Changes in E‐ and N‐cadherin expression in developing rat adenohypophysis

Our view of anterior pituitary organization has been altered with the recognition that folliculo-stellate (FS) and somatotroph cell populations form large-scale three-dimensional homotypic networks. This morphological cellular organization may optimize communication within the pituitary gland promoting coordinated pulsatile secretion adapted to physiological needs. The aim of this study was to identify the molecules involved in the formation and potential functional organization and/or signaling within these cell-cell networks. Here, we have focused on one class of cell adhesion molecules, the cadherins, since b-catenin has been detected in the GH cell network. We have characterized, by qPCR and immunohistochemistry, their cellular expression and distribution. We have also examined whether their expression could be modulated during pituitary tissue remodeling. The mouse anterior pituitary has a restricted and cell-type specific repertoire of cadherin expression: cadherin-11 is exclusively expressed in TSH cells; N-cadherin displays a ubiquitous expression pattern but with different levels of expression between endocrine cell types; E-cadherin is restricted to homotypic contacts between FS cells; while cadherin-18 is expressed both in somatotrophs and FS cells. Thus, each cell type presents a defined combinatorial expression of different subsets of cadherins. This cell-type specific cadherin expression profile emerges early during development and undergoes major changes during postnatal development. These results suggest the existence within the anterior pituitary of cell-cell contact signaling based on a defined pattern of cadherin expression, which may play a crucial role in cellular recognition during the formation and fate of pituitary cell homotypic networks.

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“…6C-L; Kikuchi et al 2007). However, the pattern of E-CAD distribution differs between endocrine cell types (Fig.…”

Section: Cadherin Expression Within the Pituitary Gland During Develomentioning

confidence: 99%

Characterization of adherens junction protein expression and localization in pituitary cell networks

Chauvet

El-Yandouzi²,

Mathieu³

et al. 2009

Journal of Endocrinology

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“…We recently found that primordial cells in the developing rat adenohypophysis co-expressed E-and N-cadherins, but endocrine cells lost E-cadherin to possess only N-cadherin at certain embryonic stages (Kikuchi et al 2006(Kikuchi et al , 2007. This phenomenon may be considered as a kind of cadherin switching (Nakagawa and Takeichi 1995;George-Weinstein et al 1997;Wheelock et al 2008).…”

Section: Introductionmentioning

confidence: 94%

Spatio-temporal relation between cadherin switching and cytogenesis of hormone-producing cells in the developing rat adenohypophysis

et al. 2009

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Cadherins are a family of transmembrane glycoproteins that mediate cell-to-cell adhesion in solid tissues and have been reported to regulate not only morphogenesis but also cell motility, proliferation, and function by activating intracellular signaling pathways. We recently found that primordial cells in the developing rat adenohypophysis co-expressed E- and N-cadherins, but endocrine cells lost E-cadherin to possess only N-cadherin at certain embryonic stages. In the present study, we aimed to elucidate the temporal relationships between cadherin expression and cell proliferation as well as between cadherin expression and the onset of hormone production in embryonic adenohypophyses. Adenohypophyses and their primordia from embryonic and postnatal rats were fixed in Bouin's fluid and paraffin sections were routinely prepared. Multiple fluorescence immunohistochemistry was performed for combinations of E-cadherin, N-cadherin, proliferating cell nuclear antigen (a marker of proliferating cells), cyclin D1, and pituitary hormones. In primordia from embryonic days 13 through 16, proliferative activities were seen in cells that co-expressed E- and N-cadherin. Cells arrested proliferation coincidentally when they lost E-cadherin after embryonic day 16. Possession of E-cadherin was closely related with expression of cyclin D1 at this stage. Moreover, hormone production was observed from embryonic day 16 only in cells that lost E-cadherin. In the developing adenohypophysis, proliferation and differentiation of hormone-producing cells have been reported to be regulated by a variety of external humoral factors. Our results raise the possibility that changes in cadherins are closely involved in these processes.

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“…During this period, the pituitary stem cell population resides in a state of activation as compared to later in life, showing higher cell numbers, higher proliferation rate and higher stem cell functionality (i.e., sphere-forming and multipotent differentiation capacity; Chen et al 2005Chen et al , 2009Gremeaux et al 2012). Moreover, stemness and embryonic markers are prominently expressed in neonatal stem cells (Chen et al 2009;Gremeaux et al 2012;Kikuchi et al 2007). The topography of the SOX2 þ cells further underlines this higher activation status, with increased numbers of clusters in the neonatal AP lobe and higher abundance of SOX2 þ cells at the junctions of the AP and IL (wedges), with signs of SOX2 þ cells sprouting from these putative germinal regions ; Fig.…”

Section: Neonatal Pituitary Maturationmentioning

confidence: 99%

Pituitary Stem Cells: Quest for Hidden Functions

Vankelecom

2016

Stem Cells in Neuroendocrinology

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The pituitary is the core endocrine gland, ruling fundamental processes of body growth, metabolism, reproduction and stress. Over the past decade, it has progressively become clear that the pituitary, like many adult tissues, harbors a population of stem cells. While the molecular depiction of these cells is constantly expanding, their function remains essentially hidden. From recent studies, the picture is developing that the stem cells of the adult pituitary are highly quiescent and mainly come into play during pathological conditions.Upon transgenic cell-ablation damage in the pituitary, the stem cell compartment is promptly turned on with expansion and expression of the missing hormone. This activation is accompanied by substantial regeneration of the lost hormonal cells, a restorative competence that was unexpected in the mature gland. This regenerative skill, however, rapidly disappears with aging, together with a decline in the number and fitness of the stem cells. One function of the adult pituitary stem cells may thus be hidden in the regenerative toolbox of the gland, at least during a specified and limited time window.Recent work also showed activation of the pituitary stem cell compartment during tumor formation in the (mouse) gland. Moreover, pituitary tumors (from patients and mice) contain a candidate 'tumor stem cell' (TSC) population. The pathogenetic steps of initiation, expansion, invasion and recurrence of pituitary tumors remain far from understood. A link between the tumor-driving TSC and the pituitary stem cells may shed new light on this tumorigenic darkness.To conclude, decoding the hidden functions of pituitary stem cells will not only lead to better fundamental insights into their role but may also expose (novel) targets for treating pituitary tumors and for regenerative intervention in pituitary deficiency, as caused by damage, tumors or aging. Yet, the journey in the 'hidden valley' of pituitary stem cell functions has only just begun, and a long distance still has to be walked.

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Changes in E‐ and N‐cadherin expression in developing rat adenohypophysis

Cited by 26 publications

References 14 publications

Characterization of adherens junction protein expression and localization in pituitary cell networks

Characterization of adherens junction protein expression and localization in pituitary cell networks

Spatio-temporal relation between cadherin switching and cytogenesis of hormone-producing cells in the developing rat adenohypophysis

Pituitary Stem Cells: Quest for Hidden Functions

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