Articles producció científica> Medicina i Cirurgia

Extracellular FABP4 uptake by endothelial cells is dependent on cytokeratin 1 expression

  • Identification data

    Identifier: imarina:5132699
    Authors:
    Martínez-Micaelo N, Rodríguez-Calvo R, Guaita-Esteruelas S, Heras M, Girona J, Masana L
    Abstract:
    Aims The aim of this study is to determine the physical and functional interplay between fatty acid-binding protein 4 (FABP4) and its membrane receptor-like candidate protein, cytokeratin 1 (CK1), and to determine the effect of hindering CK1-mediated FABP4 cellular uptake on non-disturbed or metabolically stressed endothelial cells. Methods We monitored the direct interaction between FABP4 and CK1 using surface plasmon resonance, and the effects of blocking exogenous FABP4 (eFABP4) cellular uptake were determined by using specific siRNA to knock down the expression of CK1 in human umbilical vein endothelial cells (HUVECs). The expression and nuclear translocation of transcription factors involved in oxidative stress (NRF2) and inflammation (p65 subunit of NF-ĸB transcription factor) were determined by Western blotting analysis. Results Our data showed that FABP4 and CK1 bind to each other and that the putative FABP4 binding domain would be within the 151GIQEVTINQSLLQPLNVEID170 CK1 sequence. We determined that in non-disturbed or metabolically stressed endothelial cells, eFABP4 regulates the cellular response to oxidative stress. In addition, we also found that in the presence of palmitate, eFABP4 increases the pro-inflammatory effects induced by palmitate per se, probably due to an increase in the transport of palmitate inside cells, suggesting that these FABP4-mediated pro-oxidative and pro-inflammatory effects are dependent on CK1 expression. Conclusions We demonstrated that CK1 facilitates eFABP4 cellular uptake in endothelial cells. Therefore, the CK1-targeted inhibition of exogenous FABP4 cellular uptake might be a potential therapeutic strategy to protect endothelial cells against FABP4-induced activation of inflammation and oxidative stress.
  • Others:

    Author, as appears in the article.: Martínez-Micaelo N, Rodríguez-Calvo R, Guaita-Esteruelas S, Heras M, Girona J, Masana L
    Department: Medicina i Cirurgia Ciències Mèdiques Bàsiques
    URV's Author/s: Girona Tell, Josefa / GUAITA ESTERUELAS, SANDRA / HERAS IBAÑEZ, MERCEDES / Masana Marín, Luis
    Keywords: ck1 endothelial dysfunction fabp4 Ck1 Endothelial dysfunction Fabp4 Inflammation
    Abstract: Aims The aim of this study is to determine the physical and functional interplay between fatty acid-binding protein 4 (FABP4) and its membrane receptor-like candidate protein, cytokeratin 1 (CK1), and to determine the effect of hindering CK1-mediated FABP4 cellular uptake on non-disturbed or metabolically stressed endothelial cells. Methods We monitored the direct interaction between FABP4 and CK1 using surface plasmon resonance, and the effects of blocking exogenous FABP4 (eFABP4) cellular uptake were determined by using specific siRNA to knock down the expression of CK1 in human umbilical vein endothelial cells (HUVECs). The expression and nuclear translocation of transcription factors involved in oxidative stress (NRF2) and inflammation (p65 subunit of NF-ĸB transcription factor) were determined by Western blotting analysis. Results Our data showed that FABP4 and CK1 bind to each other and that the putative FABP4 binding domain would be within the 151GIQEVTINQSLLQPLNVEID170 CK1 sequence. We determined that in non-disturbed or metabolically stressed endothelial cells, eFABP4 regulates the cellular response to oxidative stress. In addition, we also found that in the presence of palmitate, eFABP4 increases the pro-inflammatory effects induced by palmitate per se, probably due to an increase in the transport of palmitate inside cells, suggesting that these FABP4-mediated pro-oxidative and pro-inflammatory effects are dependent on CK1 expression. Conclusions We demonstrated that CK1 facilitates eFABP4 cellular uptake in endothelial cells. Therefore, the CK1-targeted inhibition of exogenous FABP4 cellular uptake might be a potential therapeutic strategy to protect endothelial cells against FABP4-induced activation of inflammation and oxidative stress.
    Thematic Areas: Biochemistry & molecular biology Biodiversidade Biophysics Biotecnología Cell biology Ciências biológicas i Ciências biológicas ii Ciências biológicas iii Engenharias ii Engenharias iii Farmacia Interdisciplinar Linguística e literatura Medicina i Medicina ii Molecular biology Química
    licence for use: https://creativecommons.org/licenses/by/3.0/es/
    Author's mail: josefa.girona@urv.cat luis.masana@urv.cat josefa.girona@urv.cat
    ISSN: 13881981
    Author identifier: 0000-0002-6267-8779 0000-0002-0789-4954 0000-0002-6267-8779
    Record's date: 2023-02-26
    Papper version: info:eu-repo/semantics/acceptedVersion
    Link to the original source: https://www.sciencedirect.com/science/article/abs/pii/S1388198118303676?via%3Dihub
    Papper original source: Biochimica Et Biophysica Acta-Molecular And Cell Biology Of Lipids. 1864 (3): 234-244
    APA: Martínez-Micaelo N, Rodríguez-Calvo R, Guaita-Esteruelas S, Heras M, Girona J, Masana L (2019). Extracellular FABP4 uptake by endothelial cells is dependent on cytokeratin 1 expression. Biochimica Et Biophysica Acta-Molecular And Cell Biology Of Lipids, 1864(3), 234-244. DOI: 10.1016/j.bbalip.2018.11.011
    Licence document URL: https://repositori.urv.cat/ca/proteccio-de-dades/
    Article's DOI: 10.1016/j.bbalip.2018.11.011
    Entity: Universitat Rovira i Virgili
    Journal publication year: 2019
    Publication Type: Journal Publications
  • Keywords:

    Biochemistry & Molecular Biology,Biophysics,Cell Biology,Molecular Biology
    ck1
    endothelial dysfunction
    fabp4
    Ck1
    Endothelial dysfunction
    Fabp4
    Inflammation
    Biochemistry & molecular biology
    Biodiversidade
    Biophysics
    Biotecnología
    Cell biology
    Ciências biológicas i
    Ciências biológicas ii
    Ciências biológicas iii
    Engenharias ii
    Engenharias iii
    Farmacia
    Interdisciplinar
    Linguística e literatura
    Medicina i
    Medicina ii
    Molecular biology
    Química
    13881981
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