Repositori institucional URV
| URV's Author/s: | Girona Tell, Josefa / GUAITA ESTERUELAS, SANDRA / HERAS IBAÑEZ, MERCEDES / Masana Marín, Luis |
| Author, as appears in the article.: | Martinez-Micaelo, N; Rodriguez-Calvo, R; Guaita-Esteruelas, S; Heras, M; Girona, J; Masana, L |
| Author's mail: | josefa.girona@urv.cat josefa.girona@urv.cat luis.masana@urv.cat |
| Author identifier: | 0000-0002-6267-8779 0000-0002-6267-8779 0000-0002-0789-4954 |
| Journal publication year: | 2019 |
| Publication Type: | Journal Publications |
| ISSN: | 13881981 |
| APA: | Martinez-Micaelo, N; Rodriguez-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 |
| Paper original source: | Biochimica Et Biophysica Acta-Molecular And Cell Biology Of Lipids. 1864 (3): 234-244 |
| 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. |
| Article's DOI: | 10.1016/j.bbalip.2018.11.011 |
| Link to the original source: | https://www.sciencedirect.com/science/article/abs/pii/S1388198118303676?via%3Dihub |
| Paper version: | info:eu-repo/semantics/acceptedVersion |
| licence for use: | https://creativecommons.org/licenses/by/3.0/es/ |
| Department: | Medicina i Cirurgia Ciències Mèdiques Bàsiques |
| Licence document URL: | https://repositori.urv.cat/ca/proteccio-de-dades/ |
| Thematic Areas: | Química Molecular biology Medicina ii Medicina i Linguística e literatura Interdisciplinar Farmacia Engenharias iii Engenharias ii Ciências biológicas iii Ciências biológicas ii Ciências biológicas i Cell biology Biotecnología Biophysics Biodiversidade Biochemistry & molecular biology |
| Keywords: | Inflammation Fabp4 Endothelial dysfunction Ck1 fabp4 endothelial dysfunction ck1 |
| Entity: | Universitat Rovira i Virgili |
| Record's date: | 2025-02-24 |
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