TY - JOUR
T1 - Id4 modulates salivary gland homeostasis and its expression is downregulated in IgG4-related disease via miR-486-5p
AU - Hayashi, Yoshikazu
AU - Kimura, Soi
AU - Yano, Ena
AU - Yoshimoto, Shohei
AU - Saeki, Ayaka
AU - Yasukochi, Atsushi
AU - Hatakeyama, Yuji
AU - Moriyama, Masafumi
AU - Nakamura, Seiji
AU - Jimi, Eijiro
AU - Kawakubo-Yasukochi, Tomoyo
N1 - Funding Information:
The authors thank Hikari Takeshima, Mayu Seida, and Nao Kuboyama for helpful technical assistance; Dr. Mizuki Sakamoto for the data sorting of human samples; Dr. Atsushi Doi, Dr. Hiroko Hagiwara, and Dr. Kaori Yasuda (Cell Innovator, Fukuoka, Japan) for assistance with the miRNA and mRNA array analyses and useful discussions. We appreciate the technical assistance of the Research Support Center, Research Center for Human Disease Modeling, Kyushu University Graduate School of Medical Sciences. We thank J. Ludovic Croxford, PhD, from Edanz (https://jp.edanz.com/ac) for editing a draft of this manuscript. This study was supported by the Japan Society for the Promotion of Science (KAKENHI grants JP20K17381 to Y.H. JP20K23114 and JP22K17003 to E.Y. JP19K10052 and JP22K09914 to T.K.-Y. JP19K10269 and JP22K10173 to A.Y. and JP20H00553 to S.N.), Takeda Science Foundation (S.Y. and T.K.-Y.), Kaibara Morikazu Medical Science Promotion Foundation (S.Y.), Fukuoka Public Health Promotion Organization Cancer Research Fund (S.Y.), Kakihara Science Technology Foundation (T.K.-Y.), Kenko Kagaku Zaidan (T.K.-Y.), Astellas Foundation for Research on Metabolic Disorders (T.K.-Y.), and Mishima Kaiun Memorial Foundation (T.K.-Y.).
Funding Information:
This study was supported by the Japan Society for the Promotion of Science (KAKENHI grants JP20K17381 to Y.H., JP20K23114 and JP22K17003 to E.Y., JP19K10052 and JP22K09914 to T.K.-Y., JP19K10269 and JP22K10173 to A.Y., and JP20H00553 to S.N.), Takeda Science Foundation (S.Y. and T.K.-Y.), Kaibara Morikazu Medical Science Promotion Foundation (S.Y.), Fukuoka Public Health Promotion Organization Cancer Research Fund (S.Y.), Kakihara Science Technology Foundation (T.K.-Y.), Kenko Kagaku Zaidan (T.K.-Y.), Astellas Foundation for Research on Metabolic Disorders (T.K.-Y.), and Mishima Kaiun Memorial Foundation (T.K.-Y.).
Publisher Copyright:
© 2022 The Authors
PY - 2023/2
Y1 - 2023/2
N2 - Salivary glands are physiologically orchestrated by the coordinated balance between cell differentiation, proliferation, apoptosis, and interactions between epithelial, mesenchymal endothelial, and neuronal cells, and they are frequent sites of manifestations of Sjögren's syndrome (SS) or IgG4-related disease (IgG4-RD). However, little is known about salivary gland homeostasis and its involvement in those diseases. Inhibitor of DNA binding/differentiation 4 (Id4) is an Id protein involved in the transcriptional control of many biological events, including differentiation. Studies of Id4-deficient mice revealed that Id4-deficient submandibular glands were smaller and exhibited accelerated differentiation, compared with those from wild-type littermates. In addition, dry mouth symptoms and Th17 expansion in splenocytes were also observed in the absence of Id4. Furthermore, Id4 levels in the salivary glands of patients with IgG4-RD, but not SS, were significantly decreased compared with those of healthy controls. miRNA-mRNA integrated analysis demonstrated that miR-486-5p was upregulated in IgG4-RD patients and that it might regulate Id4 in the lesion sites. Together, these results provide evidence for the inhibitory role of Id4 in salivary differentiation, and a critical association between Id4 downregulation and IgG4-RD.
AB - Salivary glands are physiologically orchestrated by the coordinated balance between cell differentiation, proliferation, apoptosis, and interactions between epithelial, mesenchymal endothelial, and neuronal cells, and they are frequent sites of manifestations of Sjögren's syndrome (SS) or IgG4-related disease (IgG4-RD). However, little is known about salivary gland homeostasis and its involvement in those diseases. Inhibitor of DNA binding/differentiation 4 (Id4) is an Id protein involved in the transcriptional control of many biological events, including differentiation. Studies of Id4-deficient mice revealed that Id4-deficient submandibular glands were smaller and exhibited accelerated differentiation, compared with those from wild-type littermates. In addition, dry mouth symptoms and Th17 expansion in splenocytes were also observed in the absence of Id4. Furthermore, Id4 levels in the salivary glands of patients with IgG4-RD, but not SS, were significantly decreased compared with those of healthy controls. miRNA-mRNA integrated analysis demonstrated that miR-486-5p was upregulated in IgG4-RD patients and that it might regulate Id4 in the lesion sites. Together, these results provide evidence for the inhibitory role of Id4 in salivary differentiation, and a critical association between Id4 downregulation and IgG4-RD.
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U2 - 10.1016/j.bbamcr.2022.119404
DO - 10.1016/j.bbamcr.2022.119404
M3 - Article
C2 - 36535369
AN - SCOPUS:85145242275
SN - 0167-4889
VL - 1870
JO - Biochimica et Biophysica Acta - Molecular Cell Research
JF - Biochimica et Biophysica Acta - Molecular Cell Research
IS - 2
M1 - 119404
ER -