Expression of Ror2 Associated with Fibrosis of the Submandibular Gland

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  • Takahashi Daiki
    Division of Cell Physiology, Department of Physiology and Cell Biology, Kobe University, Graduate School of Medicine Department of Oral and Maxillofacial Surgery, Kobe University, Graduate School of Medicine
  • Suzuki Hiroaki
    Department of Oral and Maxillofacial Surgery, Kobe University, Graduate School of Medicine
  • Kakei Yasumasa
    Department of Oral and Maxillofacial Surgery, Kobe University, Graduate School of Medicine
  • Yamakoshi Kimi
    Department of Mechanism of Aging, Research Institute, National Center for Geriatrics and Gerontology
  • Minami Yasuhiro
    Division of Cell Physiology, Department of Physiology and Cell Biology, Kobe University, Graduate School of Medicine
  • Komori Takahide
    Department of Oral and Maxillofacial Surgery, Kobe University, Graduate School of Medicine
  • Nishita Michiru
    Division of Cell Physiology, Department of Physiology and Cell Biology, Kobe University, Graduate School of Medicine

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Abstract

<p>The submandibular gland (SMG) is one of the major salivary glands that play important roles for variety of physiological functions, such as digestion of foods, prevention of infection, and lubrication of the mouth. Dysfunction of the SMG, often associated with a salivary inflammation, adversely influences a person’s quality of life. However, the mechanism underlying inflammation-driven dysfunction of the SMG is largely unknown. Here, we used a mouse model in which the main excretory duct of the SMG is ligated unilaterally to induce inflammation of the gland and examined the expression of Wnt5a, Ror1 and Ror2 genes, encoding Wnt5a ligand and its cognate receptors, which have been implicated in tissue damage or inflammatory responses in variety of tissues. We show that expression levels of Ror1, Ror2, and Wnt5a are increased in the ligated SMG undergoing interstitial fibrosis, which is accompanied by robust expression of fibrosis-associated genes, such as TGF-β1, TNF-α, IL-1β, and MMP-2. Increased immunostaining signal of Ror2 was detected in the fibrotic tissues with abundant accumulation of fibroblasts and collagen fibers in the ligated SMG, suggesting that Ror2-mediated signaling might be activated in response to tissue damage and associated with progression of fibrosis in the SMG.</p><p>Key words: submandibular gland, Ror2, Wnt5a, fibrosis, inflammation</p>

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