SRC-3/AIB-1 may Enhance Hepatic NFATC1 Transcription and Mediate Inflammation in a Tissue-Specific Manner in Morbid Obesity.


Journal

Endocrine, metabolic & immune disorders drug targets
ISSN: 2212-3873
Titre abrégé: Endocr Metab Immune Disord Drug Targets
Pays: United Arab Emirates
ID NLM: 101269157

Informations de publication

Date de publication:
2020
Historique:
received: 27 02 2019
revised: 14 05 2019
accepted: 16 05 2019
pubmed: 20 7 2019
medline: 20 11 2020
entrez: 20 7 2019
Statut: ppublish

Résumé

Obesity is a global epidemic which is associated with several cardiometabolic comorbidities and is characterized by chronic, low grade systemic inflammation. Numerous biomarkers have been implicated in the pathophysiology of the disease, including transcription factors and coregulators. Steroid Receptor Coactivator (SRC)-family represent the master regulators of metabolic pathways and their dysregulation is strongly associated with numerous metabolic disorders. 50 morbidly obese patients participated in the present study. Biopsies were collected from visceral adipose tissue, subcutaneous adipose tissue, skeletal muscle, extra-myocellular adipose tissue and liver. We evaluated the differential protein expression of NFATc1, SRC-2/TIF-2, SRC-3/AIB-1 and inflammatory biomarkers CD68 and CD3 by immunohistochemistry. The current study was designed to determine any correlations between the transcription factor NFATc1 and the SRC coregulators, as well as any associations with the inflammatory biomarkers. We identified SRC-3 as a hepatic NFATc1 coactivator and we demonstrated its possible role in energy homeostasis and lipid metabolism. Moreover, we revealed a complex and extensive intraand inter-tissue network among the three main investigated proteins and the inflammatory biomarkers, suggesting their potential participation in the obesity-induced inflammatory cascade. Steroid receptor coactivators are critical regulators of human metabolism with pleiotropic and tissue-specific actions. We believe that our study will contribute to the better understanding of the complex multi-tissue interactions that are disrupted in obesity and can therefore lead to numerous cardiometabolic diseases. Further on, our present findings suggest that SRC-3/AIB-1 could constitute possible future drug targets.

Sections du résumé

BACKGROUND BACKGROUND
Obesity is a global epidemic which is associated with several cardiometabolic comorbidities and is characterized by chronic, low grade systemic inflammation. Numerous biomarkers have been implicated in the pathophysiology of the disease, including transcription factors and coregulators. Steroid Receptor Coactivator (SRC)-family represent the master regulators of metabolic pathways and their dysregulation is strongly associated with numerous metabolic disorders.
METHODS METHODS
50 morbidly obese patients participated in the present study. Biopsies were collected from visceral adipose tissue, subcutaneous adipose tissue, skeletal muscle, extra-myocellular adipose tissue and liver. We evaluated the differential protein expression of NFATc1, SRC-2/TIF-2, SRC-3/AIB-1 and inflammatory biomarkers CD68 and CD3 by immunohistochemistry. The current study was designed to determine any correlations between the transcription factor NFATc1 and the SRC coregulators, as well as any associations with the inflammatory biomarkers.
RESULTS RESULTS
We identified SRC-3 as a hepatic NFATc1 coactivator and we demonstrated its possible role in energy homeostasis and lipid metabolism. Moreover, we revealed a complex and extensive intraand inter-tissue network among the three main investigated proteins and the inflammatory biomarkers, suggesting their potential participation in the obesity-induced inflammatory cascade.
CONCLUSION CONCLUSIONS
Steroid receptor coactivators are critical regulators of human metabolism with pleiotropic and tissue-specific actions. We believe that our study will contribute to the better understanding of the complex multi-tissue interactions that are disrupted in obesity and can therefore lead to numerous cardiometabolic diseases. Further on, our present findings suggest that SRC-3/AIB-1 could constitute possible future drug targets.

Identifiants

pubmed: 31322077
pii: EMIDDT-EPUB-99625
doi: 10.2174/1871530319666190715160630
doi:

Substances chimiques

Inflammation Mediators 0
NFATC Transcription Factors 0
NFATC1 protein, human 0
NCOA3 protein, human EC 2.3.1.48
Nuclear Receptor Coactivator 3 EC 2.3.1.48

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

242-255

Informations de copyright

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

Auteurs

Athina Chasapi (A)

Department of Pathology, Medical School, University of Patras, 26500 Patras, Greece.

Konstantinos Balampanis (K)

Department of Pathology, Medical School, University of Patras, 26500 Patras, Greece.
Second Department of Internal Medicine, Research Unit and Diabetes Center, Attikon University Hospital, National and Kapodistrian University of Athens, Medical School, Rimini 1, Haidari, 12462 Athens, Greece.
Department of Anatomy and Histology-Embryology, Medical School, University of Patras, 26500 Patras, Greece.

Anna Tanoglidi (A)

Department of Clinical Pathology, Akademiska University, Uppsala, Sweden.

Eleni Kourea (E)

Department of Pathology, Medical School, University of Patras, 26500 Patras, Greece.

George I Lambrou (GI)

First Department of Pediatrics, Choremeio Research Laboratory, National and Kapodistrian University of Athens, Medical School, Thivon & Levadeias 8, 11527, Goudi, Athens, Greece.

Vaia Lambadiari (V)

Second Department of Internal Medicine, Research Unit and Diabetes Center, Attikon University Hospital, National and Kapodistrian University of Athens, Medical School, Rimini 1, Haidari, 12462 Athens, Greece.

Fotios Kalfarentzos (F)

First Department of Propaedeutic Medicine, National and Kapodistrian University of Athens Medical School, Laiko General Hospital, 17, Ag. Thoma St, 11527 Athens, Greece.

Erifili Hatziagelaki (E)

Second Department of Internal Medicine, Research Unit and Diabetes Center, Attikon University Hospital, National and Kapodistrian University of Athens, Medical School, Rimini 1, Haidari, 12462 Athens, Greece.

Maria Melachrinou (M)

Department of Pathology, Medical School, University of Patras, 26500 Patras, Greece.

Georgia Sotiropoulou-Bonikou (G)

Department of Anatomy and Histology-Embryology, Medical School, University of Patras, 26500 Patras, Greece.

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Classifications MeSH