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Mitotic endosomes regulate spindle organization and function via Occludin and FIP5 binding

ABSTRACT: The genetic basis of vertebrate emergence is a major unanswered question in metazoan evolution. Understanding vertebrate-specific genes, such as Occludin (Ocln), may help answer this question. Here, we show that mammary glands lacking Ocln exhibit retarded branching, resulting from reduced cell proliferation. Interestingly, Ocln regulates spindle orientation and function, and its loss leads to a range of phenotypes, including prolonged prophase and failed nuclear and/or cytoplasmic division.

ORGANISM(S): Mus musculus

PROVIDER: GSE242842 | GEO | 2025/09/11

REPOSITORIES: GEO

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	GSE242842_processed_data_KO_vs_Control.csv.gz	Csv

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Project description:Background: Occludin is a key tight junction protein that contributes to epithelial barrier integrity and inflammatory regulation. Although its structural roles are well characterized, the physiological relevance of its C-terminal domain in airway inflammation remains poorly defined. Methods: Occludin expression in human lung disease tissues was examined by immunohistochemistry. Functional relevance was assessed using BEAS-2B cells overexpressing full-length occludin or C-terminal deletion mutants. A synthetic peptide derived from the occludin C-terminal core sequence was designed and evaluated for its anti-inflammatory and barrier-protective effects. In vitro assays included IL-8 secretion, transepithelial electrical resistance, cytoskeletal remodeling, mitochondrial function, ROS production, and transcriptomic profiling. Therapeutic efficacy was validated in a murine model of Pseudomonas aeruginosa LPS–induced airway inflammation, followed by cytokine analysis, histopathology, and immune profiling. Results: Occludin expression was markedly reduced in inflamed human lung tissues. In BEAS-2B cells, occludin overexpression suppressed LPS-induced IL-8 release, restored barrier integrity, and reduced F-actin remodeling, whereas C-terminal deletion abolished these effects. The C-terminal occludin peptide significantly decreased IL-8 production, improved barrier function, and suppressed cytoskeletal changes, while a mutant peptide was ineffective. Transcriptomic analyses identified occludin as a central suppressor of inflammatory signaling. Mechanistically, the peptide inhibited p38 activation, preserved mitochondrial structure, and reduced ROS production. In vivo, peptide pretreatment improved survival, lowered IL-6, IL-8, and TNF-α levels, and reduced goblet cell hyperplasia and inflammatory infiltration. Immune profiling further revealed restored T-cell populations, reduced myeloid expansion, and enhanced M2 macrophage polarization. Conclusion: The occludin C-terminal–derived peptide exerts robust anti-inflammatory and barrier-protective effects, representing a promising therapeutic candidate for LPS-induced and potentially broader inflammatory lung diseases.

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Mitotic endosomes regulate spindle organization and function via Occludin and FIP5 binding

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