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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Published in | Disease models & mechanisms Vol. 13; no. 9 |
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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
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
Thus, our established human salivary-gland-derived organoids would be useful for
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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AbstractList | 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. 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. Summary: Human salivary-gland-derived organoids can be used for in vitro analyses of the morphological and functional changes associated with salivary gland diseases and dysfunctions. 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 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 Thus, our established human salivary-gland-derived organoids would be useful for 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 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. |
Author | Yoshimoto, Shohei Anzai, Hiromasa Hiraki, Akimitsu Hashimoto, Shuichi Morishita, Koichiro Yoshizumi, Junko Okamura, Kazuhiko |
AuthorAffiliation | 4 Department of Morphological Biology, Division of Biomedical Sciences , Fukuoka Dental College , Fukuoka 814-0193 , Japan 1 Section of Pathology, Department of Morphological Biology, Division of Biomedical Sciences , Fukuoka Dental College , Fukuoka 814-0193 , Japan 3 Department of Oral and Maxillofacial Surgery, Division of Oral and Medical Management , Fukuoka Dental College , Fukuoka 814-0193 , Japan 2 Oral Medicine Research Center, Fukuoka Dental College , Fukuoka 814-0193 , Japan |
AuthorAffiliation_xml | – name: 1 Section of Pathology, Department of Morphological Biology, Division of Biomedical Sciences , Fukuoka Dental College , Fukuoka 814-0193 , Japan – name: 2 Oral Medicine Research Center, Fukuoka Dental College , Fukuoka 814-0193 , Japan – name: 4 Department of Morphological Biology, Division of Biomedical Sciences , Fukuoka Dental College , Fukuoka 814-0193 , Japan – name: 3 Department of Oral and Maxillofacial Surgery, Division of Oral and Medical Management , Fukuoka Dental College , Fukuoka 814-0193 , Japan |
Author_xml | – sequence: 1 givenname: Shohei surname: Yoshimoto fullname: Yoshimoto, Shohei organization: Oral Medicine Research Center, Fukuoka Dental College, Fukuoka 814-0193, Japan – sequence: 2 givenname: Junko surname: Yoshizumi fullname: Yoshizumi, Junko organization: Department of Oral and Maxillofacial Surgery, Division of Oral and Medical Management, Fukuoka Dental College, Fukuoka 814-0193, Japan – sequence: 3 givenname: Hiromasa surname: Anzai fullname: Anzai, Hiromasa organization: Department of Oral and Maxillofacial Surgery, Division of Oral and Medical Management, Fukuoka Dental College, Fukuoka 814-0193, Japan – sequence: 4 givenname: Koichiro surname: Morishita fullname: Morishita, Koichiro organization: Department of Morphological Biology, Division of Biomedical Sciences, Fukuoka Dental College, Fukuoka 814-0193, Japan – sequence: 5 givenname: Kazuhiko surname: Okamura fullname: Okamura, Kazuhiko organization: Section of Pathology, Department of Morphological Biology, Division of Biomedical Sciences, Fukuoka Dental College, Fukuoka 814-0193, Japan – sequence: 6 givenname: Akimitsu surname: Hiraki fullname: Hiraki, Akimitsu organization: Department of Oral and Maxillofacial Surgery, Division of Oral and Medical Management, Fukuoka Dental College, Fukuoka 814-0193, Japan – sequence: 7 givenname: Shuichi orcidid: 0000-0002-0637-0630 surname: Hashimoto fullname: Hashimoto, Shuichi email: hashimoto@college.fdcnet.ac.jp organization: Section of Pathology, Department of Morphological Biology, Division of Biomedical Sciences, Fukuoka Dental College, Fukuoka 814-0193, Japan hashimoto@college.fdcnet.ac.jp |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32801121$$D View this record in MEDLINE/PubMed |
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Keywords | Sialadenitis Organoid Human salivary glands TNF-α |
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SubjectTerms | Anaplastic Lymphoma Kinase - antagonists & inhibitors Anaplastic Lymphoma Kinase - metabolism Aquaporin 5 - metabolism Autoimmune diseases Bone Morphogenetic Proteins - metabolism Exocrine glands human salivary glands Humans Inflammation Kinases Morphology organoid Organoids - metabolism Organoids - ultrastructure Salivary Glands - metabolism Salivary Glands - ultrastructure sialadenitis Signal Transduction Stem cells tnf-α Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF |
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Title | Inhibition of Alk signaling promotes the induction of human salivary-gland-derived organoids |
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