A pituitary-salivary mixed gland induced by tissue recombination of embryonic pituitary epithelium and embryonic submandibular gland mesenchyme in mice

Kusakabe, Moriaki; Sakakura, Teruyo; Sano, Megumi; Nishizuka, Yasuaki

doi:10.1016/0012-1606(85)90097-1

Cited by 47 publications

(26 citation statements)

References 10 publications

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“…Instead, they form rather broad areas of dermal mesenchyme (Harunaga et al, 2011;Mikkola and Millar, 2006). As shown by heterotypic tissue recombination experiments, dynamic dermalepidermal signaling interactions nevertheless occur during both salivary gland and mammary gland development (Kratochwil, 1969;Kusakabe et al, 1985). We find that sweat glands are also comparably surrounded by sheaths of connective tissue (supplementary material Fig.…”

Section: Various Appendages Display Distinctive Signaling Interactionmentioning

confidence: 56%

Involvement of Wnt, Eda and Shh at defined stages of sweat gland development

et al. 2014

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To maintain body temperature, sweat glands develop from embryonic ectoderm by a poorly defined mechanism. We demonstrate a temporal cascade of regulation during mouse sweat gland formation. Sweat gland induction failed completely when canonical Wnt signaling was blocked in skin epithelium, and was accompanied by sharp downregulation of downstream Wnt, Eda and Shh pathway genes. The Wnt antagonist Dkk4 appeared to inhibit this induction: Dkk4 was sharply downregulated in β-catenin-ablated mice, indicating that it is induced by Wnt/β-catenin; however, its overexpression repressed Wnt target genes and significantly reduced gland numbers. Eda signaling succeeded Wnt. Wnt signaling was still active and nascent sweat gland pre-germs were still seen in Eda-null mice, but the pre-germs failed to develop further and the downstream Shh pathway was not activated. When Wnt and Eda were intact but Shh was ablated, germ induction and subsequent duct formation occurred normally, but the final stage of secretory coil formation failed. Thus, sweat gland development shows a relay of regulatory steps initiated by Wnt/β-catenin -itself modulated by Dkk4 -with subsequent participation of Eda and Shh pathways.

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Section: Various Appendages Display Distinctive Signaling Interactionmentioning

confidence: 56%

Involvement of Wnt, Eda and Shh at defined stages of sweat gland development

et al. 2014

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“…On the contrary, SMG embryonic mesenchyme was shown to induce epithelium from other glandular sources to develop into a branched gland that morphologically resembles natural salivary gland [25]. These findings therefore, demonstrated a specific need of SMG mesenchyme for proper morphogenesis and development of SMG.…”

Section: Discussionmentioning

confidence: 99%

MSCs feeder layers induce SMG self-organization and branching morphogenesis

et al. 2017

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Dysfunction of salivary glands leads to several oral health problems, including dental caries, mastication and swallowing dysfunctions and multiple oral infections. Conventional treatments for such condition fell short of providing satisfying therapeutic results. Recent advances in organ regeneration therapy which utilize tissue stem cells to fabricate bioengineered 3D organ buds, have introduced a promising therapeutic tool for full functional organ regeneration. However, finding a sustainable and easily accessible cell source for such approaches is still challenging, especially in case of severely atrophied tissues such as irradiated salivary glands. In response to this, we hypothesized that bone marrow derived mesenchymal stem cells (MSCs) could be used as feeder cells to induce salivary epithelial tissues/cells branching. Indeed, in 2D cultures, MSCs supported branching of embryonic submandibular salivary gland (SMG) epithelium. Interestingly, this enhancing effect was dependent on the initial number of MSC feeder cells. In addition, MSCs supported the self-assembly of SMG epithelial progenitor cells into well-patterned and branched 3D salivary organoids. Therefore, these findings propose MSCs as a valuable candidate cell source for induced SMG epithelial branching, which can potentially be applied in future methods for SMG regeneration approaches.

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“…For instance, embryonic mammary epithelium forms salivary rather than mammary-like structures if it is recombined with salivary gland mesenchyme and then engrafted underneath the renal capsule of a host mouse, although the epithelium still retains its ability to produce milk proteins in response to prolactin [10]. Moreover, when prospective pituitary epithelium from e8.5 Rathke's pouch is transplanted together with salivary mesenchyme, it forms salivary-like structures that in this instance contain differentiated α-amylase-producing acini [11]. Likewise, epithelium from e13 mouse skin forms milkproducing mammary ducts and alveoli if it is grown in vivo within mammary mesenchyme [12].…”

Section: Introductionmentioning

confidence: 99%

The ADAM17–amphiregulin–EGFR Axis in Mammary Development and Cancer

Sternlicht

Sunnarborg

2008

J Mammary Gland Biol Neoplasia

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In order to fulfill its function of producing and delivering sufficient milk to newborn mammalian offspring, the mammary gland first has to form an extensive ductal network. As in all phases of mammary development, hormonal cues elicit local intra-and inter-cellular signaling cascades that regulate ductal growth and differentiation. Among other things, ductal development requires the epidermal growth factor receptor (EGFR), its ligand amphiregulin (AREG), and the transmembrane metalloproteinase AD-AM17, which can cleave and release AREG from the cell surface so that it may interact with its receptor. Tissue recombination and transplantation studies demonstrate that EGFR phosphorylation and ductal development proceed only when ADAM17 and AREG are expressed on mammary epithelial cells and EGFR is present on stromal cells, and that local administration of soluble AREG can rescue the development of ADAM17-deficient transplants. Thus proper mammary morphogenesis requires the ADAM17-mediated release of AREG from ductal epithelial cells, the subsequent activation of EGFR on stromal cells, and EGFR-dependent stromal responses that in return elicit a new set of epithelial responses, all culminating in the formation of a fully functional ductal tree. This, however, raises new issues concerning what may act upstream, downstream or in parallel with the ADAM17-AREG-EGFR axis, how it may become hijacked or corrupted during the onset and evolution of cancer, and how such ill effects may be confronted.

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A pituitary-salivary mixed gland induced by tissue recombination of embryonic pituitary epithelium and embryonic submandibular gland mesenchyme in mice

Cited by 47 publications

References 10 publications

Involvement of Wnt, Eda and Shh at defined stages of sweat gland development

Involvement of Wnt, Eda and Shh at defined stages of sweat gland development

MSCs feeder layers induce SMG self-organization and branching morphogenesis

The ADAM17–amphiregulin–EGFR Axis in Mammary Development and Cancer

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