Gene expression patterns of the Bcl-2 and Bax genes in preterm birth

Objective. The apoptotic genes Bax and Bcl‐2 are both involved in the pathogenesis of preterm delivery in conjunction with additional factors. We characterized gene expression patterns of these apoptotic regulatory genes as well as relevant environmental factors. Design. A gene expression study with...

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Veröffentlicht in:Acta obstetricia et gynecologica Scandinavica 2012-10, Vol.91 (10), p.1212-1217
Hauptverfasser: DEMENDI, CSABA, BÖRZSÖNYI, BALÁZS, VÉGH, VERONIKA, NAGY, ZSOLT B., RIGÓ JR, JÁNOS, PAJOR, ATTILA, JOÓ, JÓZSEF GÁBOR
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Sprache:eng
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Zusammenfassung:Objective. The apoptotic genes Bax and Bcl‐2 are both involved in the pathogenesis of preterm delivery in conjunction with additional factors. We characterized gene expression patterns of these apoptotic regulatory genes as well as relevant environmental factors. Design. A gene expression study with evaluation of clinical data. Setting. Semmelweis University, Budapest, Hungary. Sample. Human placental samples from 104 preterm and 140 full‐term pregnancies. Methods. Gene tests were performed using real‐time PCR to assess gene expression patterns of Bax and Bcl‐2 in human placental samples. Clinical data were collected from our computerized database. Main outcome measures. Apoptotic gene expression pattern and clinical information against the background of preterm delivery. Results. In placental samples from preterm delivery pregnancies, expression of the Bcl‐2 gene was unchanged, whereas the Bax gene was overexpressed. Placental gene expression of Bax in preterm delivery was dependent on gestational age with gestational weeks 28–32 and 32–36 associated with overexpression, and no overexpression in gestational weeks 24–28. Preterm delivery began with premature rupture of membranes in 70.2% and spontaneous uterine activity in 29.8%. Conclusions. The Bax gene was overexpressed in preterm delivery, whereas expression of the Bcl‐2 gene remained unchanged. After the 28th gestational week, apoptosis appears to be a key factor in the pathogenesis of preterm delivery.
ISSN:0001-6349
1600-0412
DOI:10.1111/j.1600-0412.2012.01428.x