Birth-Related Up-Regulation of mRNA Encoding Tyrosine Hydroxylase, Dopamine β-Hydroxylase, Neuropeptide Tyrosine, and Prepro-Enkephalin in Rat Adrenal Medulla Is Dependent on Postnatal Oxygenation

Holgert, Hans; Péquignot, Jean-Marc; Lagercrantz, Hugo; Hökfelt, Tomas

doi:10.1203/00006450-199506000-00005

Cited by 22 publications

(15 citation statements)

References 39 publications

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“…Furthermore, such prenatal Hx is associated with an increased risk for neurologic abnormalities during development (17), including cognitive and behavioral disorders (18 -21). Holgert et al (22) have found that short-term Hx (11-13% O 2 ) during the last 3 d of gestation induces an increase in the level of TH mRNA in the fetal adrenal gland 1 d before birth. However, there are presently no studies available dealing with the effects of longterm Hx on the maturation of the adrenal medulla.…”

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confidence: 99%

Long-Term Prenatal Hypoxia Alters Maturation of Adrenal Medulla in Rat

Mamet¹,

Peyronnet²,

Roux³

et al. 2002

Pediatr Res

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Catecholamine release from the adrenal medulla glands plays a vital role in postnatal adaptation. A number of pathologic situations are characterized by oxygen deficiency. The objective of the present study was to determine the influence of long-term prenatal hypoxia on maturation of the adrenal medulla. Pregnant rats were subjected to hypoxia (10% O 2 ) from the fifth to the 20th d of gestation. The offspring were examined on the 19th d of gestation (E19), the day of birth (P0), and at postnatal (P) day of life P3, P7, P14, P21, and P68. The catecholamine content and activity of tyrosine hydroxylase (TH) in vivo were assayed by HPLC with electrochemical detection. Cellular expression of TH and phenylethanolamine N-methyl transferase was evaluated by protein immunohistochemistry and in situ hybridization of the corresponding mRNA species. Exposure to prenatal hypoxia reduced the epinephrine content of the adrenal medulla on E19, P0, P3, and P7 while increasing the norepinephrine content on E19, P0, and P14. Furthermore, the peak epinephrine to norepinephrine ratio appearing between P7 and P10 in the normoxic offspring was absent in the hypoxic offspring. The in vivo TH activity was increased on P3 and P14 and decreased on P68. The percentage of chromaffin cells in the medulla expressing TH and phenylethanolamine N-methyl transferase was lowered on E19, P0, and P7. TH and phenylethanolamine N-methyl transferase mRNA levels were reduced on P7. Clearly prenatal hypoxia results in major changes in adrenal catecholamine stores and synthesis during the perinatal period, which persist into adulthood. The capacity to cope with postnatal stress might be disturbed as a consequence of prenatal hypoxia. The release of catecholamines plays an essential role in initial adaptation to extrauterine life, particularly in connection with perinatal asphyxia (1). Circulating catecholamines originate to a large extent from the adrenal medulla glands and serve vital functions in relation with cardiovascular, respiratory, and metabolic responses to the stress associated with birth (1-4). In the rat, the chromaffin cells of the adrenal medulla are still immature at the time of birth and undergo extensive biochemical, morphologic, and functional changes during postnatal development.Catecholamine synthesis is catalyzed by cytoplasmic enzymes, including TH, which represents the rate-limiting step, and PNMT, which catalyzes the biosynthesis of E. At birth, increases in both the plasma and adrenal levels of catecholamines occur (5, 6). Marked increases in the levels of TH mRNA and of dopamine ␤-hydroxylase mRNA are observed in the adrenal, thus reflecting the surge in catecholamines at the

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confidence: 99%

Long-Term Prenatal Hypoxia Alters Maturation of Adrenal Medulla in Rat

Mamet¹,

Peyronnet²,

Roux³

et al. 2002

Pediatr Res

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“…However, in the rat this regulation is not mature at birth (9,11). Still, CAs are released with hypoxia (3), and synthesis of CA enzymes, and also of ENK and neuropeptide Y, is up-regulated several-fold at birth (5,6). Most likely an O 2 -sensing mechanism in the chromaffin cells plays a regulatory role at this stage (7,8).…”

Section: Discussionmentioning

confidence: 99%

“…Slides and 14 C standards [Amersham (20)] were covered with Hyperfilm ␤-max film (Kodak, Rochester, NY, U.S.A.) and exposed at Ϫ20°C for 3 and 7 d. Computerized and digitized quantification of tissue gray levels (256 levels) on the films was performed using a Nikon Microphot FX-microscope (Nikon, Tokyo, Japan), a Macintosh computer equipped with a QuickCapture frame-grabbing board (Data Translation, Marlboro, MA, U.S.A.), and a Dage-MTI 72 CCD series camera (DAGE-MTI, Michigan City, IN, U.S.A.) equipped with a Nikon 55-mm f2.8 lens, and by use of the public domain NIH Image program (http://rsb.info.nih.gov/nih-image/), as described earlier (5,6). Gray levels of the 14 C standards were determined and used in a third-degree polynomial approximation to construct a gray level to activity transfer function.…”

Section: Methodsmentioning

confidence: 99%

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Chronic Prenatal Nicotine Exposure Alters Enkephalin mRNA Regulation in the Perinatal Rat Adrenal Medulla

2003

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“…In adult rat, catecholamine secretion in adrenal medulla chromaffin cells is controlled by the cholinergic splanchnic nerve, whereas this innervation is absent at birth (39), meaning that chromaffin cells have the capacity to release catecholamines without neural stimulation during fetal life (9). It has been shown that stress, such as maternal hypoxia during the last 3 days of gestation, induces an increase in the levels of TH and D␤H mRNA in fetal adrenal glands 1 day prior to birth (18). Adrenal hypoxia in the current IUGR model is supported by microarray analysis and quantitative RT-PCR, revealing the upregulation of many genes related to hypoxia, such as Igfbp1, aldolase A, and ceruloplasmin.…”

Section: Discussionmentioning

confidence: 99%

Fetal adrenal gland alterations in a rat model of adverse intrauterine environment

Bibeau

Battista

Houde

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Given that fetal adrenal development and maturation occur during late gestation in rats, the aim of this study was to evaluate the expression of proteins and enzymes involved in steroidogenesis and catecholamine synthesis in adrenal glands from IUGR fetuses. A gene microarray was performed to investigate for alteration in the pathways participating in hormone production. Results show that increased aldosterone serum concentrations in IUGR fetuses were associated with higher mRNA adrenal levels of angiotensin II receptor type 1 (AT1R) and cytochrome P450 aldosterone synthase in response to decreased serum sodium content. Conversely, reduced serum corticosterone concentrations in these fetuses appear to result from alterations in gene expression involved in cholesterol metabolism, such as the augmented apolipoprotein E levels, and in steroidogenesis, like the decreased levels of cytochrome P45011␤-hydroxylase. Furthermore, increased AT2R expression and the presence of hypoxia and oxidative stress may, in turn, explain the higher adrenal mRNA levels of enzymes involved in catecholamine synthesis. Despite this increase, catecholamine adrenal content was reduced in males and was similar in females compared with sex-matched controls, suggesting higher catecholamine secretion. This could be associated with the induction of genes involved in inflammation-related, acute-phase response in IUGR fetuses. All of these alterations could have long-lasting health effects and may, hence, be implicated in the pathogenesis of increased blood pressure and cardiac hypertrophy observed in IUGR adult animals from this model. fetal programming; developmental plasticity; steroidogenesis; catecholamine ASSOCIATION BETWEEN LOW BIRTH weight and the increased risk of cardiovascular and metabolic diseases in adult life has been confirmed by many epidemiological and animal studies (2, 27). These links could be explained by the processes of normal developmental plasticity that can be affected in response to environmental factors during early life. Indeed, fetal adaptations as a response to impaired intrauterine environment lead to fine physiological settings (alterations in tissue anatomy or microanatomy, cellular activity, and gene expression), which, in turn, can be maladaptative to adult life (3, 13). For example, prenatal hypoxia in rats has been reported to delay the maturation of the adrenal medulla, evidenced by the lower percentage of chromaffin cells expressing tyrosine hydroxylase (TH) and phenylethanolamine N-methyl transferase (PNMT) until postnatal day 7, compared with normoxic offspring (23). Interestingly, the decreased TH activity at 10 wk of age suggests that this impaired adrenal function persists until adulthood (23). In sheep, experimental restriction of placental function (removing endometrial caruncles prior to mating) results in growth-restricted fetuses that present an increase in adrenal gland weight associated with higher plasma cortisol (32), likely due to enhanced expression of cholesterol side-chain cleavage cyt...

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Birth-Related Up-Regulation of mRNA Encoding Tyrosine Hydroxylase, Dopamine β-Hydroxylase, Neuropeptide Tyrosine, and Prepro-Enkephalin in Rat Adrenal Medulla Is Dependent on Postnatal Oxygenation

Cited by 22 publications

References 39 publications

Long-Term Prenatal Hypoxia Alters Maturation of Adrenal Medulla in Rat

Long-Term Prenatal Hypoxia Alters Maturation of Adrenal Medulla in Rat

Chronic Prenatal Nicotine Exposure Alters Enkephalin mRNA Regulation in the Perinatal Rat Adrenal Medulla

Fetal adrenal gland alterations in a rat model of adverse intrauterine environment

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