Increased myometrial contracture frequency at 96–140 days  accelerates fetal cardiovascular maturation

Shinozuka, Noriko; Yen, Andrew; Nathanielsz, Peter W.

doi:10.1152/ajpheart.2000.278.1.h41

Cited by 13 publications

(16 citation statements)

References 43 publications

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“…22 Chronic, mild fetal hypoxemia leads to premature maturation of fetal cardiovascular control, manifested as a lower heart rate and a higher blood pressure early during gestation. 23 We speculate that a suboptimal intrauterine environment may lead to altered cardiorespiratory control, which could in turn predispose an infant toward SIDS, although this hypothesis requires further study.…”

Section: Discussionmentioning

confidence: 90%

Second-Trimester Maternal Serum Levels of Alpha-Fetoprotein and the Subsequent Risk of Sudden Infant Death Syndrome

Smith

Wood²,

Pell³

et al. 2004

N Engl J Med

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Section: Discussionmentioning

confidence: 90%

Second-Trimester Maternal Serum Levels of Alpha-Fetoprotein and the Subsequent Risk of Sudden Infant Death Syndrome

Smith

Wood²,

Pell³

et al. 2004

N Engl J Med

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“…Moreover, when fertilized mouse oocytes are cultured with OT in vitro, they develop into the blastocyst stage at a higher rate than their unstimulated counterparts (46). Spontaneous myometrial contractures are known to occur during pregnancy in sheep, and controlled contractures induced by application of OT pulses to pregnant ewes have been shown to accelerate fetal cardiovascular function (47).…”

Section: Discussionmentioning

confidence: 99%

Oxytocin induces differentiation of P19 embryonic stem cells to cardiomyocytes

Paquin

Danalache

Jankowski

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

212

175

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We recently discovered the existence of the oxytocin͞oxytocin receptor (OT͞OTR) system in the heart. Activation of cardiac OTR stimulates the release of atrial natriuretic peptide (ANP), which is involved in regulation of blood pressure and cell growth. Having observed elevated OT levels in the fetal and newborn heart at a stage of intense cardiomyocyte hyperplasia, we hypothesized a role for OT in cardiomyocyte differentiation. We used mouse P19 embryonic stem cells to substantiate this potential role. P19 cells give rise to the formation of cell derivatives of all germ layers. Treatment of P19 cell aggregates with dimethyl sulfoxide (DMSO) induces differentiation to cardiomyocytes. In this work, P19 cells were allowed to aggregate from day 0 to day 4 in the presence of 0.5% DMSO, 10 ؊7 M OT and͞or 10 ؊7 M OT antagonist (OTA), and then cultured in the absence of these factors until day 14. OT alone stimulated the production of beating cell colonies in all 24 independently growing cultures by day 8 of the differentiation protocol, whereas the same result was obtained in cells induced by DMSO only after 12 days. Cells induced with OT exhibited increased ANP mRNA, had abundant mitochondria (i.e., they strongly absorbed rhodamine 123), and expressed sarcomeric myosin heavy chain and dihydropyridine receptor-␣1, confirming a cardiomyocyte phenotype. In addition, OT as well as DMSO increased OTR protein and OTR mRNA, and OTA completely inhibited the formation of cardiomyocytes in OT-and DMSO-supplemented cultures. These results suggest that the OT͞OTR system plays an important role in cardiogenesis by promoting cardiomyocyte differentiation.

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“…Because the uterus is not completely quiescent during pregnancy (Nathanielsz et al, 1998) and uterine muscle activity during pregnancy can influence fetal development (Shinozuka et al, 1999(Shinozuka et al, , 2000, inhibition of uterine contractility during midgestation may have unrecognized adverse health consequences. Additionally, interference with uterine contractility during midgestation may result in complications for spontaneous and induced abortions.…”

Section: Discussionmentioning

confidence: 99%

Phospholipase-Mediated Inhibition of Spontaneous Oscillatory Uterine Contractions by Lindane in Vitro,

Wang

Loch‐Caruso

2002

Toxicology and Applied Pharmacology

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Although regulation of uterine contractility is fundamental for parturition, mechanisms by which toxicants modify uterine muscle contractions remain poorly understood. In a previous cumulative concentration-response study, 10 μM lindane (γ-hexachlorocyclohexane) reduced contraction force and 30 μM lindane abolished contractions in Gestation Day 10 rat uterine strips when lindane was added to muscle baths at 10-min intervals. Other studies showed that brief (<10 min) exposures to 10-100 μM lindane inhibit gap junctions and activate phospholipase pathways in rat myometrial cells in culture. Consequently, lindane was used as a prototype toxicant with known uterine activity to investigate the hypothesis that activation of a specific phospholipase pathway provides a mechanistic link between inhibition of uterine contraction and inhibition of myometrial gap junctions. Uterine tissue and cells were pretreated with phospholipase pathway inhibitors to evaluate the role of phospholipase pathways in lindane's actions in the uterus. Concentrations of inhibitors were selected based on previous reports of effective concentrations for the enzyme activity and on pilot toxicity studies of the inhibitors on uterine contraction and gap junction communication. To monitor uterine contractions, longitudinal uterine strips were excised from Gestation Day 10 rats and suspended in isometric muscle baths, consistent with previous experiments. Exposure in vitro for 60 min to 10-50 μM lindane, an effective concentration range for the uterine responses of interest, revealed that 30 μM lindane rapidly abolished contractions. Subsequently, uterine strips were pretreated with phospholipase pathway inhibitors and then challenged with 30 μM lindane, the lindane concentration that elicited maximal inhibition of uterine contraction. Pretreatment with 20-50 μM of the phosphatidylinositol-specific phospholipase C inhibitor 1-O-octadecyl-2-O-methyl-sn -glycerol-3-phosphorylcholine (ET-18-OCH 3 ) reversed lindane-induced inhibition of spontaneous uterine contractions. Gap junction intercellular communication was monitored by injecting the fluorescent dye Lucifer yellow into rat myometrial cells grown in culture and assessing dye transfer to adjacent cells using epifluorescence microscopy. Similar to uterine contraction, pretreatment of cell cultures with phospholipase C inhibitors (30 μM ET-18-OCH 3 , 50 μM tricyclodecan-p-yl-xanthogenate · K [D609] or 50 μM tricyclodecan-p-yl-xanthogenate · K or 2-nitro-4-carboxyphenyl-N,Ndophenylcarbamate [NCDC]) partially reversed inhibition of dye transfer by 100 μM lindane, a 4To whom correspondence and reprint requests should be addressed at 1420 Washington Heights, Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, MI 48109-2029. Fax: (734) lindane concentration previously shown to abolish myometrial Lucifer yellow dye transfer under similar culture conditions. In contrast, pretreatment with 20 μM of bromoenol lactone (BEL) to inhibit the calcium-i...

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Increased myometrial contracture frequency at 96–140 days accelerates fetal cardiovascular maturation

Cited by 13 publications

References 43 publications

Second-Trimester Maternal Serum Levels of Alpha-Fetoprotein and the Subsequent Risk of Sudden Infant Death Syndrome

Second-Trimester Maternal Serum Levels of Alpha-Fetoprotein and the Subsequent Risk of Sudden Infant Death Syndrome

Oxytocin induces differentiation of P19 embryonic stem cells to cardiomyocytes

Phospholipase-Mediated Inhibition of Spontaneous Oscillatory Uterine Contractions by Lindane in Vitro,

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