Folliculo-stellate cells and intercellular communication within the rat anterior pituitary gland

Soji, Tśuyoshi; Mabuchi, Yoshio; Kurono, Chieko; Herbert, Damon C.

doi:10.1002/(sici)1097-0029(19971015)39:2<138::aid-jemt5>3.0.co;2-h

Cited by 54 publications

(55 citation statements)

References 26 publications

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“…However, the mechanisms by which pituitary cells develop functional homotypic connections are far from clear. Different contact and signaling mechanisms in the pituitary include gap junctions, adherens junctions, integrin, and cadherin complexes (Soji et al 1997, Guerineau et al 1998, Ezzat & Asa 2005, Paez-Pereda et al 2005. In addition to gap junctions, physical contacts between FS cells are mediated by adherens junctions (Soji et al 1997), and we have shown that adherens junctions between GH cells actually resist physical dissociation, revealing the strong homotypic robustness of the GH cell network (Bonnefont et al 2005).…”

Section: Introductionmentioning

confidence: 73%

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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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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Section: Introductionmentioning

confidence: 73%

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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“…A similar role of cadherins may enable folliculo-stellate cells to separate from hormone-producing cells and aggregate homologously to construct pseudofollicles. In addition, zonula adherens is known to be specific to folliculo-stellate cells in the pituitary gland (Soji et al, 1997). Zonula adherens is a specialized form of cadherin-mediated cell-to-cell adhesion, but cadherins can also mediate adhesion without the formation of morphologically apparent adhesive junctions (Yap et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Distinctive localization of N‐ and E‐cadherins in rat anterior pituitary gland

et al. 2006

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In the rat anterior pituitary gland, folliculo-stellate cells aggregate preferably to form pseudofollicles, and each type of hormone-producing cell shows adhesive affinity with particular types of heterologous hormone-producing cells. Distribution of cadherin types in the rat anterior pituitary was examined immunohistochemically to clarify the unique cell arrangements caused by homologous and heterologous affinities among cells. N-and E-cadherins were detected continuously along cell membranes, while P-cadherin was not. N-and E-cadherins showed distinct isolation in localization, with N-cadherins localized in hormone-producing cells of distal and intermediate lobes in various amounts, and E-cadherins limited to folliculo-stellate cells and marginal layer cells facing the residual lumen of Rathke's pouch. A similar distribution of cadherins was observed in cell clusters of primary cultured anterior pituitary cells. These findings suggest that differential expression of cell adhesion molecules may be partially responsible for localization of hormone-producing cells and folliculo-stellate cells.

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“…It has also been shown that FS cells communicate with other FS cells and with endocrine cells, including prolactin-secreting lactotropes [87]. The gapjunctional number in the anterior pituitary varied during the estrous cycle; it was highest in proestrous and in estrous and increased during middle to late pregnancy in rats [85]. This suggests that gonadal factors such as estradiol may regulate the rate of occurrence of gap junction in the anterior pituitary gland.…”

Section: Gap-junctional Communicationmentioning

confidence: 98%

“…In the rat pituitary, formation of gap junctions between FS cells has been demonstrated using electron microscopic methods [85,86]. It has also been shown that FS cells communicate with other FS cells and with endocrine cells, including prolactin-secreting lactotropes [87].…”

Section: Gap-junctional Communicationmentioning

confidence: 99%

Genesis of Prolactinomas: Studies Using Estrogen-Treated Animals

Sarkar

2006

Frontiers of Hormone Research

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Prolactin-secreting adenomas (prolactinomas) are the most prevalent form of pituitary tumors in humans. Our knowledge of the formation of these tumors is limited. Experimental work in animal has uncovered that estradiol exposure leads to prolactinoma formation via orchestrated events involving dopamine D2 receptors, transforming growth factor-β (TGF-β) isoforms and their receptors, as well as factors secondary to TGF-β action. Additionally, these studies determined that TGF-β and b-FGF interact to facilitate the communication between lactotropes and folliculo-stellate cells that is necessary for the mitogenic action of estradiol. The downstream signaling that governs lactotropic cell proliferation involves activation of the MAP kinase p44/42-dependent pathway.Pituitary tumors are primarily adenomas; they account for approximately 10-15% of intracranial tumors. They cause significant morbidity due to local invasion, hypopituitarism or hormone hypersecretion [1,2]. Pituitary tumors are classified as either functioning and secreting excessive amounts of active hormones, or as endocrinologically inactive and secreting no hormones or inactive hormones. Pituitary tumors are also classified by virtue of their size into the arbitrary division of those less than 1 cm as microadenomas and those more than 1 cm as macroadenomas. Pituitary tumors secreting excess prolactin are characterized as prolactinomas. Prolactinomas are the most frequently occurring neoplasm in the human pituitary [3,4]. In the general population, 1:2,800 men and 1:1,050 women are considered to have prolactinomas [5]. In human subjects, prolactinomas occur as both macroadenomas and microadenomas. In addition, mixed growth hormone and prolactin-secreting adenomas are documented to exist in a substantial number of acromegaly patients.Hyperprolactinoma is a condition in which plasma prolactin (PRL) levels are elevated above normal levels. Hyperprolactinemia, with elevation of serum prolactin of more than 200 ng/ml, is characteristically associated with prolactinomas [6]. Hyperprolactinemia causes reproductive dysfunction such as amenorrhea, galactorrhea, and infertility in women [7]. Amenorrhea and galactorrhea may occur alone or together [8]. Up to 25% of patients with secondary amenorrhea have been diagnosed with hyperprolactinemia. Many of these patients showed micro-prolactin adenomas or macro-prolactin adenomas in the pituitary. Although treatments that alter central dopaminergic neuronal functions cause an elevated serum PRL level, in most cases hyperprolactinemia is due to a pituitary tumor. In women, prolactinomas are mainly microadenomas. These microadenomas are rarely associated with hypopituitarism or central nervous system dysfunction. Idiopathic hyperprolactinemia, without demonstrable pituitary or hypothalamic disease, has also been identified. In men, prolactinomas are mainly

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Folliculo-stellate cells and intercellular communication within the rat anterior pituitary gland

Cited by 54 publications

References 26 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

Distinctive localization of N‐ and E‐cadherins in rat anterior pituitary gland

Genesis of Prolactinomas: Studies Using Estrogen-Treated Animals

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