INCREASED EXPRESSION OF CARDIOTROPHIN-1
IN CARDIOMYOPATHY PATIENTS
Sharif S1,*, Saleem A1, Naz S1, Rashid F1, Iqtedar M2, Kaleem A2, Latif A1
*Corresponding Author: Dr. Saima Sharif, Department of Zoology, Lahore College for Women
University, Jail Road, Lahore, Pakistan. Tel: +92-333-409-2232. Fax: +92-042-9920-3077. E-mail:
saimasharif04@ gmail.com
page: 21
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DISCUSSION
Among cardiovascular problems, CM is one of the
leading causes of heart transplantation. Dilated CM occupies
a significant position among all types of CM. In CM,
more than 1400 mutations are linked [4]. Approximately
80.0% of identified mutations relating to cardiac β-myosin
heavy chain and cardiac myosin binding protein C are present
in eight sarcomere genes in CM [11]. Left ventricular
dilation and dysfunction characterized by primary myocardial
disease is known as DCM. Ventricular hypertrophy is
increased mainly due to volume overload [12]. Prevalence
of CM in the USA is as low as 0.02 to 0.2% in the population.
It is found to be only 0.5% within unselected patients
referred for echocardiography examination. Occurrence
of one form of CM in Japan is the same as in the western
population, namely 17.3/100,000 [13]. In Pakistan, data
regarding the occurrence of CM has hardly been reported.
In comparison to the control group, the alteration
in “CT-1 gene expression” in the blood cells of cardiomyopathic
subjects was observed at the molecular level.
In our study, RT-PCR analysis revealed 5.2-times more
expression and upregulation of the CT-1 gene in the CM
group than controls. Another study by Jougasaki et al.
[14], confirmed the overexpression of cardiotrophin level
in CM patients, in which levels of cardiotrophin mRNA
in failing LV cardiotrophin from the DCM patients was
assessed by semi-quantitative RT-PCR. It demonstrated
the CT-1 gene expression by northern blot analysis and
found that the level of gene was high in HF models. Strong
positive correlation exists between left ventricular mass
index and CT-1 mRNA. In congestive HF (CHF) models
immunoreactivity of CT-1 was more intense in atrium and
ventricle of model heart as compare to normal heart [14].
The studies revealed that direct relationship exist
between increased expression of CT-1 gene and dilation
of the LV. Cardiotrophin-1 acts as a marker in the
progression of ventricular hypertrophy. It is obvious that
early developmental genes are related to the onset of CM.
Additionally, researchers recently used human myocardial
tissue and found changes in the expression of these genes
in heart disease patients. Our results for the expression of the CT-1 gene in CM patients compared to healthy individuals
are similar to the study by Freed et al. [15]. Our
data indicated that adipose tissues are identified as a CT-1
source in CM subjects, as significant direct association
between BMI and CT-1 expression was observed. High
levels of CT-1 in metabolic syndrome was also reported
by Natal et al. [16]. Circulating stem cell progenitor cells
expressed early cardiovascular genes in peripheral blood
system that resides in the bone marrow. This indicates that
the peripheral blood system can be used as a marker to
detect the gene expression in response to a disease. Our
results supported this hypothesis that gene expression in
blood cells may be the reflection of the disease harshness
as high levels of plasma CT-1 were found in patients with
CM. Furthermore, in another study by Tsutamoto et al.
[17], the association between plasma level CT-1 and the
mass index of the LV and neurohumoral factors such as
norepinephrine and angiotensin II, which can stimulate
in vitro production of CT-1 in CM subjects, was reported.
Thus, it was concluded that expression of CT-1 gene is
increased in CM patients. Increased expression of gene
alters the activity of myocytes that result in the proliferation
of cells and increase ventricular mass, resulting in
cardiac failure.
Conclusions. It was concluded that expression of the
CT-1 gene was significantly greater in CM subjects when
compared to control subjects. Moreover, age and BMI also
influence the expression.
Acknowledgments. We are sincerely grateful to
the subjects for their help in the clinical evaluation and
data collection. I am also grateful to the Pakistan Science
Foundation for funding the presentation of this article
at the 5th International Conference on Prehypertension,
Hypertension and Cardiometabolic Syndrome, held at
Venice, Italy, February 22-25 2018.
Declaration of Interest. The authors report no conflicts
of interest. The authors alone are responsible for the
content and writing of this article.
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