ArticlePloS one2015
Lysosomal trafficking of TGFBIp via caveolae-mediated endocytosis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 35 citations in OpenAlex.
- A Novel Mouse Model of Granular Corneal Dystrophy Type II Reveals Impaired Autophagy and Recapitulates Human Pathogenesis.Investigative ophthalmology & visual science · 2025Article
- Molecular genetic analysis of R124H TGFBIp in one family Avellino corneal dystrophy.Molecular vision · 2024Article
- Endoplasmic reticulum stress: molecular mechanism and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Review
- Mini-Review: Clinical Features and Management of Granular Corneal Dystrophy Type 2.Korean journal of ophthalmology : KJO · 2023Article
- All-natural-molecule, bioluminescent photodynamic therapy results in complete tumor regression and prevents metastasis.Biomaterials · 2023Article
- Article
- Strategies for Delivering Nanoparticles across Tumor Blood Vessels.Advanced functional materials · 2021Article
- Lysosomal dysfunction of corneal fibroblasts underlies the pathogenesis of Granular Corneal Dystrophy Type 2 and can be rescued by TFEB.Journal of cellular and molecular medicine · 2020Article
- Article
- Caveolae, CD109, and endothelial cells as targets for treating Alzheimer's disease.Alzheimer's & dementia (New York, N. Y.) · 2020Article
- Generation of TGFBI knockout ABCG2+/ABCB5+ double-positive limbal epithelial stem cells by CRISPR/Cas9-mediated genome editing.PloS one · 2019Article
- Fascinating Fasciclins: A Surprisingly Widespread Family of Proteins that Mediate Interactions between the Cell Exterior and the Cell Surface.International journal of molecular sciences · 2018Review
- Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis.Scientific reports · 2017Article
- Role of TGFBIp in Wound Healing and Mucin Expression in Corneal Epithelial Cells.Yonsei medical journal · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-beta-induced protein (TGFBIp) is ubiquitously expressed in the extracellular matrix (ECM) of various tissues and cell lines. Progressive accumulation of mutant TGFBIp is directly involved in the pathogenesis of TGFBI-linked corneal dystrophy. Recent studies reported that mutant TGFBIp accumulates in cells; however, the trafficking of TGFBIp is poorly understood. Therefore, we investigated TGFBIp trafficking to determine the route of its internalization and secretion and to elucidate its roles in the pathogenesis of granular corneal dystrophy type 2 (GCD2). Our data indicate that newly synthesized TGFBIp was secreted via the endoplasmic reticulum/Golgi-dependent secretory pathway, and this secretion was delayed in the corneal fibroblasts of patients with GCD2. We also found that TGFBIp was internalized by caveolae-mediated endocytosis, and the internalized TGFBIp accumulated after treatment with bafilomycin A1, an inhibitor of lysosomal degradation. In addition, the proteasome inhibitor MG132 inhibits the endocytosis of TGFBIp. Co-immunoprecipitation revealed that TGFBIp interacted with integrin αVβ3. Moreover, treatment with arginine-glycine-aspartic acid (RGD) tripeptide suppressed the internalization of TGFBIp. These insights on TGFBIp trafficking could lead to the identification of novel targets and the development of new therapies for TGFBI-linked corneal dystrophy.
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