Influence of adenovirus 36 seropositivity on the expression of adipogenic microRNAs in obese subjects.


Journal

International journal of obesity (2005)
ISSN: 1476-5497
Titre abrégé: Int J Obes (Lond)
Pays: England
ID NLM: 101256108

Informations de publication

Date de publication:
11 2020
Historique:
received: 20 01 2020
accepted: 11 08 2020
revised: 15 07 2020
pubmed: 23 8 2020
medline: 4 11 2021
entrez: 23 8 2020
Statut: ppublish

Résumé

Infection by Adenovirus 36 (Ad-36) has been associated with adipogenesis using cell and animal models, and a high risk of developing obesity has been reported in Ad-36-seropositive individuals. However, molecular mechanisms involved in the maintenance over the years of adipogenesis associated with Ad-36 has not been investigated in human adipose tissue. Epigenetic mechanisms, such as micro-RNAs (miRNAs) that regulate gene expression at the post-transcriptional level, have shown an important role in the development and maintenance of metabolic diseases. This study investigated the expression of miRNA associated with the adipogenic process in visceral adipose tissue from obese individuals according to Ad-36 serology. Obese individuals were separated according to their status of Ad-36 serology in seropositive (Ad-36 (+); n = 29) and seronegative (Ad-36 (-); n = 28) groups. Additionally, a group of lean controls (n = 17) was selected to compare with obese individuals. Biopsies of visceral adipose tissue were obtained to evaluate miRNA and gene expression. The study of Ad-36 serology was carried out by ELISA. The expression of pro-adipogenic (miR-17 and miR-210) and anti-adipogenic (miR-155, miR-130 and miR-27a) miRNAs was evaluated using Taqman advanced miRNA assays by qPCR. The expression of adipogenes encoding LEP, ADIPOQ, and PPARγ was evaluated by Taqman predesigned assays through qPCR. The obese group had higher LEP (p < 0.001) and PPARγ (p = 0.016) expression and lower ADIPOQ expression (p = 0.017), and also had higher expression of miR-210 (p = 0.039), whereas lower expression of miR-155 (p = 0.019) and miR-27a (p = 0.028) as compared to lean controls. Higher PPARγ expression (p = 0.008), but no influence on LEP or ADIPOQ expression was observed in Ad-36 (+) group. Those seropositive individuals also had higher expression of the miR-17 (p = 0.028) and lower levels of miR-155 (p = 0.031) in adipose tissue as compared to seronegative subjects. Individuals with previous infection by Ad-36 had higher expression of the pro-adipogenic miR-17 and lower expression of the anti-adipogenic miR-155, which could lead to an increased adipogenic status by positively modulating PPARγ expression in adipose tissue from obese subjects.

Sections du résumé

BACKGROUND
Infection by Adenovirus 36 (Ad-36) has been associated with adipogenesis using cell and animal models, and a high risk of developing obesity has been reported in Ad-36-seropositive individuals. However, molecular mechanisms involved in the maintenance over the years of adipogenesis associated with Ad-36 has not been investigated in human adipose tissue. Epigenetic mechanisms, such as micro-RNAs (miRNAs) that regulate gene expression at the post-transcriptional level, have shown an important role in the development and maintenance of metabolic diseases.
AIM
This study investigated the expression of miRNA associated with the adipogenic process in visceral adipose tissue from obese individuals according to Ad-36 serology.
METHODS
Obese individuals were separated according to their status of Ad-36 serology in seropositive (Ad-36 (+); n = 29) and seronegative (Ad-36 (-); n = 28) groups. Additionally, a group of lean controls (n = 17) was selected to compare with obese individuals. Biopsies of visceral adipose tissue were obtained to evaluate miRNA and gene expression. The study of Ad-36 serology was carried out by ELISA. The expression of pro-adipogenic (miR-17 and miR-210) and anti-adipogenic (miR-155, miR-130 and miR-27a) miRNAs was evaluated using Taqman advanced miRNA assays by qPCR. The expression of adipogenes encoding LEP, ADIPOQ, and PPARγ was evaluated by Taqman predesigned assays through qPCR.
RESULTS
The obese group had higher LEP (p < 0.001) and PPARγ (p = 0.016) expression and lower ADIPOQ expression (p = 0.017), and also had higher expression of miR-210 (p = 0.039), whereas lower expression of miR-155 (p = 0.019) and miR-27a (p = 0.028) as compared to lean controls. Higher PPARγ expression (p = 0.008), but no influence on LEP or ADIPOQ expression was observed in Ad-36 (+) group. Those seropositive individuals also had higher expression of the miR-17 (p = 0.028) and lower levels of miR-155 (p = 0.031) in adipose tissue as compared to seronegative subjects.
CONCLUSIONS
Individuals with previous infection by Ad-36 had higher expression of the pro-adipogenic miR-17 and lower expression of the anti-adipogenic miR-155, which could lead to an increased adipogenic status by positively modulating PPARγ expression in adipose tissue from obese subjects.

Identifiants

pubmed: 32826973
doi: 10.1038/s41366-020-00654-9
pii: 10.1038/s41366-020-00654-9
doi:

Substances chimiques

MIRN155 microRNA, human 0
MIRN17 microRNA, human 0
MicroRNAs 0
PPAR gamma 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

2303-2312

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Auteurs

Víctor Manríquez (V)

Centro de Excelencia en Medicina Traslacional, CEMT-BIOREN, Universidad de La Frontera, Temuco, Chile.

Alvaro Gutierrez (A)

Centro de Excelencia en Medicina Traslacional, CEMT-BIOREN, Universidad de La Frontera, Temuco, Chile.

Alexis Morales (A)

Centro de Excelencia en Medicina Traslacional, CEMT-BIOREN, Universidad de La Frontera, Temuco, Chile.

Roberto Brito (R)

Centro de Excelencia en Medicina Traslacional, CEMT-BIOREN, Universidad de La Frontera, Temuco, Chile.

Monica Pavez (M)

Centro de Excelencia en Medicina Traslacional, CEMT-BIOREN, Universidad de La Frontera, Temuco, Chile.

Jorge Sapunar (J)

Centro de Excelencia en Medicina Traslacional, CEMT-BIOREN, Universidad de La Frontera, Temuco, Chile.
Centro de Investigación en Epidemiología Cardiovascular y Nutricional, EPICYN, Universidad de La Frontera, Temuco, Chile.
Department of Internal Medicine, Universidad de La Frontera, Temuco, Chile.

Luis Fonseca (L)

Centro de Tratamiento de la Obesidad, Clinica Alemana de Temuco, Temuco, Chile.

Víctor Molina (V)

Centro de Tratamiento de la Obesidad, Clinica Alemana de Temuco, Temuco, Chile.

Eugenia Ortiz (E)

Centro de Tratamiento de la Obesidad, Clinica Alemana de Temuco, Temuco, Chile.

Maria Ines Barra (MI)

Department of Internal Medicine, Universidad de La Frontera, Temuco, Chile.
Centro de Tratamiento de la Obesidad, Clinica Alemana de Temuco, Temuco, Chile.

Camila Reimer (C)

Department of Internal Medicine, Universidad de La Frontera, Temuco, Chile.
Centro de Tratamiento de la Obesidad, Clinica Alemana de Temuco, Temuco, Chile.

Maria Charles (M)

Centro de Tratamiento de la Obesidad, Clinica Alemana de Temuco, Temuco, Chile.

Constance Schneider (C)

Centro de Tratamiento de la Obesidad, Clinica Alemana de Temuco, Temuco, Chile.

Alvaro Cerda (A)

Centro de Excelencia en Medicina Traslacional, CEMT-BIOREN, Universidad de La Frontera, Temuco, Chile. alvaro.cerda@ufrontera.cl.
Centro de Investigación en Epidemiología Cardiovascular y Nutricional, EPICYN, Universidad de La Frontera, Temuco, Chile. alvaro.cerda@ufrontera.cl.
Department of Basic Sciences, Universidad de La Frontera, Temuco, Chile. alvaro.cerda@ufrontera.cl.

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