Tissue Remodelling in the Adrenal Gland

Wolkersdörfer, Gernot W.; Bornstein, Stefan R.

doi:10.1016/s0006-2952(98)00067-7

Cited by 56 publications

(32 citation statements)

References 68 publications

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“…Patterns of expression of the DKK3 gene suggest that it could be a morphogen in the adrenal cortex. Previous studies of differences in gene expression among the zones have yielded information on receptors, signal transduction mechanisms, and steroid biosynthetic enzymes, but have so far not yielded clues as to the underlying mechanisms of zonal differentiation (Wolkersdorfer & Bornstein 1998, Mitani et al 1999, Rainey 1999, Whitworth & Vinson 2000, Alesci & Bornstein 2001. In the present experiments we found that the DKK3 gene was expressed in the ZG at a higher level than in the ZF and ZR.…”

Section: Discussioncontrasting

confidence: 46%

“…At various times in the past they have been thought of as entirely separate cell types, sustained by proliferation within each zone, but currently it is generally thought that the three zones of the cortex represent forms of differentiation of a single cell type (Wolkersdorfer & Bornstein 1998, Mitani et al 1999, Rainey 1999, Whitworth & Vinson 2000, Alesci & Bornstein 2001. However, questions of the nature of stem cells within the adrenal cortex, if they exist, have not yet been resolved (Hornsby 2001).…”

Section: Introductionmentioning

confidence: 99%

“…However, questions of the nature of stem cells within the adrenal cortex, if they exist, have not yet been resolved (Hornsby 2001). The concept that cells of one of the three zonal cell types may re-differentiate into another zonal cell type has been derived from observations on the growth of the adrenal cortex and experiments involving adrenocortical regeneration and cell transplantation (Okamoto et al 1998, Wolkersdorfer & Bornstein 1998, Mitani et al 1999, Teebken & Scheumann 2000, Hornsby 2001). …”

Section: Introductionmentioning

confidence: 99%

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Zonal expression of dickkopf-3 and components of the Wnt signalling pathways in the human adrenal cortex

Suwa¹,

Chen²,

Hawks³

et al. 2003

Journal of Endocrinology

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The mechanisms underlying the differentation of the adrenal cortex into zones are unclear. Microarray studies on RNA from microdissected zona reticularis (ZR) and zona fasciculata/zona glomerulosa (ZF/ZG) derived from adult human adrenal glands showed that a gene of the dickkopf family (DKK), DKK3, is differentially expressed in the zones. The Dickkopf proteins are morphogens involved in Wnt signalling. Northern blotting showed higher DKK3 transcript levels in ZF/ZG than ZR samples. In situ hybridization on adult human adrenal gland sections showed that DKK3 expression was much higher in the ZG than in the ZF or ZR. DKK3 expression was also higher in the medulla. We screened for expression of other members of the DKK family and the related Wingless-type mouse mammary tumor virus integration site gene family (WNT), frizzled (FZD), and dishevelled (DVL) gene families. Among dickkopf family members, only DKK3 was expressed at a detectable level in both human and mouse adrenocortical RNA samples. Consistent with previously published data on the effects of Wnt4 gene disruption in the mouse, we found only WNT4 expression within the WNT family in both human and mouse RNA. Northern blotting showed that WNT4 was expressed at a higher level in ZF/ZG cells than in ZR. The higher level of DKK3 and WNT4 expression in ZF/ZG cells was confirmed by real-time PCR. In the frizzled and dishevelled families we found FZD1, FZD2 and DVL3 transcripts in human adrenocortical RNA, and FZD2 and DVL3 in mouse adrenocortical RNA. These data show that a variety of genes of the Wnt signalling pathways are expressed in the adrenal cortex. The zonal distribution of DKK3 expression suggests that it could be involved in zonal differentiation or growth.

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Section: Discussioncontrasting

confidence: 46%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Zonal expression of dickkopf-3 and components of the Wnt signalling pathways in the human adrenal cortex

Suwa¹,

Chen²,

Hawks³

et al. 2003

Journal of Endocrinology

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“…Apoptosis is also known to occur in the adrenal cortex during the adult period. It has been assumed that adrenocortical cells proliferate in the outermost layers of the cortex and then migrate towards the inner cortex and die through an apoptotic mechanism in the ZR (reviewed in Wolkersdörfer & Bornstein 1998). The mechanisms controlling apoptosis in the adrenal cortex are complicated, but it is possible that activins play a role in this process as their signaling system is expressed in the same area as the most active apoptosis (Sasano et al 1995).…”

Section: Figurementioning

confidence: 99%

Expression of activin/inhibin signaling components in the human adrenal gland and the effects of activins and inhibins on adrenocortical steroidogenesis and apoptosis

Vänttinen

Liu²,

Kuulasmaa³

et al. 2003

Journal of Endocrinology

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Activins and inhibins are structurally related glycoprotein hormones modulating pituitary FSH secretion and gonadal steroidogenesis. Activins and inhibins are also produced in the adrenal cortex where their physiological role is poorly known. Hormonally active human adrenocortical tumors express and secrete inhibins, while in mice adrenal inhibins may function as tumor suppressors. To clarify the significance of adrenal activins and inhibins we investigated the localization of activin/inhibin signaling components in the adrenal gland, and the effects of activins and inhibins on adrenocortical steroidogenesis and apoptosis.Activin receptor type II/IIB and IB, activin signal transduction proteins Smad2/3, and inhibin receptor betaglycan were expressed throughout the adrenal cortex, whereas Smad4 expression was seen mainly in the zona reticularis and the innermost zona fasciculata as evaluated by immunohistochemistry. Treatment of cultured adrenocortical carcinoma NCI-H295R cells with activin A inhibited steroidogenic acute regulatory protein and 17 -hydroxylase/17,20-lyase mRNA accumulation as evaluated by the Northern blot technique, and decreased cortisol, androstenedione, dehydroepiandrosterone and dehydroepiandrosterone sulfate secretion as determined by specific enzyme immunoassays. Activin A increased apoptosis as measured by a terminal deoxynucleotidyl transferase in situ apoptosis detection method. Inhibins had no effect on steroidogenesis or apoptosis.In summary, activin/inhibin signaling components are coexpressed in the zona reticularis and the innermost zona fasciculata indicating full signaling potential for adrenal activins and inhibins in these layers. Activin inhibits steroidogenic enzyme gene expression and steroid secretion, and increases apoptosis in human adrenocortical cells. Thus, the activin-inhibin system may have a significant role in the regulation of glucocorticoid and androgen production and apoptotic cell death in the human adrenal cortex.

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“…It undergoes dynamic structural changes under physiological and pathological conditions (Wolkersdorfer and Bornstein 1998;Bornstein et al 1994). Those dynamic changes are covered by cell proliferation as well as cell death.…”

Section: Discussionmentioning

confidence: 99%

Morphology of Adrenal Gland and Lymph Organs is Impaired in Neurodeficient Lurcher Mutant Mice

Beranova¹,

Mandakova²,

Šíma³

et al. 2002

Acta Vet. Brno

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Beranová M., P. Manìáková, P. ·íma, J. Slípka, F. VoÏeh, J. Koãová, M. âervinková, J. S˘kora: Morphology of Adrenal Gland and Lymph Organs is Impaired in Neurodeficient Lurcher Mutant Mice. Acta Vet. Brno 2002, 71: 23-28. There is a tight structural relation and functional co-operation between the nervous, endocrine and immune systems. A dense network of soluble neuro-endocrine and immune mediators exists to ensure close interactions. These hormones, cytokines and neurotransmitters all interact through positive and negative feed-forward and feedback loops. The mediators, once considered specific to the central nervous system (CNS), the endocrine system (ES) or the immune system (IS), do in fact act in all three systems, forming that way the united neuro-endocrine-immune system. The complex neuro-endocrine-immune networks operate under both physiological and pathological conditions.In the presented study microscopical analyses of selected immune organs (the thymus, spleen, inguinal and subscapular lymph nodes) and of the adrenal gland of the neurodeficient Lurcher mutant mice and control C3H mice were performed. In the neurodeficient mice the morphology of the immune organs was impaired. The changes followed in the spleen, especially the increased number of megakaryocytes, lead to the hypothesis of enhanced extramedullar hemopoiesis in the neurodeficient Lurcher mutant mice. Histopathological analysis of the adrenal gland showed the relative hypertrophy of the adrenal medulla. Regarding the adrenal cortex, the three cortical zones, zona glomerularis, fasciculata and reticularis, are difficult to be distinguished. It has been supposed that structural changes of adrenal medulla could document the increased secretion of catecholamines in the neurodeficient animals.Our observations confirm the idea of the tight cooperation of neuro-endocrine-immune structures and contribute to its better understanding, specifically in the conditions of postnatally progressing neurodeficiency. Lurcher mutant mice, homeostatic relatioships, neuro-endocrine-immune system, adrenal gland, megakaryocytesThe intrinsic condition for the individual survival is a balance of the internal enviromenthomeostasis. There are many proofs of the existence of a unified neuro-endocrine-immune regulatory system that is responsible for maintaining the homeostasis (Michael and Chapman 1990;Weigent and Blalock 1995;Besedovsky et al. 1983). The regulatory relations within that system are mutual and complex (Jankovic 1989;Csaba 1994; ·íma and Vûtviãka 1990;Provinciali and Fabris 1991;Pertseva 1991; Slípka 1961).To contribute to the explanation of these relations we used in our previous study "an experiment of the nature", gross-brain malformation -anencephaly -which eliminates the central nervous system and consequently the neuro-endocrine part of the homeostatic system (Slípka et al. 1997; B e ranová 1994). The spontaneously aborted human foetuses without any external malformation and human anencephalic foetuses were compared with

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Tissue Remodelling in the Adrenal Gland

Cited by 56 publications

References 68 publications

Zonal expression of dickkopf-3 and components of the Wnt signalling pathways in the human adrenal cortex

Zonal expression of dickkopf-3 and components of the Wnt signalling pathways in the human adrenal cortex

Expression of activin/inhibin signaling components in the human adrenal gland and the effects of activins and inhibins on adrenocortical steroidogenesis and apoptosis

Morphology of Adrenal Gland and Lymph Organs is Impaired in Neurodeficient Lurcher Mutant Mice

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