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Page 37
Biochemistry & Molecular Biology Journal
ISSN: 2471-8084
Internat i ona l Conference on
Biotechnology, Biomarkers
& Systems Biology
M a r c h 0 4 - 0 5 , 2 0 1 9
Am s t e r d a m , N e t h e r l a n d s
Biotechnology, Biomarkers & Systems Biology 2019
Background:
Atherosclerosis is the leading cause of cardiovascular diseases
and a worldwide health burden imposing a considerable health toll. Vascular
fibrosis and inflammation in the vessel walls are among the risk factors of
atherosclerosis development, characterized by vessel stiffness and subsequent
loss of elasticity. Bradykinin (BK) and leptin have been previously shown to be
involved in the development of atherosclerosis through their effect on vascular
fibrosis and inflammation processes.
Aim:
In this study, we investigate the effect of BK and leptin on the global
protein profile in vascular smooth muscle cell (VSMC), employing the LC-MS/
MS technique and systems biology analysis, to gain insight into the different
pathways modified by BK and leptin, and the diseases and biological pathways
they are involved in, and to search for a candidate molecule(s) that would serve
as a biomarker for the progression of vascular injury.
Results:
In our study, we identified 1837 proteins in the control samples. Among
these proteins, BK modified 70 (3.8%) and 120 (6.5%) proteins compared to
controls after 24 and 48 hrs, respectively. BK induced the expression of the
leptin receptor, TGFβ and COX1 in VSMC by promoting vascular fibrosis and
inflammation. On the other hand, leptin modified 189 (10.2%) and 127 (6.5%)
proteins compared to controls after 24 and 48 hrs, respectively. For instance,
leptin induced the expression of collagen IV suggesting a role of leptin in
the development of vascular fibrosis. Furthermore, leptin reduced cofilin
expression, confirming the role of leptin in actin remodeling. Finally, pathway
analyses indicated that the activation of MAPKs and AKT pathways to be a
common mediator between BK and leptin signaling.
Conclusion(s):
BK stimulation showed a proteomic pattern favoring vascular
fibrosis, inflammation and the involvement of the leptin pathway. On the other
hand, leptin stimulation induced ECM proteins and reduced actin remodeling
proteins. These findings point to a possible interaction between BK and leptin
pathways in VSMC to promote vascular injury.
Biography
Moustafa Al Hariri is Co-ordinator of Department of Emergency
Medicine Research Unit at the American University of Beirut
Medical Center (AUBMC). He has graduated with a PhD degree
in 2017 fromthe AmericanUniversity of Beirut. After Graduation,
he has joined the Department of Emergency Medicine at
AUBMC to coordinate and manage the clinical and biomedical
research activities in the department. His research work since
included oversea and supervise the quality of research activities
in the department, search for funding opportunities for the
projects, and increase the research visibility of the department
research activities.
ma147@aub.edu.lbProteome profiling in the vascular smooth muscle cell in
response to bradykinin and leptin
Al Hariri M
1
, Jaffa MA
1
, Saoud R
1
, Zhao J
3
, Zhu R
3
, Kobeissy F
1
,
Anwarul Hassan
4
, Ziyadeh FN
1
, Mechref Y
3
and Jaffa AA
1
1
American University of Beirut, Lebanon
2
Texas Tech University, USA
3
Qatar University, Qatar
Al Hariri M et al., Biochem Mol biol J 2019, Volume:5
DOI: 10.21767/2471-8084-C1-023