Functional glucocorticoid receptors in the mesonephros of the ovine fetus

Peers, Arianne; Hantzis, Vicky; Dodic, Miodrag; Koukoulas, Irene; Gibson, A. P.; Baird, R.; Salemi, Renato; Wintour, E. M.

doi:10.1046/j.1523-1755.2001.059002425.x

Cited by 18 publications

(18 citation statements)

References 26 publications

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“…Growth restriction is a common finding in models of long-term glucocorticoid exposure [35], [36], whereas short-term exposure to glucocorticoids does not usually result in restricted growth [37], [38], [39], [40], [41], [42]. In the present study, however, 48 h of DEX exposure, did lead to significantly reduced body size in the period during the DEX exposure at E14.5, but body size was restored to normal by E17.5 and there was no evidence of postnatal growth restriction.…”

Section: Discussionmentioning

confidence: 99%

Prenatal Exposure to Dexamethasone in the Mouse Alters Cardiac Growth Patterns and Increases Pulse Pressure in Aged Male Offspring

et al. 2013

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Exposure to synthetic glucocorticoids during development can result in later cardiovascular and renal disease in sheep and rats. Although prenatal glucocorticoid exposure is associated with impaired renal development, less is known about effects on the developing heart. This study aimed to examine the effects of a short-term exposure to dexamethasone (60 hours from embryonic day 12.5) on the developing mouse heart, and cardiovascular function in adult male offspring. Dexamethasone (DEX) exposed fetuses were growth restricted compared to saline treated controls (SAL) at E14.5, but there was no difference between groups at E17.5. Heart weights of the DEX fetuses also tended to be smaller at E14.5, but not different at E17.5. Cardiac AT1aR, Bax, and IGF-1 mRNA expression was significantly increased by DEX compared to SAL at E17.5. In 12-month-old offspring DEX exposure caused an increase in basal blood pressure of ∼3 mmHg. In addition, DEX exposed mice had a widened pulse pressure compared to SAL. DEX exposed males at 12 months had an approximate 25% reduction in nephron number compared to SAL, but no difference in cardiomyocyte number. Exposure to DEX in utero appears to adversely impact on nephrogenesis and heart growth but is not associated with a cardiomyocyte deficit in male mice in adulthood, possibly due to compensatory growth of the myocardium following the initial insult. However, the widened pulse pressure may be indicative of altered vascular compliance.

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Section: Discussionmentioning

confidence: 99%

Prenatal Exposure to Dexamethasone in the Mouse Alters Cardiac Growth Patterns and Increases Pulse Pressure in Aged Male Offspring

et al. 2013

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“…23,24 Control reactions that did not include reverse transcriptase were included in a separate reverse transcription reaction with all total RNA samples. A comparative C T (cycle of threshold fluorescence) method was used to determine relative mRNA expression levels of the angiotensin II type 1 and type 2 receptors (AT 1 and AT 2 ) and angiotensinogen in fetal brain tissues.…”

Section: Gene Expression Studiesmentioning

confidence: 99%

“…The real-time polymerase chain reaction (PCR) has been described in more detail elsewhere. 23,24 Optimal concentrations of primers and probe have been determined in preliminary experiments and are previously shown. 25,26 cDNA (50 ng) was amplified at 50°C for 2 minutes and at 95°C for 10 minutes followed by 40 cycles of 95°C for 15 seconds and 60°C for 1 minute…”

Section: Gene Expression Studiesmentioning

confidence: 99%

Programming Effects of Short Prenatal Exposure to Dexamethasone in Sheep

et al. 2002

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Abstract-Recent studies have linked fetal exposure to a suboptimal intrauterine environment with adult hypertension. The aims of the present study were to see whether prenatal dexamethasone administered intravenously to the ewe between 26 to 28 days of gestation (1) resulted in high blood pressure in male and female offspring and whether hypertension in males was modulated by testosterone status, and (2) altered gene expression for angiotensinogen and angiotensin type 1 (AT 1 ) receptors in the brain in late gestation and in the adult. Basal mean arterial pressure (MAP) at 2 years of age was significantly higher in wethers exposed to prenatal dexamethasone (group D; 106Ϯ5 mm Hg, nϭ9) compared with the control group (group S; 91Ϯ3 mm Hg, nϭ8; PϽ0.01). Infusion of testosterone for 3 weeks had no effect on MAP in either treatment group. Key Words: brain Ⅲ glucocorticoids Ⅲ hypertension, experimental Ⅲ sheep E pidemiological evidence suggests that babies born small for gestational age have an increased incidence of adultonset diseases or dysfunction, including syndrome X (hypertension, non-insulin-dependent diabetes mellitus, and hyperlipidemia). [1][2][3] It is hypothesized that a suboptimal intrauterine environment during a critical stage of development permanently alters, or "programs," the development of fetal tissues. This may ensure the short-term survival of the fetus but also may bring adverse consequences in postnatal life.Animal models using maternal undernutrition or restriction of specific dietary components (iron, protein), either throughout pregnancy or during parts of gestation, have confirmed that restriction of fetal growth leads to elevated blood pressure in the progeny of rats. 4 -6 A second type of animal model has examined the long-term/programming effects caused by prenatal glucocorticoid exposure. When adult rats were exposed to large doses of carbenoxolone (an 11␤-hydroxysteroid dehydrogenase [HSD] inhibitor, which blocks placental inactivation of endogenous glucocorticoids) throughout gestation, offspring were of low birth weight and had high blood pressure. 7-9 The synthetic glucocorticoid dexamethasone, which is poorly metabolized by placental 11␤-HSD, given throughout rat pregnancy resulted in offspring with high blood pressure. 10 In the sheep, we 11 have shown that exposure to dexamethasone, for 2 days very early in gestation (at a mean age of 27 days of the 150-day gestation period) results in hypertensive female offspring by 3 to 4 months of age. This hypertension amplifies with age and is associated with an increased cardiac output. 12 By 7 years of age, these animals had developed left ventricular hypertrophy with reduced cardiac functional reserve. 13 In these studies, only female offspring were studied. However, in many models, the programming effects of the prenatal treatment are only seen in male offspring, 14 or they were more pronounced in male offspring compared with female offspring. 4 These studies proposed that programming, at least in some models, may be gender specific....

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“…This dose of dexamethasone had previously produced hypertension in female offspring (Dodic et al 1998(Dodic et al , 2000 and the dose of cortisol was suffi cient to produce maternal blood cortisol values of 392 (SE 66) nmol/l (Peers et al 2001). After birth, lambs were transported with their dams to the Institute and housed in pens.…”

Section: Maternal Treatmentmentioning

confidence: 99%

Blood pressure, heart rate, hormonal and other acute responses to rubber-ring castration and tail docking of lambs

Peers

Mellor²,

Wintour

et al. 2002

New Zealand Veterinary Journal

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Functional glucocorticoid receptors in the mesonephros of the ovine fetus

Abstract: These results suggest that functional GRs are present in the early ovine mesonephros.

Cited by 18 publications

References 26 publications

Prenatal Exposure to Dexamethasone in the Mouse Alters Cardiac Growth Patterns and Increases Pulse Pressure in Aged Male Offspring

Prenatal Exposure to Dexamethasone in the Mouse Alters Cardiac Growth Patterns and Increases Pulse Pressure in Aged Male Offspring

Programming Effects of Short Prenatal Exposure to Dexamethasone in Sheep

Blood pressure, heart rate, hormonal and other acute responses to rubber-ring castration and tail docking of lambs

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