ArticleJournal of hepatology2015
Epiplakin attenuates experimental mouse liver injury by chaperoning keratin reorganization.
Article in Journal of hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 24 citations in OpenAlex.
- Transcriptome sequencing reveals the expression profiles of lncRNAs and mRNAs in goat skin tissues with different types of wool coats.Scientific reports · 2025Article
- Epiplakin expression is lost in psoriatic skin lesions and is downregulated by IFN-γ inFrontiers in cell and developmental biology · 2025Article
- Paxillin regulates liver fibrosis via actin polymerization and ERK activation in hepatic stellate cells.Journal of cell science · 2023Article
- A CaCells · 2022Article
- Comparative genomics reveals evolutionary loss of epiplakin in cetaceans.Scientific reports · 2022Article
- Review
- The attributes of plakins in cancer and disease: perspectives on ovarian cancer progression, chemoresistance and recurrence.Cell communication and signaling : CCS · 2021Review
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsEpiplakin is a member of the plakin protein family and exclusively expressed in epithelial tissues where it binds to keratins. Epiplakin-deficient (Eppk1(-/-)) mice displayed no obvious spontaneous phenotype, but their keratinocytes showed a faster keratin network breakdown in response to stress. The role of epiplakin in the stressed liver remained to be elucidated.
methodsWild-type (WT) and Eppk1(-/-) mice were subjected to common bile duct ligation (CBDL) or fed with a 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-containing diet. The importance of epiplakin during keratin reorganization was assessed in primary hepatocytes.
resultsOur experiments revealed that epiplakin is expressed in hepatocytes and cholangiocytes, and binds to keratin 8 (K8) and K18 via multiple domains. In several liver stress models epiplakin and K8 genes displayed identical expression patterns and transgenic K8 overexpression resulted in elevated hepatic epiplakin levels. After CBDL and DDC treatment, Eppk1(-/-) mice developed a more pronounced liver injury and their livers contained larger amounts of hepatocellular keratin granules, indicating impaired disease-induced keratin network reorganization. In line with these findings, primary Eppk1(-/-) hepatocytes showed increased formation of keratin aggregates after treatment with the phosphatase inhibitor okadaic acid, a phenotype which was rescued by the chemical chaperone trimethylamine N-oxide (TMAO). Finally, transfection experiments revealed that Eppk1(-/-) primary hepatocytes were less able to tolerate forced K8 overexpression and that TMAO treatment rescued this phenotype.
conclusionOur data indicate that epiplakin plays a protective role during experimental liver injuries by chaperoning disease-induced keratin reorganization.
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Registered trials
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