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The matrix metalloproteases and endothelin-1 in infection-associated preterm birth.

Olgun NS, Reznik SE - Obstet Gynecol Int (2010)

Bottom Line: While the risk factors for PTB are numerous, the single most common cause is intrauterine infection.As there is currently no FDA-approved therapy for infection-associated PTB, understanding the pathogenesis of preterm labor (PTL) and delivery should be given high priority.Several lines of evidence also suggest a role for endothelin-1 (ET-1) in infection-associated preterm delivery.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmaceutical Sciences, College of Pharmacy and Allied Health Professions, St. John's University, St. Albert Hall G018-B, 8000 Utopia Parkway, Jamaica, NY 11439, USA.

ABSTRACT
Preterm birth (PTB) is clinically defined as any delivery which occurs before the completion of 37 weeks of gestation, and is currently the most important problem in obstetrics. In the United States, PTB accounts for 12-13% of all live births, and, with the exception of fetuses suffering from anomalies, is the primary cause of perinatal mortality. While the risk factors for PTB are numerous, the single most common cause is intrauterine infection. As there is currently no FDA-approved therapy for infection-associated PTB, understanding the pathogenesis of preterm labor (PTL) and delivery should be given high priority. The matrix metalloproteinases (MMPs) are a family of enzymes that have been implicated in normal parturition as well as infection-triggered rupture of membranes and preterm birth. Several lines of evidence also suggest a role for endothelin-1 (ET-1) in infection-associated preterm delivery. This paper focuses on the evidence that the MMPs and ET-1 act in the same molecular pathway in preterm birth.

No MeSH data available.


Related in: MedlinePlus

Effect of ET-1 blockade on preterm delivery in the mouse model. (a) Incidence of preterm delivery in the mouse model in the absence, presence of high-dose, or presence of low-dose BQ-123 (P < .01 between control and high-dose groups, Fisher's exact test). (b) Effect of SiRNA for ECE-1 in the animal model of infection-associated PTB (P < .001, Fisher's exact test).
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fig2: Effect of ET-1 blockade on preterm delivery in the mouse model. (a) Incidence of preterm delivery in the mouse model in the absence, presence of high-dose, or presence of low-dose BQ-123 (P < .01 between control and high-dose groups, Fisher's exact test). (b) Effect of SiRNA for ECE-1 in the animal model of infection-associated PTB (P < .001, Fisher's exact test).

Mentions: We reported in 2004 that inhibition of endothelin-converting enzyme-1 (ECE-1), which colocalizes with ET-1 in the placenta [66], controls PTD in a mouse model of infection-associated PTL [67]. Subsequently, we have shown that ECE-1 is upregulated in our mouse model of PTL and that PTD is controlled with the ETA receptor antagonist BQ-123 and with silencing of ECE-1 mRNA [68] (Figure 2).


The matrix metalloproteases and endothelin-1 in infection-associated preterm birth.

Olgun NS, Reznik SE - Obstet Gynecol Int (2010)

Effect of ET-1 blockade on preterm delivery in the mouse model. (a) Incidence of preterm delivery in the mouse model in the absence, presence of high-dose, or presence of low-dose BQ-123 (P < .01 between control and high-dose groups, Fisher's exact test). (b) Effect of SiRNA for ECE-1 in the animal model of infection-associated PTB (P < .001, Fisher's exact test).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2913859&req=5

fig2: Effect of ET-1 blockade on preterm delivery in the mouse model. (a) Incidence of preterm delivery in the mouse model in the absence, presence of high-dose, or presence of low-dose BQ-123 (P < .01 between control and high-dose groups, Fisher's exact test). (b) Effect of SiRNA for ECE-1 in the animal model of infection-associated PTB (P < .001, Fisher's exact test).
Mentions: We reported in 2004 that inhibition of endothelin-converting enzyme-1 (ECE-1), which colocalizes with ET-1 in the placenta [66], controls PTD in a mouse model of infection-associated PTL [67]. Subsequently, we have shown that ECE-1 is upregulated in our mouse model of PTL and that PTD is controlled with the ETA receptor antagonist BQ-123 and with silencing of ECE-1 mRNA [68] (Figure 2).

Bottom Line: While the risk factors for PTB are numerous, the single most common cause is intrauterine infection.As there is currently no FDA-approved therapy for infection-associated PTB, understanding the pathogenesis of preterm labor (PTL) and delivery should be given high priority.Several lines of evidence also suggest a role for endothelin-1 (ET-1) in infection-associated preterm delivery.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmaceutical Sciences, College of Pharmacy and Allied Health Professions, St. John's University, St. Albert Hall G018-B, 8000 Utopia Parkway, Jamaica, NY 11439, USA.

ABSTRACT
Preterm birth (PTB) is clinically defined as any delivery which occurs before the completion of 37 weeks of gestation, and is currently the most important problem in obstetrics. In the United States, PTB accounts for 12-13% of all live births, and, with the exception of fetuses suffering from anomalies, is the primary cause of perinatal mortality. While the risk factors for PTB are numerous, the single most common cause is intrauterine infection. As there is currently no FDA-approved therapy for infection-associated PTB, understanding the pathogenesis of preterm labor (PTL) and delivery should be given high priority. The matrix metalloproteinases (MMPs) are a family of enzymes that have been implicated in normal parturition as well as infection-triggered rupture of membranes and preterm birth. Several lines of evidence also suggest a role for endothelin-1 (ET-1) in infection-associated preterm delivery. This paper focuses on the evidence that the MMPs and ET-1 act in the same molecular pathway in preterm birth.

No MeSH data available.


Related in: MedlinePlus