Serum coding and non-coding RNAs as biomarkers of NAFLD and fibrosis severity.


Journal

Liver international : official journal of the International Association for the Study of the Liver
ISSN: 1478-3231
Titre abrégé: Liver Int
Pays: United States
ID NLM: 101160857

Informations de publication

Date de publication:
09 2019
Historique:
received: 20 12 2018
revised: 28 05 2019
accepted: 31 05 2019
pubmed: 7 6 2019
medline: 10 10 2020
entrez: 7 6 2019
Statut: ppublish

Résumé

In patients with non-alcoholic fatty liver disease (NAFLD), liver biopsy is the gold standard to detect non-alcoholic steatohepatitis (NASH) and stage liver fibrosis. We aimed to identify differentially expressed mRNAs and non-coding RNAs in serum samples of biopsy-diagnosed mild and severe NAFLD patients with respect to controls and to each other. We first performed a whole transcriptome analysis through microarray (n = 12: four Control: CTRL; four mild NAFLD: NAS ≤ 4 F0; four severe NAFLD NAS ≥ 5 F3), followed by validation of selected transcripts through real-time PCRs in an independent internal cohort of 88 subjects (63 NAFLD, 25 CTRL) and in an external cohort of 50 NAFLD patients. A similar analysis was also performed on liver biopsies and HepG2 cells exposed to oleate:palmitate or only palmitate (cellular model of NAFL/NASH) at intracellular/extracellular levels. Transcript correlation with histological/clinical data was also analysed. We identified several differentially expressed coding/non-coding RNAs in each group of the study cohort. We validated the up-regulation of UBE2V1, BNIP3L mRNAs, RP11-128N14.5 lncRNA, TGFB2/TGFB2-OT1 coding/lncRNA in patients with NAS ≥ 5 (vs NAS ≤ 4) and the up-regulation of HBA2 mRNA, TGFB2/TGFB2-OT1 coding/lncRNA in patients with Fibrosis stages = 3-4 (vs F = 0-2). In in vitro models: UBE2V1, RP11-128N14.5 and TGFB2/TGFB2-OT1 had an increasing expression trend ranging from CTRL to oleate:palmitate or only palmitate-treated cells both at intracellular and extracellular level, while BNIP3L was up-regulated only at extracellular level. UBE2V1, RP11-128N14.5, TGFB2/TGFB2-OT1 and HBA2 up-regulation was also observed at histological level. UBE2V1, RP11-128N14.5, BNIP3L and TGFB2/TGFB2-OT1 correlated with histological/biochemical data. Combinations of TGFB2/TGFB2-OT1 + Fibrosis Index based on the four factors (FIB-4) showed an Area Under the Curve (AUC) of 0.891 (P = 3.00E-06) or TGFB2/TGFB2-OT1 + Fibroscan (AUC = 0.892, P = 2.00E-06) improved the detection of F = 3-4 with respect to F = 0-2 fibrosis stages. We identified specific serum coding/non-coding RNA profiles in severe and mild NAFLD patients that possibly mirror the molecular mechanisms underlying NAFLD progression towards NASH/fibrosis. TGFB2/TGFB2-OT1 detection improves FIB-4/Fibroscan diagnostic performance for advanced fibrosis discrimination.

Sections du résumé

BACKGROUND & AIMS
In patients with non-alcoholic fatty liver disease (NAFLD), liver biopsy is the gold standard to detect non-alcoholic steatohepatitis (NASH) and stage liver fibrosis. We aimed to identify differentially expressed mRNAs and non-coding RNAs in serum samples of biopsy-diagnosed mild and severe NAFLD patients with respect to controls and to each other.
METHODS
We first performed a whole transcriptome analysis through microarray (n = 12: four Control: CTRL; four mild NAFLD: NAS ≤ 4 F0; four severe NAFLD NAS ≥ 5 F3), followed by validation of selected transcripts through real-time PCRs in an independent internal cohort of 88 subjects (63 NAFLD, 25 CTRL) and in an external cohort of 50 NAFLD patients. A similar analysis was also performed on liver biopsies and HepG2 cells exposed to oleate:palmitate or only palmitate (cellular model of NAFL/NASH) at intracellular/extracellular levels. Transcript correlation with histological/clinical data was also analysed.
RESULTS
We identified several differentially expressed coding/non-coding RNAs in each group of the study cohort. We validated the up-regulation of UBE2V1, BNIP3L mRNAs, RP11-128N14.5 lncRNA, TGFB2/TGFB2-OT1 coding/lncRNA in patients with NAS ≥ 5 (vs NAS ≤ 4) and the up-regulation of HBA2 mRNA, TGFB2/TGFB2-OT1 coding/lncRNA in patients with Fibrosis stages = 3-4 (vs F = 0-2). In in vitro models: UBE2V1, RP11-128N14.5 and TGFB2/TGFB2-OT1 had an increasing expression trend ranging from CTRL to oleate:palmitate or only palmitate-treated cells both at intracellular and extracellular level, while BNIP3L was up-regulated only at extracellular level. UBE2V1, RP11-128N14.5, TGFB2/TGFB2-OT1 and HBA2 up-regulation was also observed at histological level. UBE2V1, RP11-128N14.5, BNIP3L and TGFB2/TGFB2-OT1 correlated with histological/biochemical data. Combinations of TGFB2/TGFB2-OT1 + Fibrosis Index based on the four factors (FIB-4) showed an Area Under the Curve (AUC) of 0.891 (P = 3.00E-06) or TGFB2/TGFB2-OT1 + Fibroscan (AUC = 0.892, P = 2.00E-06) improved the detection of F = 3-4 with respect to F = 0-2 fibrosis stages.
CONCLUSIONS
We identified specific serum coding/non-coding RNA profiles in severe and mild NAFLD patients that possibly mirror the molecular mechanisms underlying NAFLD progression towards NASH/fibrosis. TGFB2/TGFB2-OT1 detection improves FIB-4/Fibroscan diagnostic performance for advanced fibrosis discrimination.

Identifiants

pubmed: 31169972
doi: 10.1111/liv.14167
pmc: PMC6771597
doi:

Substances chimiques

Biomarkers 0
RNA, Untranslated 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1742-1754

Informations de copyright

© 2019 The Authors. Liver International Published by John Wiley & Sons Ltd.

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Auteurs

Stefania Di Mauro (S)

Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi-Nesima Hospital, University of Catania, Catania, Italy.

Alessandra Scamporrino (A)

Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi-Nesima Hospital, University of Catania, Catania, Italy.

Salvatore Petta (S)

Section of Gastroenterology, Di.Bi.M.I.S, University of Palermo, Palermo, Italy.

Francesca Urbano (F)

Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi-Nesima Hospital, University of Catania, Catania, Italy.

Agnese Filippello (A)

Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi-Nesima Hospital, University of Catania, Catania, Italy.

Marco Ragusa (M)

Department of BioMedical Sciences and BioTechnology, Section of Biology and Genetics Giovanni Sichel, Unit of Molecular, Genome and Complex Systems BioMedicine, Catania, Italy.
Oasi Research Institute - IRCCS, Troina, 94018, Italy.

Maria T Di Martino (MT)

Department of Experimental and Clinical Medicine, Magna Graecia University, Catanzaro, Italy.

Francesca Scionti (F)

Department of Experimental and Clinical Medicine, Magna Graecia University, Catanzaro, Italy.

Stefania Grimaudo (S)

Section of Gastroenterology, Di.Bi.M.I.S, University of Palermo, Palermo, Italy.

Rosaria M Pipitone (RM)

Section of Gastroenterology, Di.Bi.M.I.S, University of Palermo, Palermo, Italy.

Graziella Privitera (G)

Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi-Nesima Hospital, University of Catania, Catania, Italy.

Antonino Di Pino (A)

Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi-Nesima Hospital, University of Catania, Catania, Italy.

Roberto Scicali (R)

Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi-Nesima Hospital, University of Catania, Catania, Italy.

Luca Valenti (L)

Translational Medicine, University of Milan, Fondazione IRCCS Ca' Granda Pad Marangoni, Milan, Italy.

Paola Dongiovanni (P)

Department of Pathophysiology and Transplantation, Section of Internal Medicine, University of Milan, Fondazione Ca' Granda IRCCS Ospedale Maggiore Policlinico, Milan, Italy.

Anna Fracanzani (A)

Department of Pathophysiology and Transplantation, Section of Internal Medicine, University of Milan, Fondazione Ca' Granda IRCCS Ospedale Maggiore Policlinico, Milan, Italy.

Agata M Rabuazzo (AM)

Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi-Nesima Hospital, University of Catania, Catania, Italy.

Antonio Craxì (A)

Section of Gastroenterology, Di.Bi.M.I.S, University of Palermo, Palermo, Italy.

Michele Purrello (M)

Department of BioMedical Sciences and BioTechnology, Section of Biology and Genetics Giovanni Sichel, Unit of Molecular, Genome and Complex Systems BioMedicine, Catania, Italy.

Francesco Purrello (F)

Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi-Nesima Hospital, University of Catania, Catania, Italy.

Salvatore Piro (S)

Department of Clinical and Experimental Medicine, Internal Medicine, Garibaldi-Nesima Hospital, University of Catania, Catania, Italy.

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