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Commentary

Comment on “A series of microRNA in the chromosome

14q32.2 maternally imprinted region related to progression

of non-alcoholic fatty liver disease in a mouse model”

1
Pietro Di Fazio , Thaddeus Till Wissniowski 2
1 Department of Visceral, Thoracic and Vascular Surgery, Philipps University Marburg, 35043 Marburg, Germany.
2 Department of Gastroenterology, Philipps University Marburg, 35043 Marburg, Germany.
Corresponding Author:
Dr. Pietro Di Fazio, Department of Visceral, Thoracic and Vascular Surgery, Philipps University Marburg, Baldinger strasse, 35043 Marburg,
Germany. E-mail: difazio@med.uni-marburg.de
Received: 06-06-2016, Accepted: 08-06-2016

Okamoto K, Koda M, Okamoto T, Onoyama T, Miyoshi K, Kishina affinity mature mRNAs forming a double RNA sequence. The
M, Kato J, Tokunaga S, Sugihara TA, Hara Y, Hino K, Murawaki duplex impedes the translational machinery and stabilizes
Y. A series of microRNA in the chromosome 14q32.2 maternally the mRNA or promote its degradation.
imprinted region related to progression of non-alcoholic fatty liver
disease in a mouse model. PLoS One 2016;11:e0154676. So the exact role exerted by miRNAs is based on the
inhibition of gene products expression. This fine regulatory
[6]
Non-alcoholic fatty liver disease (NAFLD) is a liver disease mechanism is responsible of several cellular processes and
related to metabolic syndrome with rising socio-economic can be altered in several diseases including NAFLD. [7-10]
impact worldwide. NAFLD is defined by significant lipid
[11]
deposition in hepatocytes that is unrelated to alcohol Okamoto et al. present an outstanding study concerning
consumption. This high prevalence of liver disease occurs a broad range analysis of miRNAs characterizing NAFLD
after a protracted inflammatory status caused by insulin mouse model and serum from patients affected by this
resistance derived from high consumption of fructose-rich disease.
goods as shown by the multi-parallel hit theory. [2,3]
[1]
They performed a microarray in order to identify
NAFLD is currently classified in simple steatosis (SS) and the expression variation of miRNAs and their possible
non alcoholic steatohepatitis (NASH). NAFLD is a benign identification with NAFLD. The data obtained in the
condition without histological signs of inflammation and closest mouse model for NAFLD fatty liver shionogi ob/
could be reversed by change of life style, recovering from ob characterized by mice bearing a spontaneous obesity
hyperinsulinism and the metabolic syndrome. However, a mutation of the leptin gene (Lepob, commonly known as ob)
protracted inflammation and elevated serum transaminases were processed for similarity with human expressed miRNAs.
determine a severe stage of disease, so called NASH, that
affects the liver irreversibly leading to liver fibrosis, cirrhosis Interestingly, analysis of similarity conservation of miRNAs
and cancer. [4] between rodent and human confirmed the expression of
the same miRNAs in patient affected by SS and NASH. These
MicroRNAs (miRNAs) represent one of the key regulators of miRNAs were identified at the maternally imprinted region
epigenetic modifications. They are normally expressed in (mat) of the chromosome 14q32.2.
clusters and their mature forms are able to combine together
with proteins and form the RNA-inducing silencing complex Seven miRNAs were identified as markers for NAFLD, especially
(RISC). Once the RISC is formed, miRNAs bind the high for NASH, all belonging to the Dlk1-Dio3 mat cluster.
[5]
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How to cite this article: Di Fazio P, Wissniowski TT. Comment
DOI: on “A series of microRNA in the chromosome 14q32.2 maternally
10.20517/2394-5079.2016.19 imprinted region related to progression of non-alcoholic fatty liver
disease in a mouse model”. Hepatoma Res 2016;2:205-6.
© 2016 Hepatoma Research | Published by OAE Publishing Inc. 205