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TGF-β–mediated epithelial–mesenchymal transition of keratinocytes promotes fibrosis in secondary lymphedema
Hyeung Ju Park, … , Babak J. Mehrara, Raghu P. Kataru
Hyeung Ju Park, … , Babak J. Mehrara, Raghu P. Kataru
Published July 29, 2025
Citation Information: JCI Insight. 2025. https://doi.org/10.1172/jci.insight.192890.
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Research In-Press Preview Cell biology Dermatology Inflammation

TGF-β–mediated epithelial–mesenchymal transition of keratinocytes promotes fibrosis in secondary lymphedema

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Abstract

Secondary lymphedema is characterized by fibrosis and impaired lymphatic function. Although TGF-β is a key regulator of fibrosis in this disease, the cellular mechanisms regulating this process remain unknown. Epithelial–mesenchymal transition (EMT), a mechanism by which TGF-β induces fibrosis in other skin diseases, is characterized by loss of epithelial cell markers and cellular polarity, upregulation of fibrotic gene expression, and gain of migratory capacity. Using clinical lymphedema biopsy specimens and animal models, we show that keratinocytes in the basal layer of the epidermis undergo EMT in lymphedematous skin, migrate into the dermis, and contribute to dermal fibrosis. In vitro studies using cultured primary human keratinocytes treated with lymphatic fluid from the affected limbs of patients with secondary lymphedema resulted in a TGF-β–mediated increased expression of EMT markers. We show for the first time that EMT is activated by TGF-β in secondary lymphedema and that this process plays an important role in regulating skin fibrosis in this disease.

Authors

Hyeung Ju Park, Jinyeon Shin, Ananta Sarker, Mark G. Klang, Elyn Riedel, Michelle Coriddi, Joseph H. Dayan, Sarit Pal, Babak J. Mehrara, Raghu P. Kataru

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