Differential response of human fetal smooth muscle cells from arterial duct to retinoid acid

Wu, Lihui; Xu, Shiwen; Jiang, Teng; Wu, Wei; Ye, Duyun; Wu, Xingzhong

doi:10.1111/j.1745-7254.2008.00766.x

Cited by 5 publications

(3 citation statements)

References 23 publications

(24 reference statements)

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“…Importantly, such activation was absent in adjacent aortic or pulmonary arterial segments (18). Similarly, several other studies support the role of RAR in DA closure (19–21). However, further investigation is needed to determine the therapeutic potential of these pathways for treating PDA.…”

Section: Discussionsupporting

confidence: 65%

Microarray gene expression analysis in ovine ductus arteriosus during fetal development and birth transition

Goyal

Longo

et al. 2016

Pediatr Res

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BACKGROUND Patent ductus arteriosus (PDA) in the newborn is the most common congenital heart anomaly and is significantly more common in preterm infants. Contemporary pharmacological treatment is effective in only 70–80% of the cases. Moreover, indomethacin or ibuprofen, which are used to close a PDA may be accompanied by serious side effects in premature infants. To explore the novel molecular pathways, which may be involved in the maturation and closure of the ductus arteriosus (DA), we used fetal and neonatal sheep to test the hypothesis that maturational development of DA is associated with significant alterations in specific mRNA expression. METHODS We conducted oligonucleotide microarray experiments on the isolated mRNA from DA and ascending aorta from three study groups (premature fetus—97 ± 0 d, near-term fetus—136 ± 0.8 d, and newborn lamb—12 ± 0 h). We compared the alterations in mRNA expression in DA and aorta to identify genes specifically involved in DA maturation. RESULTS Results demonstrate significant changes in wingless–integrin1, thrombospondin 1, receptor activator of nuclear factor-kappa B, nitric oxide synthase, and retinoic acid receptor activation signaling pathways. CONCLUSION We conclude that these pathways may play an important role during both development and postnatal DA closure and warrant further investigation.

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Section: Discussionsupporting

confidence: 65%

Microarray gene expression analysis in ovine ductus arteriosus during fetal development and birth transition

Goyal

Longo

et al. 2016

Pediatr Res

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“…Retinoic acid also participates in vascular remodeling via promoting SMC and ECM proliferation. Wu et al showed that retinoic acid stimulated the growth of DASMCs by the stimulation of proliferating cell nuclear antigen expression and decreased apoptosis [ 54 ]. Yokoyama et al demonstrated that maternally administrated vitamin A increased the production of fibronectin and hyaluronic acid, promoting intimal thickening in the DA at preterm rats [ 55 ].…”

Section: Anatomical Closurementioning

confidence: 99%

Molecular Mechanisms for Regulating Postnatal Ductus Arteriosus Closure

Hung

Yeh

Hsu

2018

IJMS

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The ductus arteriosus (DA) connects the main pulmonary artery and the aorta in fetal circulation and closes spontaneously within days after birth in normal infants. Abnormal patent DA (PDA) causes morbidities and mortality, especially in preterm infants. Closure of the DA is a complex interactive process involving two events: functional and anatomic closure. Functional closure by smooth muscle contraction was achieved through the regulatory factors of vaso-reactivity. These factors include oxygen sensing system, glutamate, osmolality, prostaglandin E2, nitric oxide, and carbon monoxide. Anatomic closure by vascular remodeling involved several vascular components including endothelium, extracellular matrix, smooth muscle cells, and intraluminal blood cells. Despite advances in understanding of PDA pathogenesis, the molecular mechanism for regulation of DA closure is complex and not fully understood. In this article we review recent evidence regarding the molecular mechanisms of DA closure.

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“…Retinoic acid stimulates the growth of SMCs and decreases apoptosis ( 86 ). Prenatal administration of vitamin A increases the production of fibronectin and hyaluronic acid, leading to intimal tickening, as well as the intracellular calcium response and the contractile response of the ductus to oxygen ( 50 ).…”

Section: Anatomic Closure and Remodelingmentioning

confidence: 99%

Molecular and Mechanical Mechanisms Regulating Ductus Arteriosus Closure in Preterm Infants

Ovalı

2020

Front. Pediatr.

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Failure of ductus arteriosus closure after preterm birth is associated with significant morbidities. Ductal closure requires and is regulated by a complex interplay of molecular and mechanical mechanisms with underlying genetic factors. In utero patency of the ductus is maintained by low oxygen tension, high levels of prostaglandins, nitric oxide and carbon monoxide. After birth, ductal closure occurs first by functional closure, followed by anatomical remodeling. High oxygen tension and decreased prostaglandin levels mediated by numerous factors including potassium channels, endothelin-1, isoprostanes lead to the contraction of the ductus. Bradykinin and corticosteroids also induce ductal constriction by attenuating the sensitivity of the ductus to PGE2. Smooth muscle cells of the ductus can sense oxygen through a mitochondrial network by the role of Rho-kinase pathway which ends up with increased intracellular calcium levels and contraction of myosin light chains. Anatomical closure of the ductus is also complex with various mechanisms such as migration and proliferation of smooth muscle cells, extracellular matrix production, endothelial cell proliferation which mediate cushion formation with the interaction of blood cells. Regulation of vessel walls is affected by retinoic acid, TGF-β1, notch signaling, hyaluronan, fibronectin, chondroitin sulfate, elastin, and vascular endothelial cell growth factor (VEGF). Formation of the platelet plug facilitates luminal remodeling by the obstruction of the constricted ductal lumen. Vasa vasorum are more pronounced in the term ductus but are less active in the preterm ductus. More than 100 genes are effective in the prostaglandin pathway or in vascular smooth muscle development and structure may affect the patency of ductus. Hemodynamic changes after birth including fluid load and flow characteristics as well as shear forces within the ductus also stimulate closure. Current pharmacological treatment for the closure of a patent ductus is based on the blockage of the prostaglandin pathway mainly through COX or POX inhibition, albeit with some limitations and side effects. Further research for new agents aiming ductal closure should focus on a clear understanding of vascular biology of the ductus.

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Differential response of human fetal smooth muscle cells from arterial duct to retinoid acid

Cited by 5 publications

References 23 publications

Microarray gene expression analysis in ovine ductus arteriosus during fetal development and birth transition

Microarray gene expression analysis in ovine ductus arteriosus during fetal development and birth transition

Molecular Mechanisms for Regulating Postnatal Ductus Arteriosus Closure

Molecular and Mechanical Mechanisms Regulating Ductus Arteriosus Closure in Preterm Infants

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