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Your search keyword '"Fernandez‐Rojo, Manuel A."' showing total 4 results
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4 results on '"Fernandez‐Rojo, Manuel A."'

1. Caveolin-1 Is Necessary for Hepatic Oxidative Lipid Metabolism: Evidence for Crosstalk between Caveolin-1 and Bile Acid Signaling

Author

Fernandez-Rojo, Manuel A, Gongora, Milena, Fitzsimmons, Rebecca L, Martel, Nick, Martin, Sheree D, Nixon, Susan J, Brooks, Andrew J, Ikonomopoulou, Maria P, Martin, Sally, Lo, Harriet P, Myers, Stephen A, Restall, Christina, Ferguson, Charles, Pilch, Paul F, McGee, Sean L, Anderson, Robin L, Waters, Michael J, Hancock, John F, Grimmond, Sean M, Muscat, George EO, Parton, Robert G, Fernandez-Rojo, Manuel A, Gongora, Milena, Fitzsimmons, Rebecca L, Martel, Nick, Martin, Sheree D, Nixon, Susan J, Brooks, Andrew J, Ikonomopoulou, Maria P, Martin, Sally, Lo, Harriet P, Myers, Stephen A, Restall, Christina, Ferguson, Charles, Pilch, Paul F, McGee, Sean L, Anderson, Robin L, Waters, Michael J, Hancock, John F, Grimmond, Sean M, Muscat, George EO, and Parton, Robert G

Abstract

Caveolae and caveolin-1 (CAV1) have been linked to several cellular functions. However, a model explaining their roles in mammalian tissues in vivo is lacking. Unbiased expression profiling in several tissues and cell types identified lipid metabolism as the main target affected by CAV1 deficiency. CAV1−/− mice exhibited impaired hepatic peroxisome proliferator-activated receptor α (PPARα)-dependent oxidative fatty acid metabolism and ketogenesis. Similar results were recapitulated in CAV1-deficient AML12 hepatocytes, suggesting at least a partial cell-autonomous role of hepatocyte CAV1 in metabolic adaptation to fasting. Finally, our experiments suggest that the hepatic phenotypes observed in CAV1−/− mice involve impaired PPARα ligand signaling and attenuated bile acid and FXRα signaling. These results demonstrate the significance of CAV1 in (1) hepatic lipid homeostasis and (2) nuclear hormone receptor (PPARα, FXRα, and SHP) and bile acid signaling.

Published
2013

2. Enhancing European capabilities for application of multi-omics studies in biology and biomedicine space research.

Author

Manzano A, Weging S, Bezdan D, Borg J, Cahill T, Carnero-Diaz E, Cope H, Deane CS, Etheridge T, Giacomello S, Hardiman G, Leys N, Madrigal P, Mastroleo F, Medina FJ, Mieczkowski J, Fernandez-Rojo MA, Siew K, Szewczyk NJ, Walsh SB, da Silveira WA, and Herranz R

Abstract

Following on from the NASA twins' study, there has been a tremendous interest in the use of omics techniques in spaceflight. Individual space agencies, NASA's GeneLab, JAXA's ibSLS, and the ESA-funded Space Omics Topical Team and the International Standards for Space Omics Processing (ISSOP) groups have established several initiatives to support this growth. Here, we present recommendations from the Space Omics Topical Team to promote standard application of space omics in Europe. We focus on four main themes: i) continued participation in and coordination with international omics endeavors, ii) strengthening of the European space omics infrastructure including workforce and facilities, iii) capitalizing on the emerging opportunities in the commercial space sector, and iv) capitalizing on the emerging opportunities in human subjects research., Competing Interests: F.M. is CEO/Co-Founder at Genegoggle, D.B. is a cofounder of Poppy Health, Inc. and CSO of Yuri Gravity GmbH and declares affiliations at the NGS Competence Center Tübingen (NCCT), University of Tübingen, Tübingen and Yuri Gravity, Meckenbeuren, Germany. M.F.R. declares additional affiliation at Diamantina Institute, The University of Queensland, St Lucia, Queensland 4072, Australia. S.G. is a scientific consultant of 10x Genomics., (© 2023 The Authors.)

Published
2023
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3. Filling the Gap on Caveolin-1 in Liver Carcinogenesis.

Author

Fernandez-Rojo MA and Ramm GA

Subjects
Animals, Carcinogenesis, Hepatocytes metabolism, Humans, Liver Neoplasms drug therapy, Liver Neoplasms metabolism, Caveolin 1 metabolism, Liver Neoplasms pathology
Abstract

Caveolin-1 (CAV1) has emerged as a promoter of proliferation, metastasis, and chemoresistance in hepatoma cells, as well as a marker of poor prognosis in liver cancer. We discuss here current knowledge and future approaches to elucidating the molecular mechanisms underlying CAV1 action during hepatocarcinogenesis and evaluate its potential use in clinical therapies., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Published
2016
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4. Hepatic oxidative stress promotes insulin-STAT-5 signaling and obesity by inactivating protein tyrosine phosphatase N2.

Author

Gurzov EN, Tran M, Fernandez-Rojo MA, Merry TL, Zhang X, Xu Y, Fukushima A, Waters MJ, Watt MJ, Andrikopoulos S, Neel BG, and Tiganis T

Subjects
Animals, Cells, Cultured, Diet, High-Fat, Female, Glutathione Peroxidase deficiency, Glutathione Peroxidase genetics, Glutathione Peroxidase metabolism, Growth Hormone metabolism, Hepatocytes cytology, Hepatocytes metabolism, Insulin pharmacology, Insulin-Like Growth Factor I metabolism, Liver enzymology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Obesity metabolism, Obesity pathology, Protein Tyrosine Phosphatase, Non-Receptor Type 2 deficiency, Protein Tyrosine Phosphatase, Non-Receptor Type 2 genetics, Reactive Oxygen Species metabolism, STAT1 Transcription Factor metabolism, STAT3 Transcription Factor metabolism, STAT5 Transcription Factor genetics, Signal Transduction drug effects, Glutathione Peroxidase GPX1, Insulin metabolism, Liver metabolism, Oxidative Stress, Protein Tyrosine Phosphatase, Non-Receptor Type 2 metabolism, STAT5 Transcription Factor metabolism
Abstract

Hepatic insulin resistance is a key contributor to the pathogenesis of obesity and type 2 diabetes (T2D). Paradoxically, the development of insulin resistance in the liver is not universal, but pathway selective, such that insulin fails to suppress gluconeogenesis but promotes lipogenesis, contributing to the hyperglycemia, steatosis, and hypertriglyceridemia that underpin the deteriorating glucose control and microvascular complications in T2D. The molecular basis for the pathway-specific insulin resistance remains unknown. Here we report that oxidative stress accompanying obesity inactivates protein-tyrosine phosphatases (PTPs) in the liver to activate select signaling pathways that exacerbate disease progression. In obese mice, hepatic PTPN2 (TCPTP) inactivation promoted lipogenesis and steatosis and insulin-STAT-5 signaling. The enhanced STAT-5 signaling increased hepatic IGF-1 production, which suppressed central growth hormone release and exacerbated the development of obesity and T2D. Our studies define a mechanism for the development of selective insulin resistance with wide-ranging implications for diseases characterized by oxidative stress., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Published
2014
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