Animal models of placental angiogenesis

Reynolds, Lawrence P.; Borowicz, P. P.; Vonnahme, K. A.; Johnson, Mary Lynn; Grazul-Bilska, Anna T.; Wallace, Jacqueline M.; Caton, J. S.; Redmer, Dale A.

doi:10.1016/j.placenta.2004.11.010

Cited by 159 publications

(172 citation statements)

References 157 publications

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“…Placenta nutrient transport has long been known to be dependent on vascular development. Placental vascularity in sheep during pregnancy occurs through an increase in the number and surface density of capillaries, particularly on the fetal side of the placentome (Stegeman 1974, Reynolds et al 2005. Placental surface area for nutrient exchange increases through elongation and increased branching of the fetal villi (Stegeman 1974, Macdonald & Fowden 1997.…”

Section: Discussionmentioning

confidence: 99%

Maternal betamethasone administration reduces binucleate cell number and placental lactogen in sheep

Braun

Li²,

Moss³

et al. 2007

Journal of Endocrinology

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The placenta may mediate glucocorticoid-induced fetal growth restriction. Previous studies have examined effects of fetal cortisol in sheep, which reduces placental binucleate cell (BNC) number; the source of ovine placental lactogen (oPL). The effects of maternal GC are unknown. Therefore, this study examined the effects of maternal betamethasone (BET) administration on BNC number, distribution, placental oPL protein levels, and maternal and fetal plasma oPL levels. Pregnant ewes were randomized to receive injections of saline or one (104 days of gestation; dG), two (104 and 111 dG), or three (104, 111, and 118 dG) doses of BET (0 . 5 mg/kg). Placental tissue was collected before, during, and after the period of BET treatment. Fetal (121-146 dG) and placental (121 dG) weights were decreased after BET when compared with controls. In controls, the mean number of BNCs increased until 132 dG and decreased thereafter. Placental oPL protein levels peaked at 109 dG and remained stable thereafter. Maternal plasma oPL levels in controls increased across gestation; fetal plasma oPL levels decreased. BNCs were reduced by 24% to 47% after BET when compared with controls at all ages studied. Placental oPL protein levels, maternal, and fetal plasma oPL levels were also reduced after BET injections, but recovered to values that were not different to controls near term. BET disrupted the normal distribution of BNCs within the placentome. These data may suggest a placental role in growth restrictive effects of prenatal maternal BET exposure through alterations in placental output of oPL, a key metabolic hormone of pregnancy.

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Section: Discussionmentioning

confidence: 99%

Maternal betamethasone administration reduces binucleate cell number and placental lactogen in sheep

Braun

Li²,

Moss³

et al. 2007

Journal of Endocrinology

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“…0 to 30 days gestation), or continuing up to the time at which fetal growth becomes exponential (i.e. 0 to 110 days gestation) (Reynolds et al, 2005), has no effect on either placental or fetal weight in later gestation (Yiallourides et al, 2009). A decrease in maternal food intake from , 28 days gestation continuing up to the end of the period of maximal placental growth that is 80 days gestation, does restrict placental mass primarily as a consequence of reducing growth of the placental component (Heasman et al, 1998).…”

Section: Symonds Sebert and Budgementioning

confidence: 99%

Nutritional regulation of fetal growth and implications for productive life in ruminants

Symonds¹,

Sebért²,

Budge³

2010

Animal

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The maternal nutritional and metabolic environment is critical in determining not only the reproductive success but also the long-term health and viability of the offspring. Changes in maternal diet at defined stages of gestation coincident with different stages of development can have pronounced effects on organ and tissue function in later life. This includes adipose tissue for which differential effects are observed between brown and white adipose tissues. One early, critical window of organ development in the ruminant relates to the period covering uterine attachment, or implantation, and rapid placental growth. During this period, there is pronounced cell division within developing organelles in many fetal tissues, leading to their structural development. In sheep, a 50% global reduction in caloric intake over this specific period profoundly affects placental growth and morphology, resulting in reduced placentome weight. This occurs in conjunction with a lower capacity to inactivate maternal cortisol through the enzyme 11b-hydroxysteroid dehydrogenase type 2 in response to a decrease in maternal plasma cortisol in early gestation. The birth weight of the offspring is, however, unaffected by this dietary manipulation and, although they possess more fat, this adaptation does not persist into adulthood when they become equally obese as those born to control fed mothers. Subsequently, after birth, further changes in fat development occur which impact on both glucocorticoid action and inflammatory responses. These adaptations can include changes in the relative populations of both brown and white adipocytes for which prolactin acting through its receptor appears to have a prominent role. Earlier when in utero nutrient restricted (i.e. between earlyto-mid gestation) offspring are exposed to an obesogenic postnatal environment; they exhibit an exaggerated insulin response, which is accompanied by a range of amplified and thus, adverse, physiological or metabolic responses to obesity. These types of adaptations are in marked contrast to the effect of late gestational nutrient restriction, which results in reduced fat mass at birth. As young adults, however, fat mass is increased and, although basal insulin is unaffected, these offspring are insulin resistant. In conclusion, changes in nutrient supply to either the mother and/or her fetus can have profound effects on a range of metabolically important tissues. These have the potential to either exacerbate, or protect from, the adverse effects of later obesity and accompanying complications in the resulting offspring.

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“…Angiogenesis and vasodilation within placentomes are mediated by various angiogenic factors, including vascular endothelial growth factor (VEGF) and nitric oxide (NO). While the cotyledonary capillary beds grow primarily by branching (angiogenesis) to provide a very high density of small capillaries, the caruncular capillary beds grow mainly by increasing the size of the capillaries (vasodilation), with smaller increases in capillary density (Reynolds and Redmer, 2001;Reynolds et al, 2005a and2005b).…”

Section: Placental Formationmentioning

confidence: 99%

Litter-size-dependent intrauterine growth restriction in sheep

Gootwine

Spencer

Bazer

2007

Animal

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Regulation of foetal development in sheep depends on interactions between the intrinsic capacity of the foetus for growth and the maternal environment. Lambs born in multi-foetus litters have relatively small placentae with fewer cotelydons, and lower birth weights. Litter-size-dependent intrauterine growth restriction (IUGR) is evident at mid gestation when metabolic needs of the conceptus are moderate, and overnutrition of ewes with multiple foetuses does not promote growth of their foetuses to the size of singletons. Those observations suggest that placental and conceptus growth in multi-foetus pregnancies is reprogrammed at mid gestation by an as yet undefined mechanism to attenuate foetal growth. This may protect the foetus from severe nutritional insult during late gestation, when its daily growth rate is at a maximum. In that way, lambs born in large litters with relatively lower birth weights may not experience the long-term physiological insults that can be observed in small lambs born to undernourished ewes.

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Animal models of placental angiogenesis

Cited by 159 publications

References 157 publications

Maternal betamethasone administration reduces binucleate cell number and placental lactogen in sheep

Maternal betamethasone administration reduces binucleate cell number and placental lactogen in sheep

Nutritional regulation of fetal growth and implications for productive life in ruminants

Litter-size-dependent intrauterine growth restriction in sheep

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