Effects of Antenatal Betamethasone on Maternal and Fetoplacental Matrix Metalloproteinases 2 and 9 Activities in Human Singleton Pregnancies

Gharraee, Z.; Beharry, Kay D.; Valencia, Arwin M.; Cho, Steve; Guajardo, Leonel; Nageotte, Michael P.; Modanlou, Houchang D.

doi:10.2310/6650.2006.05060

Cited by 5 publications

(2 citation statements)

References 39 publications

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“…While glucocorticoids exert a range of positive effects in establishing early pregnancy such as stimulation of human chorionic gonadotropin (hCG) secretion and suppression of uterine natural killer cells [79], they can also adversely influence the progression of a healthy pregnancy. For example, it has been reported that glucocorticoids stimulate growth of the early trophoblast -now known to be a key factor in the development of pre-eclampsia [80,81]. These effects, however, are not consistent and it has also been demonstrated that dexamethasone impairs the ability of human trophoblasts to invade a matrigel matrix in vitro [82].…”

Section: Effects Of Cortisol On the Trophoblastmentioning

confidence: 98%

Endocrine aspects of pre-eclampsia

Currie

Carty

Connell

et al. 2015

Cardiovascular Endocrinology

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Section: Effects Of Cortisol On the Trophoblastmentioning

confidence: 98%

Endocrine aspects of pre-eclampsia

Currie

Carty

Connell

et al. 2015

Cardiovascular Endocrinology

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“…Free elastase activity in newborn tracheal aspirate is associated with increased risk of developing PIE [83]; which almost inevitably leads to BPD. Glucocorticoids may therefore influence airway remodeling by increasing activity of MMP-2 and MMP-9 and decreasing activity of TIMP-1 [84].…”

Section: The Role Of Matrix Metalloproteinases (Mmp's) In Airway Remomentioning

confidence: 99%

Pathophysiology and Prevention of Bronchopulmonary Dysplasia

Davis¹

2008

CPR

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BPD is the major respiratory complication of preterm delivery and is typified by chronic oxygen dependency and respiratory insufficiency beyond 36 weeks' postconceptional age. It is caused by a combination of insults on the developing lung precipitated by preterm birth and its subsequent respiratory management. The common pathway linking the various causative factors is inflammation, which may be initiated prior to birth in the setting of maternal chorioamnionitis, or after birth by mechanical ventilation, infection or oxidative stress. Inflammation in the developing lung induces airways remodeling which adversely affects lung function. Multiple inflammatory mediators are implicated in this process and modifying the course of the disease has proven difficult. The emphasis of management should be directed towards prevention with strategies aimed at minimizing early lung injury and oxidative stress. These include delivery room stabilization and mechanical ventilation techniques that aim to avoid volutrauma and atelectotrauma. Drugs may also influence BPD progression and can broadly be divided into three categories; those administered prenatally to accelerate lung maturation, those administered postnatally to reduce initiation of inflammatory stimuli and those to modify any established inflammatory response. In this review we have examined recent evidence for each of these ventilatory and therapeutic strategies to prevent BPD. A better understanding of the pathophysiology of airways remodeling in BPD could have significant implications for future potential targeted interventions.

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