Effects of dexamethasone on the expression of myelin basic protein, proteolipid protein, and glial fibrillary acidic protein genes in developing rat brain

Tsuneishi, Syuichi; Takada, Satoshi; Motoike, Toshiyuki; Ohashi, Tamaki; Sano, Kimihiko; Nakamura, Hajime

doi:10.1016/0165-3806(91)90121-x

Cited by 60 publications

(33 citation statements)

References 32 publications

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“…ous studies have indicated that GC treatment results in decreased cerebellar volumes in the rodent and human brain (19,20). To confirm the effects of GC treatment on early neonatal cerebellar development involving multiple courses, we treated C57BL/6J mouse pups with Dex daily for 1 week from P0 to P7 (Figure 1).…”

Section: Gc Treatment Inhibits Cerebellar Growth and Cgnp Proliferatimentioning

confidence: 99%

Hedgehog signaling has a protective effect in glucocorticoid-induced mouse neonatal brain injury through an 11βHSD2-dependent mechanism

Heine¹,

Rowitch²

2009

J. Clin. Invest.

136

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Glucocorticoids (GCs) are administered to human fetuses at risk of premature delivery and to infants with life-threatening respiratory and cardiac conditions. However, there are ongoing concerns about adverse effects of GC treatment on the developing human brain, although the precise molecular mechanisms underlying GCinduced brain injury are unclear. Here, we identified what we believe to be novel cross-antagonistic interactions of Sonic hedgehog (Shh) and GC signaling in proliferating mouse cerebellar granule neuron precursors (CGNPs). Chronic GC treatment (from P0 through P7) in mouse pups inhibited Shh-induced proliferation and upregulation of expression of N-myc, Gli1, and D-type cyclin protein in CGNPs. Conversely, acute GC treatment (on P7 only) caused transient apoptosis. Shh signaling antagonized these effects of GCs, in part by induction of 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2). Importantly, 11βHSD2 antagonized the effects of the GCs corticosterone, hydrocortisone, and prednisolone, but not the synthetic GC dexamethasone. Our findings indicate that Shh signaling is protective in the setting of GC-induced mouse neonatal brain injury. Furthermore, they led us to propose that 11βHSD2-sensitive GCs (e.g., hydrocortisone) should be used in preference to dexamethasone in neonatal human infants because of the potential for reduced neurotoxicity.

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Section: Gc Treatment Inhibits Cerebellar Growth and Cgnp Proliferatimentioning

confidence: 99%

Hedgehog signaling has a protective effect in glucocorticoid-induced mouse neonatal brain injury through an 11βHSD2-dependent mechanism

Heine¹,

Rowitch²

2009

J. Clin. Invest.

136

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“…Außerdem wurde die Expression der mRNA der Proteine MBP und PLP durch Gabe von Dexamethason in der frühen postnatalen Periode unterdrückt [Tsuneishi et al, 1991].…”

Section: Einfluss Auf Myelin Und Oligodendrocytenunclassified

“…Auch Beeinträchtigungen der Myelinisierung bzw. der Expression Myelin-spezifischer mRNA wurde in einigen in vivo Studien beobachtet [Tsuneishi et al, 1991;Dunlop et al, 1997;Huang et al, 2001]. In diesen Versuchen wurden jedoch mehrfach sehr hohe Dosen an Corticosteroiden gegeben, wie sie in der Perinatalmedizin nicht zur Anwendung kommen würden.…”

Section: Vorläuferzellen?unclassified

15 Periventrikuläre Leukomalazie

Attenberger¹,

Runge²,

Morelli³

et al. 2012

Essentials Der Klinischen MRT

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“…2, 3, 4 and 5 weeks and adults (8 -10 weeks) were used for this study. The animals were injected with Dex solution subcutaneously (s.c.) at a dose of 2 mg Dex/Kg body weight for three alternative days prior to the day of sacrifice [8,[18][19][20]. Thus in the 2-week group, the animals received Dex treatment on day 8, 10 and 12; and the animals were sacrificed on day 14.…”

Section: Animals and Treatment With Dexmentioning

confidence: 99%

“…Due to its distinct anti-inflammatory properties, it is being used for the treatment of wide range of diseases. These include skin diseases; bronchial asthma; chronic lung disease (CLD) in extremely low birth weight (ELBW) and very low weight (VLBW) infants; bronchopulmonary dysplasia (BPD); metastasis of brain, spine and meninges, respiratory distress syndrome (RDS) in fetuses and rheumatoid arthritis [1,[3][4][5][6][7][8]. Glucocorticoids like dexamethasone and betamethasone are choice drugs of clinicians to prevent lung diseases in immature newborns.…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone treatment alters kinetics properties of liver mitochondrial F<sub>0</sub>.F<sub>1</sub>-ATPase and membrane lipid profiles in developing and adult rats

Pandya¹,

Agarwal²,

Modi³

et al. 2013

AER

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Dexamethasone-a potent synthetic glucocorticoid-has multiple diagnostic and therapeutic applications in wide range of age groups. However, the side-effects of dexamethasone (Dex) treatment including those on development are becoming increasingly apparent. Since the developmental processes are energy-dependent, we examined the effects of chronic Dex treatment on kinetics properties of liver mitochondrial F 0 .F 1 -ATPase and mitochondrial membrane lipid profiles in rats belonging to different developmental age groups (2, 3, 4 and 5 weeks) and in adults (~8 weeks). The animals were treated with a subcutaneous dose of 2 mg of Dex/kg body weight (or saline as vehicle) for three alternative days (at around 7.00 A.M.) prior to the day of sacrifice. Dex treatment resulted in significant reduction in F 0 .F 1 -ATPase activity in developmental age groups and in adults as compared to their age-matched vehicle-treated control group. The substrate kinetics analysis of F 0 .F 1 -ATPase resolved Km and Vmax values in 3 components in all the control age groups; whereas Dex treatment significantly altered the Km and Vmax values or abolished the entire components in age-specific manner. Dex treatment significantly lowered the energy of activation and altered phase transition temperature (Tt˚C) in all the developmental age groups and in adults. Dex treatment significantly increased the contents of total phospholipid (TPL), individual phospholipids classes and cholesterol (CHL) in all the developmental age groups whereas opposite pattern was observed in adults. The mitochondrial membrane became more fluidized in the developing age groups (2, 4 and 5 weeks); whereas no change was observed in 3-week and adult groups following Dex treatment. In present study, our data demonstrate comprehensive deleterious effects of chronic Dex treatment on liver mitochondrial membrane structure and F 0 .F 1 -ATPase functional properties with respect to energy metabolism. At the same time, our data also warns against excessive repeated use of antenatal DEX in treatments in growing and adult human patients.

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Effects of dexamethasone on the expression of myelin basic protein, proteolipid protein, and glial fibrillary acidic protein genes in developing rat brain

Cited by 60 publications

References 32 publications

Hedgehog signaling has a protective effect in glucocorticoid-induced mouse neonatal brain injury through an 11βHSD2-dependent mechanism

Hedgehog signaling has a protective effect in glucocorticoid-induced mouse neonatal brain injury through an 11βHSD2-dependent mechanism

15 Periventrikuläre Leukomalazie

Dexamethasone treatment alters kinetics properties of liver mitochondrial F<sub>0</sub>.F<sub>1</sub>-ATPase and membrane lipid profiles in developing and adult rats

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Effects of dexamethasone on the expression of myelin basic protein, proteolipid protein, and glial fibrillary acidic protein genes in developing rat brain

Cited by 60 publications

References 32 publications

Hedgehog signaling has a protective effect in glucocorticoid-induced mouse neonatal brain injury through an 11βHSD2-dependent mechanism

Hedgehog signaling has a protective effect in glucocorticoid-induced mouse neonatal brain injury through an 11βHSD2-dependent mechanism

15 Periventrikuläre Leukomalazie

Dexamethasone treatment alters kinetics properties of liver mitochondrial F&lt;sub&gt;0&lt;/sub&gt;.F&lt;sub&gt;1&lt;/sub&gt;-ATPase and membrane lipid profiles in developing and adult rats

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Dexamethasone treatment alters kinetics properties of liver mitochondrial F<sub>0</sub>.F<sub>1</sub>-ATPase and membrane lipid profiles in developing and adult rats