Messenger; D013449:Sulfonamides; D015149:Tocolytic Agents; C047046:atosiban; D009543:Nifedipine; D000068579:Celecoxib; D015232:Dinoprostone; D014668:Vasotocin