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Study · Animal study (in vivo) · mouse · 2025

3 results

Loss of tricellular tight junction tricellulin leads to hyposalivation in Sjögren's syndrome.

Mao X, Li H, Min S, Su J, Wei P, Zhang Y, He Q, Wu L, Yu G, Cong X

International journal of oral science19 Mar 2025Cited by 7 (Europe PMC)

PMID40108118 (opens in a new tab)PMCIDPMC11923234 (opens in a new tab)DOI10.1038/s41368-025-00349-9 (opens in a new tab)PepBankPUB-40108118
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Summary

Tricellulin, a key tricellular tight junction (TJ) protein, is essential for maintaining the barrier integrity of acinar epithelia against macromolecular passage in salivary glands. This study aims to explore the role and regulatory mechanism of tricellulin in the development of salivary gland hypofunction in Sjögren's syndrome (SS). Employing a multifaceted approach involving patient biopsies, non-obese diabetic (NOD) mice as a SS model, salivary gland acinar cell-specific tricellulin conditional knockout (TricCKO) mice, and IFN-γ-stimulated salivary gland epithelial cells, we investigated the role of tricellulin in SS-related hyposalivation. Our data revealed diminished levels of tricellulin in salivary glands of SS patients. Similarly, NOD mice displayed a reduction in tricellulin expression from the onset of the disease, concomitant with hyposecretion and an increase in salivary albumin content. Consistent with these findings, TricCKO mice exhibited both hyposecretion and leakage of macromolecular tracers when compared to control animals. Mechanistically, the JAK/STAT1/miR-145 axis was identified as mediating the IFN-γ-induced downregulation of tricellulin. Treatment with AT1001, a TJ sealer, ameliorated epithelial barrier dysfunction, restored tricellulin expression, and consequently alleviated hyposalivation in NOD mice. Importantly, treatment with miR-145 antagomir to specifically recover the expression of tricellulin in NOD mice significantly alleviated hyposalivation and macromolecular leakage. Collectively, we identified that tricellulin deficiency in salivary glands contributed to hyposalivation in SS. Our findings highlight tricellulin as a potential therapeutic target for hyposecretion, particularly in the context of reinforcing epithelial barrier function through preventing leakage of macromolecules in salivary glands.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

3 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In NOD mice, AT1001 ameliorated epithelial barrier dysfunction.

    In plain wordsIn mice, AT1001 reduced epithelial barrier dysfunction.

    Peptide
    Larazotide
    Outcome
    DecreaseEpithelial barrier dysfunction
    Study

    mousen: not reported in source

    NOD mice with Sjögren's syndrome
    Outcome group
    Organ injury · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment with AT1001, a TJ sealer, ameliorated epithelial barrier dysfunction, restored tricellulin expression, and consequently alleviated hyposalivation in NOD mice.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In NOD mice, AT1001 restored tricellulin expression.

    In plain wordsIn mice, AT1001 restored tricellulin expression.

    Peptide
    Larazotide
    Outcome
    IncreaseTricellulin expression
    Study

    mousen: not reported in source

    NOD mice with Sjögren's syndrome
    Outcome group
    Receptor activity and mechanism · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment with AT1001, a TJ sealer, ameliorated epithelial barrier dysfunction, restored tricellulin expression, and consequently alleviated hyposalivation in NOD mice.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In NOD mice, AT1001 alleviated hyposalivation.

    In plain wordsIn mice, AT1001 alleviated abnormally low saliva production.

    Peptide
    Larazotide
    Outcome
    DecreaseHyposalivation
    Study

    mousen: not reported in source

    NOD mice with Sjögren's syndrome
    Outcome group
    Gastrointestinal function · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment with AT1001, a TJ sealer, ameliorated epithelial barrier dysfunction, restored tricellulin expression, and consequently alleviated hyposalivation in NOD mice.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    22 Oct 2026, 02:26 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 18:59 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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