Peptide growth factors and the adrenal cortex

Ho, Mei Mei; Vinson, Gavin P.

doi:10.1002/(sici)1097-0029(19970315)36:6<558::aid-jemt12>3.0.co;2-n

Cited by 24 publications

(11 citation statements)

References 170 publications

(167 reference statements)

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“…In addition, we identified basic fibroblast growth factor as a potential candidate for CITED2 regulation since it is a potent mitogen for fetal and adult adrenocortical cells (Mesiano et al 1991, Basile & Holzwarth 1993, Ho & Vinson 1997, Boulle et al 2000 and since it is expressed in several adrenal tissues (Schweigerer et al 1987, Westermann et al 1990, Ho & Vinson 1995. Our in vitro experiments demonstrated that CITED2 promotor activity, mRNA-and protein levels were increased by bFGF in the NCI-H295R cell-line.…”

Section: Discussionmentioning

confidence: 75%

“…Secondly, we analyzed if CITED2 is under control of factors that are relevant for adrenal function. Since corticotropin (ACTH) is a key regulator of adrenal physiology and basic fibroblast growth factor (bFGF) has been implicated in the control of adrenocortical growth (Mesiano et al 1991, Basile & Holzwarth 1993, Ho & Vinson 1997, Feige et al 1998, Boulle et al 2000 we hypothesized that CITED2 may be a downstream effector of these factors. Therefore, we applied NCI-H295R cells to study the regulation of CITED2 by ACTH and bFGF in adrenocortical cells.…”

Section: Introductionmentioning

confidence: 99%

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CITED2 is expressed in human adrenocortical cells and regulated by basic fibroblast growth factor

Schott¹,

Bornstein²,

Malendowicz³

et al. 2007

Journal of Endocrinology

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CITED2 gene deletion in mice leads to adrenal agenesis. Therefore, we analyzed CITED2, a CBP/p300 interacting transactivator with transforming activity, in the human adrenal gland. In this study, we examined CITED2 expression in human embryonic and adult adrenal glands as well as adrenocortical carcinomas. As ACTH and basic fibroblast growth factor (bFGF) are connected to the physiology and growth of adrenocortical cells we studied the regulation of CITED2 by these factors in the NCI-H295R adrenocortical carcinoma cell line. We found CITED2 expression in the adult adrenal cortex as well in adrenocortical carcinomas. At an early stage of human adrenal organogenesis CITED2 could be located to the definitive zone of the developing adrenal gland using immunohistochemistry. In NCI-H295R cells, stimulation by bFGF led to a dose-dependent increase in CITED2 promotor activity, mRNA and protein expression while ACTH had no significant effect. The stimulatory effect of bFGF could be reduced by blocking mitogen-activated protein kinase activity using the MAPkinase kinase (MEK1)-inhibitor PD98059. CITED2 is expressed in embryonic and adult human adrenal glands as well as in adrenocortical cancer. It is connected to the signaling cascades of bFGF and its expression is modulated by mitogen-activated protein kinases. This suggests a novel role for CITED2 in human adrenal growth and possibly in adrenal tumorigenesis.

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Section: Discussionmentioning

confidence: 75%

Section: Introductionmentioning

confidence: 99%

CITED2 is expressed in human adrenocortical cells and regulated by basic fibroblast growth factor

Schott¹,

Bornstein²,

Malendowicz³

et al. 2007

Journal of Endocrinology

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“…4). Measurements of ACTH, a potent activator of adrenal cortex growth and steroidogenesis (22), indicated that the impaired corticosterone response to fasting was not due to a decrease in ACTH levels as SR-BI KO and SR-BI KO/CETP Tg mice displayed a 2-to 3-fold increase (P , 0.05) in plasma ACTH levels compared with WT controls under fasting conditions (Fig. 5A).…”

Section: Resultsmentioning

confidence: 97%

Scavenger receptor class B type I-mediated uptake of serum cholesterol is essential for optimal adrenal glucocorticoid production

Hoekstra¹,

Ye²,

Hildebrand³

et al. 2009

Journal of Lipid Research

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Impaired scavenger receptor class B type I (SR-BI)-mediated uptake of HDL-cholesterol esters (HDL-CE) induces adrenal insufficiency in mice. Humans contain an alternative route of HDL-CE clearance, namely through the transfer by cholesteryl ester transfer protein (CETP) to apolipoprotein B lipoproteins for subsequent uptake via the LDL receptor. In this study, we determined whether CETP can compensate for loss of adrenal SR-BI. Transgenic expression of human CETP (CETP Tg) in SR-BI knockout (KO) mice increased adrenal HDL-CE clearance from 33-58% of the control value. SR-BI KO/CETP Tg and SR-BI KO mice displayed adrenal hypertrophy due to equally high plasma adrenocorticotropic hormone levels. Adrenal cholesterol levels and plasma corticosterone levels were 38-52% decreased in SR-BI KO mice with and without CETP expression. SR-BI KO/CETP Tg mice also failed to increase their corticosterone level after lipopolysaccharide challenge, leading to an identical .4-fold increased tumor necrosis factor-a response compared with controls. These data indicate that uptake of CE via other routes than SR-BI is not sufficient to generate the cholesterol pool needed for optimal adrenal steroidogenesis. In conclusion, we have shown that CETP-mediated transfer of HDL-CE is not able to reverse adrenal insufficiency in SR-BI knockout mice. Thus, SR-BI-mediated uptake of serum cholesterol is essential for optimal adrenal function.-Hoekstra, M., D. Ye, R. B. Hildebrand, Y. Zhao, B. Lammers, M. Stitzinger, J. Kuiper, T. J. C. Van Berkel, and M. Van Eck. Scavenger receptor class B type I-mediated uptake of serum cholesterol is essential for optimal adrenal glucocor ticoid production.

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“…Importantly, Trigatti et al (27) have shown that female SR-BIdeficient mice are infertile, probably because of a similarly impaired steroidogenesis in the ovaries. Given the fact that SR-BI-deficient mice have very high circulating levels of ACTH, a potent activator of adrenal cortex glucocorticoid production (28), and a concomitant increase in adrenal weight under fasting conditions, it is suggested that SR-BI-deficient mice are unable to respond adequately to physiological stress impulses, as they suffer from adrenal glucocorticoid insufficiency. Probably as a consequence of the hampered response in plasma corticosterone levels, SR-BI deficiency also resulted in a significant attenuation of hepatic glucocorticoid signaling, as judged from the marked changes in the hepatic expression of the glucocorticoid-responsive genes CYP7A1, HMGCS, ApoA-IV, CBG, IL-6, and TNF-a.…”

Section: Discussionmentioning

confidence: 99%

Absence of HDL cholesteryl ester uptake in mice via SR-BI impairs an adequate adrenal glucocorticoid-mediated stress response to fasting

Hoekstra¹,

Meurs²,

Koenders³

et al. 2008

Journal of Lipid Research

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Receptor-mediated cholesterol uptake has been suggested to play a role in maintaining the adrenal intracellular free cholesterol pool and the ability to produce hormones. Therefore, in the current study, we evaluated the importance of scavenger receptor class B type I (SR-BI)-mediated cholesteryl ester uptake from HDL for adrenal glucocorticoid hormone synthesis in vivo. No difference was observed in the plasma level of corticosterone between SR-BI-deficient and wild-type mice under ad libitum feeding conditions. Overnight fasting (?16 h) stimulated the plasma level of corticosterone by 2-fold in wild-type mice. In contrast, no effect of fasting on plasma corticosterone levels was observed in SR-BI-deficient mice, leading to a 44% lower plasma corticosterone level compared with their wild-type littermate controls. In parallel, an almost complete depletion of lipid stores in the adrenal cortex of fasted SR-BIdeficient mice was observed. Plasma adrenocorticotropic hormone levels were increased by 5-fold in fasted SR-BIdeficient mice. SR-BI deficiency induced marked changes in the hepatic expression of the glucocorticoid-responsive genes cholesterol 7a-hydroxylase, HMG-CoA synthase, apolipoprotein A-IV, corticosteroid binding globulin, interleukin-6, and tumor necrosis factor-a, which coincided with a 42% decreased plasma glucose level under fasting conditions. In conclusion, we show that the absence of adrenal HDL cholesteryl ester uptake in SR-BI-deficient mice impairs the adrenal glucocorticoid-mediated stress response to fasting as a result of adrenal glucocorticoid insufficiency and attenuated liver glucocorticoid receptor signaling, leading to hypoglycemia under fasting conditions.-Hoekstra, M., I. Meurs, M. Koenders, R. Out, R. B. Hildebrand, J. K. Kruijt, M. Van Eck, and T. J. C. Van Berkel. Absence of HDL cholesteryl ester uptake in mice via SR-BI impairs an adequate adrenal glucocorticoid-mediated stress response to fasting. J. Lipid Res. 2008. 49: 738-745.

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Peptide growth factors and the adrenal cortex

Cited by 24 publications

References 170 publications

CITED2 is expressed in human adrenocortical cells and regulated by basic fibroblast growth factor

CITED2 is expressed in human adrenocortical cells and regulated by basic fibroblast growth factor

Scavenger receptor class B type I-mediated uptake of serum cholesterol is essential for optimal adrenal glucocorticoid production

Absence of HDL cholesteryl ester uptake in mice via SR-BI impairs an adequate adrenal glucocorticoid-mediated stress response to fasting

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