Interleukin-15 Inhibits Smooth Muscle Cell Proliferation and Hyaluronan Production in Rat Ductus Arteriosus

Iwasaki, Shigeo; Minamisawa, Susumu; Yokoyama, Utako; Akaike, Toru; Quan, Hong; Nagashima, Yoji; Nishimaki, Shigeru; Ishikawa, Yoshihiro; Yokota, Shumpei

doi:10.1203/pdr.0b013e31813c9339

Cited by 15 publications

(11 citation statements)

References 35 publications

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“…Several 'classical' angiogenic and vasculogenic signaling pathways are involved in ductus development and remodeling. VEGF regulates remodeling during permanent closure [23] , PDGF-BB mediates VSMC proliferation [101] , and the AGTR1 gene is upregulated in the neonatal ductus. In addition, angiotensin has been suggested as a novel effector of ductus closure [49] .…”

Section: Resultsmentioning

confidence: 99%

Insights into the Pathogenesis and Genetic Background of Patency of the Ductus Arteriosus

Bökenkamp¹,

DeRuiter²,

Munsteren³

et al. 2009

Neonatology

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The unique differentiation program of the ductus arteriosus (DA) is essential for its specific task during fetal life and for the adapting circulation after birth. Phenotypic changes occur in the DA during the normal maturation and definitive closure. Morphological abnormalities of the vessel wall characterize the persistent DA (PDA) in older children. Here, we give an overview of the animal models of DA regulation and remodeling. Genetic research has identified the cause of syndromic forms of PDA, such as the TFAP2B mutations in Char syndrome. Genes that interfere with the remodeling of vascular smooth muscle cells (VSMCs) of the ductal media are affected in virtually all of these anomalies. Therefore, the pivotal regulatory role of VSMCs is emphasized. A better understanding of the genetic background of this developmental process may help develop new strategies to manipulate the DA in premature infants, neonates with duct-dependent anomalies, and patients with syndromic and non-syndromic PDA.

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Section: Resultsmentioning

confidence: 99%

Insights into the Pathogenesis and Genetic Background of Patency of the Ductus Arteriosus

Bökenkamp¹,

DeRuiter²,

Munsteren³

et al. 2009

Neonatology

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“…In addition, growth factors and cytokines regulate HA production in smooth muscle cells. For example, PDGF stimulates HA production in vascular smooth muscle cells (318, 319), while IL-15 inhibits HA production and smooth muscle cell migration (161). Furthermore, HA binding proteins regulate smooth muscle cell proliferation and migration during tissue injury.…”

Section: Ha and Non-leukocytesmentioning

confidence: 99%

Hyaluronan as an Immune Regulator in Human Diseases

Jiang

Liang

Noble

2011

Physiological Reviews

882

914

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Accumulation and turnover of extracellular matrix components are the hallmarks of tissue injury. Fragmented hyaluronan stimulates the expression of inflammatory genes by a variety of immune cells at the injury site. Hyaluronan binds to a number of cell surface proteins on a variety of cell types. Hyaluronan fragments signal through both Toll-like receptor (TLR) 4 and TLR2 as well as CD44 to stimulate inflammatory genes in inflammatory cells. Hyaluronan is also present on the cell surface of epithelial cells and provides protection against tissue damage by interacting with TLR2 and TLR4 on these parenchymal cells. Hyaluronan and hyaluronan-binding proteins regulate inflammation, tissue injury and repair through regulating inflammatory cell recruitment, release of inflammatory cytokines, and stem cell migration. This review focuses on the role of hyaluronan as an immune regulator in human diseases.

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“…This mechanism of vascular remodeling is similar to the development of atherosclerosis seen after vascular wall injury 140,142 . Cytokines, such as IL-17, play a role in vascular remodeling in atherosclerosis and may similarly mediate remodeling of the ductus 143,144 . IL-17 has also been shown to affect the aorta (large vessel) and the coronaries (small vessels) in different ways revealing that IL-17 has variable expression in different tissues 145 .…”

Section: The Role Of Il-17 In the Patent Ductus Arteriosusmentioning

confidence: 99%

IL‐17 in neonatal health and disease

Lawrence

Ruoss

Wynn

2017

American J Rep Immunol

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Over the last few years, scientific interest in the cytokine IL-17A has intensified as its role in human health and disease has been elucidated. Discovered almost a quarter century ago, IL-17A is known to have poor biologic activity when acting alone, but attains robust actions when working synergistically with potent mediators of proinflammatory immune responses, such as IL-6 and IL-8. IL-17A is produced by specialized innate immune cells that protect host barriers from the outside world. Like sentries, these innate immune cells can “sound the alarm” through increased production of IL-17A, causing activation and recruitment of primed neutrophils and monocytes when pathogens escape initial host defenses. In this way, IL-17A promulgates mechanisms responsible for pathogen death and clearance. However, when IL-17A pathways are triggered during fetal development, due to chorioamnionitis or in utero inflammatory conditions, IL-17A can instigate and/or exacerbate fetal inflammatory responses that increase neonatal morbidities and mortality associated with common neonatal conditions such as sepsis, bronchopulmonary dysplasia (BPD), patent ductus arteriosus (PDA), and necrotizing enterocolitis (NEC). This review details the ontogeny of IL-17A in the fetus and newborn, discusses how derangements in its production can lead to pathology, and describes known and evolving therapies that may attenuate IL-17A-mediated human conditions.

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Interleukin-15 Inhibits Smooth Muscle Cell Proliferation and Hyaluronan Production in Rat Ductus Arteriosus

Cited by 15 publications

References 35 publications

Insights into the Pathogenesis and Genetic Background of Patency of the Ductus Arteriosus

Insights into the Pathogenesis and Genetic Background of Patency of the Ductus Arteriosus

Hyaluronan as an Immune Regulator in Human Diseases

IL‐17 in neonatal health and disease

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