scholarly journals Effects of prenatal glucocorticoid exposure on cardiac calreticulin and calsequestrin protein expression during early development and in adulthood

2003 ◽  
Vol 371 (1) ◽  
pp. 61-69 ◽  
Author(s):  
Maria L. LANGDOWN ◽  
Mark J. HOLNESS ◽  
Mary C. SUGDEN
Keyword(s):  
Cardiac Function ◽  
Protein Expression ◽  
Growth Retardation ◽  
Premature Death ◽  
Fetal Life ◽  
Dexamethasone Treatment ◽  
Increased Risk ◽  
Uterine Growth ◽  
Intra Uterine Growth Retardation ◽  
Glucocorticoid Action

Overexpression of the conserved Ca2+-binding proteins calreticulin and calsequestrin impairs cardiac function, leading to premature death. Calreticulin is vital for embryonic development, but also impairs glucocorticoid action. Glucocorticoid overexposure during late fetal life causes intra-uterine growth retardation and programmed hypertension in adulthood. To determine whether intra-uterine growth retardation or programmed hypertension was associated with altered calreticulin or calsequestrin expression, effects of prenatal glucocorticoid overexposure (maternal dexamethasone treatment on days 15—21 of pregnancy) were examined during fetal life and postnatal development until adulthood (24 weeks). Dexamethasone (100 or 200μg/kg of maternal body weight) was administered via osmotic pump. Calreticulin was detected as a 55kDa band and calsequestrin as 55 and 63kDa bands in 21 day fetal hearts. Only the 55kDa calsequestrin band was detected postnatally. Prenatal glucocorticoid overexposure at the higher dose decreased calreticulin protein expression (26%; P<0.05) but increased calsequestrin protein expression, both 55 and 63kDa bands, by 87% (P<0.01) and 78% (P<0.01); only the 55kDa calsequestrin band was increased at the lower dose (66%; P<0.05). Offspring of dams treated at the lower dexamethasone dose were studied further. In control offspring, cardiac calreticulin protein expression declined between 2 and 3 weeks of age, and remained suppressed until adulthood. Cardiac calsequestrin protein expression increased 2-fold between fetal day 21 and postnatal day 1 and continued to increase until adulthood, at which time it was 3.4-fold higher (P<0.001). Prenatal dexamethasone exposure minimally affected postnatal calsequestrin protein expression, but the postnatal decline in calreticulin protein expression was abrogated and calreticulin protein expression in adulthood was 2.2-fold increased (P<0.001) compared with adult controls. In view of the known associations between cardiac calreticulin overexpression and impaired cardiac function, targeted up-regulation of calreticulin may contribute to the increased risk of adult heart disease introduced as a result of prenatal overexposure to glucocorticoids.

Preterm birth and intra-uterine growth retardation among children of women with schizophrenia

1999 ◽  
Vol 175 (3) ◽  
pp. 239-245 ◽  
Author(s):  
B. E. Bennedsen ◽  
P. B. Mortensen ◽  
A. V. Olesen ◽  
T. B. Henriksen
Keyword(s):  
Birth Weight ◽  
Preterm Birth ◽  
Relative Risk ◽  
Low Birth Weight ◽  
Growth Retardation ◽  
Adverse Pregnancy Outcome ◽  
Increased Risk ◽  
Uterine Growth ◽  
Adverse Pregnancy ◽  
Intra Uterine Growth Retardation

BackgroundThere is conflicting evidence about the frequency of adverse pregnancy outcomes among women with schizophrenia.AimsTo investigate the risk of preterm birth, low birth weight and intra-uterine growth retardation among women with schizophrenia.MethodA total of 2212 births to 1537 women with schizophrenia in Denmark were compared with a random sample of all deliveries in Denmark in 1973–1993 (122 931 births to 72 742 women)ResultsThe children of women with schizophrenia were at increased risk of preterm delivery (relative risk=1.46, 95% CI=1.19–1.79), low birth weight (relative risk=1.57, 95% 0=1.36–1.82) and small for gestational age (relative risk=1.34, 95% CI=1.17–1.53)ConclusionsWomen with schizophrenia are at increased risk of adverse pregnancy outcome. This may be associated with an increased mortality and general morbidity and risk of schizophrenia in their children.

Association of increased maternal ferritin levels with gestational diabetes and intra-uterine growth retardation

2010 ◽  
Vol 36 (1) ◽  
pp. 58-63 ◽  
Author(s):  
V. Soubasi ◽  
S. Petridou ◽  
K. Sarafidis ◽  
Ch. Tsantali ◽  
E. Diamanti ◽  
...  
Keyword(s):  
Gestational Diabetes ◽  
Growth Retardation ◽  
Uterine Growth ◽  
Intra Uterine Growth Retardation

Tyrosine α ketoglutarate transaminase in the liver of rats with intra-uterine growth retardation

Life Sciences ◽  
1971 ◽  
Vol 10 (19) ◽  
pp. 1115-1123
Author(s):  
C. Degremont ◽  
J.M. Roux ◽  
E. Swierczewski ◽  
C. Tordet-Caridroit
Keyword(s):  
Growth Retardation ◽  
Uterine Growth ◽  
Intra Uterine Growth Retardation

Umbilical Artery Doppler Waveform in Pregnancies with Uncomplicated Intra-Uterine Growth Retardation

1988 ◽  
Vol 26 (3) ◽  
pp. 206-210 ◽  
Author(s):  
N.G. Haddad ◽  
F.D. Johnstone ◽  
P.R. Hoskins ◽  
S.E. Chambers ◽  
B.B. Muir ◽  
...  
Keyword(s):  
Growth Retardation ◽  
Umbilical Artery ◽  
Doppler Waveform ◽  
Uterine Growth ◽  
Umbilical Artery Doppler ◽  
Intra Uterine Growth Retardation

scholarly journals Early growth retardation induced by excessive exposure to glucocorticoids in utero selectively increases cardiac GLUT1 protein expression and Akt/protein kinase B activity in adulthood

2001 ◽  
Vol 169 (1) ◽  
pp. 11-22 ◽  
Author(s):  
ML Langdown ◽  
MJ Holness ◽  
MC Sugden
Keyword(s):  
Protein Kinase ◽  
Protein Expression ◽  
Adult Male ◽  
Growth Retardation ◽  
Glucose Transporter ◽  
Protein Kinase B ◽  
Early Growth ◽  
Male Offspring ◽  
Dexamethasone Treatment ◽  
Glut1 Protein

In the rat, dexamethasone treatment during late pregnancy leads to intrauterine growth retardation and is used as a model of early programming of adult onset disease. The present study investigated whether pre-natal dexamethasone treatment modifies cardiac glucose transporter (GLUT) protein expression in adulthood and identified signalling pathways involved in the response. Dexamethasone (100 microg/kg body wt per day) administered via an osmotic pump to pregnant rats (day 15 to day 21; term=22 to 23 days) reduced fetal weight at day 21 and caused hypertension, hyperinsulinaemia and elevated corticosterone levels in the adult (24-week-old) male offspring. Cardiac GLUT1 protein expression was selectively up-regulated (2.5-fold; P<0.001), in the absence of altered cardiac GLUT4 protein expression, in adult male offspring of dexamethasone-treated dams. Maternal dexamethasone treatment did not influence cardiac GLUT1 protein expression during fetal or early post-natal life. We examined potential regulatory signalling proteins that might mediate up-regulation of cardiac GLUT1 protein expression in adulthood. We observed marked (2.2-fold; P<0.01) activation of Akt/protein kinase B (PKB), together with modest activation of the anti-apoptotic protein kinase C (PKC) isoforms PKC alpha (88%, P<0.05) and PKC epsilon (56%, P<0.05) in hearts of the early-growth-retarded male offspring. These effects were, however, observed in conjunction with up-regulation of cardiac protein expression of PKC beta(1) (191%, P<0.01), PKC beta(2) (49%, P<0.05) and PKC delta (35%; P<0.01), effects that may have adverse consequences. Maternal dexamethasone treatment was without effect on cardiac extracellular signal-related kinase (ERK) 1 or ERK2 activity in adulthood. In conclusion, our data demonstrate an effect of maternal dexamethasone treatment to up-regulate cardiac GLUT1 protein expression in early-growth-retarded, hypertensive, hyperinsulinaemic adult male offspring, an effect observed in conjunction with activation of Akt/PKB.

Effect of lycopene on pre-eclampsia and intra-uterine growth retardation in primigravidas

2003 ◽  
Vol 81 (3) ◽  
pp. 257-262 ◽  
Author(s):  
J.B. Sharma ◽  
Ashok Kumar ◽  
A. Kumar ◽  
M. Malhotra ◽  
R. Arora ◽  
...  
Keyword(s):  
Growth Retardation ◽  
Uterine Growth ◽  
Intra Uterine Growth Retardation
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