Inhibition of Alk signaling promotes the induction of human salivary-gland-derived organoids

Hyposalivation and xerostomia are the cause of several morbidities, such as dental caries, painful mucositis, oral fungal infections, sialadenitis and dysphagia. For these reasons, preservation of normal saliva secretion is critical for the maintenance of functionally normal oral homeostasis and for...
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Gespeichert in:

Autor*in:	Shohei Yoshimoto [verfasserIn] Junko Yoshizumi [verfasserIn] Hiromasa Anzai [verfasserIn] Koichiro Morishita [verfasserIn] Kazuhiko Okamura [verfasserIn] Akimitsu Hiraki [verfasserIn] Shuichi Hashimoto [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	human salivary glands organoid sialadenitis tnf-α

Übergeordnetes Werk:	In: Disease Models & Mechanisms - The Company of Biologists, 2011, 13(2020), 9
Übergeordnetes Werk:	volume:13 ; year:2020 ; number:9

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1242/dmm.045054

Katalog-ID:	DOAJ077872290

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authorswithroles_txt_mv	Shohei Yoshimoto @@aut@@ Junko Yoshizumi @@aut@@ Hiromasa Anzai @@aut@@ Koichiro Morishita @@aut@@ Kazuhiko Okamura @@aut@@ Akimitsu Hiraki @@aut@@ Shuichi Hashimoto @@aut@@
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callnumber-first	R - Medicine
author	Shohei Yoshimoto
spellingShingle	Shohei Yoshimoto misc RB1-214 misc human salivary glands misc organoid misc sialadenitis misc tnf-α misc Medicine misc R misc Pathology Inhibition of Alk signaling promotes the induction of human salivary-gland-derived organoids
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topic_title	RB1-214 Inhibition of Alk signaling promotes the induction of human salivary-gland-derived organoids human salivary glands organoid sialadenitis tnf-α
topic	misc RB1-214 misc human salivary glands misc organoid misc sialadenitis misc tnf-α misc Medicine misc R misc Pathology
topic_unstemmed	misc RB1-214 misc human salivary glands misc organoid misc sialadenitis misc tnf-α misc Medicine misc R misc Pathology
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title	Inhibition of Alk signaling promotes the induction of human salivary-gland-derived organoids
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title_sort	inhibition of alk signaling promotes the induction of human salivary-gland-derived organoids
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title_auth	Inhibition of Alk signaling promotes the induction of human salivary-gland-derived organoids
abstract	Hyposalivation and xerostomia are the cause of several morbidities, such as dental caries, painful mucositis, oral fungal infections, sialadenitis and dysphagia. For these reasons, preservation of normal saliva secretion is critical for the maintenance of functionally normal oral homeostasis and for keeping good health. Several strategies for restoring salivary gland function have been reported, from different points of view, based on the use of salivary-gland-derived epithelial stem/progenitor cells and tissue engineering approaches to induce organoids that mimic in vivo salivary glands. In this study, we clarified that inhibition of activin receptor-like kinase (Alk) signaling was essential for the induction of human salivary-gland-derived organoids, and demonstrated the usefulness of such organoids as an inflammatory disease model. In inflammatory conditions like sialadenitis, in general, pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α, also known as TNF) are upregulated, but their function is still unclear. In our established human salivary-gland-derived organoid culture system, we successfully induced organoid swelling by stimulation with carbachol, a non-selective cholinergic agonist, and forskolin, an activator of cystic fibrosis transmembrane conductance regulator (CFTR). Furthermore, we found that this organoid swelling was inhibited by TNF-α. From these results, we could clarify the inhibitory function of TNF-α on saliva secretion in vitro. Thus, our established human salivary-gland-derived organoids would be useful for in vitro analyses of the morphological and functional changes involved in salivary gland dysfunctions in several research fields, such as pathobiology, inflammation and regenerative medicine. This article has an associated First Person interview with the first author of the paper.
abstractGer	Hyposalivation and xerostomia are the cause of several morbidities, such as dental caries, painful mucositis, oral fungal infections, sialadenitis and dysphagia. For these reasons, preservation of normal saliva secretion is critical for the maintenance of functionally normal oral homeostasis and for keeping good health. Several strategies for restoring salivary gland function have been reported, from different points of view, based on the use of salivary-gland-derived epithelial stem/progenitor cells and tissue engineering approaches to induce organoids that mimic in vivo salivary glands. In this study, we clarified that inhibition of activin receptor-like kinase (Alk) signaling was essential for the induction of human salivary-gland-derived organoids, and demonstrated the usefulness of such organoids as an inflammatory disease model. In inflammatory conditions like sialadenitis, in general, pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α, also known as TNF) are upregulated, but their function is still unclear. In our established human salivary-gland-derived organoid culture system, we successfully induced organoid swelling by stimulation with carbachol, a non-selective cholinergic agonist, and forskolin, an activator of cystic fibrosis transmembrane conductance regulator (CFTR). Furthermore, we found that this organoid swelling was inhibited by TNF-α. From these results, we could clarify the inhibitory function of TNF-α on saliva secretion in vitro. Thus, our established human salivary-gland-derived organoids would be useful for in vitro analyses of the morphological and functional changes involved in salivary gland dysfunctions in several research fields, such as pathobiology, inflammation and regenerative medicine. This article has an associated First Person interview with the first author of the paper.
abstract_unstemmed	Hyposalivation and xerostomia are the cause of several morbidities, such as dental caries, painful mucositis, oral fungal infections, sialadenitis and dysphagia. For these reasons, preservation of normal saliva secretion is critical for the maintenance of functionally normal oral homeostasis and for keeping good health. Several strategies for restoring salivary gland function have been reported, from different points of view, based on the use of salivary-gland-derived epithelial stem/progenitor cells and tissue engineering approaches to induce organoids that mimic in vivo salivary glands. In this study, we clarified that inhibition of activin receptor-like kinase (Alk) signaling was essential for the induction of human salivary-gland-derived organoids, and demonstrated the usefulness of such organoids as an inflammatory disease model. In inflammatory conditions like sialadenitis, in general, pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α, also known as TNF) are upregulated, but their function is still unclear. In our established human salivary-gland-derived organoid culture system, we successfully induced organoid swelling by stimulation with carbachol, a non-selective cholinergic agonist, and forskolin, an activator of cystic fibrosis transmembrane conductance regulator (CFTR). Furthermore, we found that this organoid swelling was inhibited by TNF-α. From these results, we could clarify the inhibitory function of TNF-α on saliva secretion in vitro. Thus, our established human salivary-gland-derived organoids would be useful for in vitro analyses of the morphological and functional changes involved in salivary gland dysfunctions in several research fields, such as pathobiology, inflammation and regenerative medicine. This article has an associated First Person interview with the first author of the paper.
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title_short	Inhibition of Alk signaling promotes the induction of human salivary-gland-derived organoids
url	https://doi.org/10.1242/dmm.045054 https://doaj.org/article/c0b01b3b4eaa4e3fa90b985e9efb0117 http://dmm.biologists.org/content/13/9/dmm045054 https://doaj.org/toc/1754-8403 https://doaj.org/toc/1754-8411
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In our established human salivary-gland-derived organoid culture system, we successfully induced organoid swelling by stimulation with carbachol, a non-selective cholinergic agonist, and forskolin, an activator of cystic fibrosis transmembrane conductance regulator (CFTR). Furthermore, we found that this organoid swelling was inhibited by TNF-α. From these results, we could clarify the inhibitory function of TNF-α on saliva secretion in vitro. Thus, our established human salivary-gland-derived organoids would be useful for in vitro analyses of the morphological and functional changes involved in salivary gland dysfunctions in several research fields, such as pathobiology, inflammation and regenerative medicine. 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Inhibition of Alk signaling promotes the induction of human salivary-gland-derived organoids

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