Plectin controls biliary tree architecture and stability in cholestasis

Jiroušková, Markéta; Nepomucká, Kateřina; Oyman-Eyrilmez, Gizem; Kalendová, Alžběta; Havelková, Helena; Sarnová, Lenka; Chalupský, Karel; Schuster, Bjoern; Benada, Oldřich; Mikšátková, Petra; Kuchař, Martin; Fabián, Ondřej; Sedláček, Radislav; Wiche, Gerhard; Gregor, Martin

doi:10.1016/j.jhep.2017.12.011

Cited by 28 publications

(45 citation statements)

References 37 publications

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“…(4) The role of PLEC in the liver was first demonstrated in Plec Δalb mice. (3) Our data shared some similarities to the finding of Plec Δalb mice challenged with cholestatic stress, including scattered K8 signals in the cytoplasm of hepatocytes, distorted bile ducts, and dilated bile canaliculi. The impaired BSEP canalicular expression and elevated bile acid levels suggested that the PLEC mutations may affect BSEP targeting and cause cholestasis.…”

Section: Discussionsupporting

confidence: 85%

“…Mutations in different PLEC isoform transcripts cause various phenotypes in a tissue trophic manner . The role of PLEC in the liver was first demonstrated in Plec Δalb mice …”

Section: Discussionmentioning

confidence: 99%

“…Shang-Hsin Wu, 1 Jacob Shujui Hsu, [2][3][4] Hui-Ling Chen, 5 Mu-Ming Chien, 6 Jia-Feng Wu, 6 Yen-Hsuan Ni, 5,6 Bang-Yu Liou, 6 Ming-Chih Ho, 7 Yung-Ming Jeng, 8 Mei-Hwei Chang, 1,5,6 Pei-Lung Chen, 2,9,10 and Huey-Ling Chen 5,6,11 N eonates and infants are susceptible to cholestatic liver diseases. At least six genes are causative for progressive familial intrahepatic cholestasis (PFIC), and more genetic defects are known to cause infant cholestasis.…”

Section: Plectin Mutations In Progressive Familial Intrahepatic Cholementioning

confidence: 99%

“…(2) The cytoskeleton linker plectin (PLEC) was recently found to protect the liver from cholestatic injuries in a liver-specific PLEC knockout (Plec Δalb ) mouse model. (3) However, the PLEC mutation has not been reported in human PFIC patients. In this study, we report a pair of siblings who had severe cholestasis with compound heterozygous PLEC mutations.…”

Section: Plectin Mutations In Progressive Familial Intrahepatic Cholementioning

confidence: 99%

“…Approximately one‐third of patients with PFIC do not have mutations in these genes . The cytoskeleton linker plectin (PLEC) was recently found to protect the liver from cholestatic injuries in a liver‐specific PLEC knockout ( Plec Δalb ) mouse model . However, the PLEC mutation has not been reported in human PFIC patients.…”

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confidence: 99%

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Plectin Mutations in Progressive Familial Intrahepatic Cholestasis

Hsu

Chen

et al. 2019

Hepatology

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Section: Discussionsupporting

confidence: 85%

“…Mutations in different PLEC isoform transcripts cause various phenotypes in a tissue trophic manner . The role of PLEC in the liver was first demonstrated in Plec Δalb mice …”

Section: Discussionmentioning

confidence: 99%

Section: Plectin Mutations In Progressive Familial Intrahepatic Cholementioning

confidence: 99%

Section: Plectin Mutations In Progressive Familial Intrahepatic Cholementioning

confidence: 99%

mentioning

confidence: 99%

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Plectin Mutations in Progressive Familial Intrahepatic Cholestasis

Hsu

Chen

et al. 2019

Hepatology

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Differentially expressed proteins obtained by label‐free quantitative proteomic analysis reveal affected biological processes and functions in Western diet‐induced steatohepatitis

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Ferron

Francisqueti-Ferron

et al. 2021

J Biochem & Molecular Tox

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Nonalcoholic steatohepatitis (NASH) is a pathological manifestation with a progressive incidence in response to the epidemic of hepatic steatosis caused primarily by excessive energy intake. The present study unravels affected biological processes and functions by the presence of NASH in rats using a label-free quantitative proteomic strategy. NASH was induced by a Western high-sugar and high-fat diet for 20 weeks. The liver tissue was collected for histology and for a mass spectrometrybased proteomic protocol. The NASH group showed severe lipidosis, hepatocyte ballooning, and the presence of collagen deposition. Among upregulated proteins in NASH perilipin-2 (Plin-2; F6QBA3; difference [diff]: 2.29), ferritin heavy (Fth1; Q66HI5; diff: 2.19) and light (Ftl1; P02793; diff: 1.75) chains, macrophage migration inhibitory factor 1 (Mif; P30904; diff: 1.69), and fibronectin (Fn1; F1LST1; diff: 0.35) were observed, whereas among downregulated proteins, plectin (Q6S399; diff: −3.34), some Cyp2 family proteins of the cytochrome P450 complex, glutathione S-transferases, flavin-containing monooxygenase 1 (Fmo1; P36365; diff: −2.08), acetyl-CoA acetyltransferase 2 (Acat2; Q5XI22; diff: −2.25), acyl-CoA oxidase 2 (Acox2; F1LNW3; diff: −1.59), and acyl-CoA oxidase 3 (Acox3; F1M9A7; diff: −2.41) were observed. Also, biological processes and functions such as LPS/IL-1 inhibition of RXR, fatty acid metabolism, Nrf2-mediated oxidative stress response, xenobiotic metabolism, and PXR/RXR and CAR/RXR activations were predicted to be affected.In conclusion, the liver of rats with NASH induced by Western diet shows a decreased capacity of metabolizing lipids, fatty acids, and xenobiotic compounds that predispose fibrosis development.

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Cytoskeleton | Intermediate Filament Linker Proteins: Plectin and BPAG1

Wiche

Castañón

2021

Encyclopedia of Biological Chemistry III

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Plectin controls biliary tree architecture and stability in cholestasis

Cited by 28 publications

References 37 publications

Plectin Mutations in Progressive Familial Intrahepatic Cholestasis

Plectin Mutations in Progressive Familial Intrahepatic Cholestasis

Differentially expressed proteins obtained by label‐free quantitative proteomic analysis reveal affected biological processes and functions in Western diet‐induced steatohepatitis

Cytoskeleton | Intermediate Filament Linker Proteins: Plectin and BPAG1

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