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Genes upregulated in human fetal membranes by infection or labor
L S Tashima1, L K Millar, G D Bryant-Greenwood
1Pacific Biomedical Research Center, University of Hawaii, Honolulu, USA.
Objective:
To determine whether suppression subtractive hybridization can detect genes in fetal membranes that are upregulated by infection, preterm premature rupture of membranes (PROM), or labor.
Methods:
Using suppression subtractive hybridization, messenger RNAs from a preterm fetal membrane obtained at cesarean delivery without labor (control) were subtracted from a pool of messenger RNAs of three patients with preterm PROM and vaginal delivery. Eight candidate genes identified as upregulated were quantitated by Northern analysis in each of the tissues and in additional patient subgroups.
Results:
Eight differentially upregulated genes were identified in preterm labor with PROM. Four of the genes are known to be involved in the response to inflammation or infection, and subsequent histologic examination showed one of the preterm PROM tissues to be infected. F-actin capping protein and chitinase precursor, not previously known to be involved in infection, were also upregulated in the infected tissue from preterm PROM. Northern blots using additional subgroups of patients showed that a regulatory G-protein signaling protein gene was significantly upregulated at term by labor in addition to significant upregulation of interleukin-8. There was a strong correlation between the gene expression for complement factor-B and duration of membrane rupture in the patients with preterm PROM.
Conclusion:
Two novel genes potentially involved in the response to inflammation or infection have been identified. A regulatory G-protein signaling protein and interleukin-8 gene expression were upregulated by labor. Complement factor-B gene expression was directly related to the duration of membrane rupture.
Insights
This study identified novel genes in fetal membranes upregulated by infection and preterm premature rupture of membranes (PROM). Labor also upregulated specific genes, with complement factor-B correlating to rupture duration.
Area of Science:
- Reproductive Biology
- Genomics
- Infectious Diseases
Background:
- Fetal membrane gene expression changes are critical in pregnancy complications.
- Understanding molecular responses to infection, preterm premature rupture of membranes (PROM), and labor is essential.
Purpose of the Study:
- To identify genes in fetal membranes upregulated by infection, PROM, or labor using suppression subtractive hybridization.
- To investigate the role of novel genes in pregnancy complications.
Main Methods:
- Suppression subtractive hybridization (SSH) was employed to compare gene expression profiles.
- Messenger RNAs from control and PROM/labor samples were analyzed.
- Quantitative Northern analysis validated candidate gene upregulation.
Main Results:
- Eight differentially upregulated genes were identified in preterm labor with PROM.
- Four known inflammation/infection-related genes and two novel genes (F-actin capping protein, chitinase precursor) were upregulated in infected PROM tissues.
- A regulatory G-protein signaling protein and interleukin-8 were upregulated by labor.
- Complement factor-B gene expression correlated with the duration of membrane rupture in PROM.
Conclusions:
- Two novel genes potentially involved in inflammation or infection responses were identified.
- Labor upregulates regulatory G-protein signaling protein and interleukin-8.
- Complement factor-B expression is linked to the duration of membrane rupture.