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Virology Research Journal
|
Volume 2
Page 24
Note:
allied
academies
IMMUNOLOGY AND CELL BIOLOGY
BACTERIOLOGY AND INFECTIOUS DISEASES
&
Global Summit on
Global Congress on
J u n e 2 5 - 2 6 , 2 0 1 8 | A m s t e r d a m , N e t h e r l a n d s
Joint Event on
THE ROLE OF B CELLS IN DIABETIC
CARDIOMYOPATHY
Khadija Rafiq
and
Amrita Sarkar
Thomas Jefferson University, USA
D
iabetic cardiomyopathy (DCM) is typified by alterations in cardiac
morphology and function, independent of hypertension or coronary
disease. The disease is characterized by intramyocardial inflammation,
cardiomyocytes apoptosis and cardiac fibrosis. The molecular mechanism
that links inflammation to DCM is incompletely understood. This study
investigates the role of B cells on the development of DCM. Induction of
diabetes inWTmice resulted a significant decrease in B cell infiltration into the
left ventricular heart, but not in other organs, during the development of DCM.
Interestingly, decreased B cell numbers correlate with the downregulation
of the expression of a B cell inflammatory molecule, Allograft Inflammatory
Factor-1(AIF-1), which has been reported to enhance lymphocyte activation.
However, the molecular mechanism(s) responsible for the decrease of B cell
homing and AIF-1 expression in diabetic hearts as well as their relationship
duringthedevelopmentofDCMisunknown.Focusedongaininginsightintothe
role of AIF-1 in B cell migration, our
in vitro
study showed that B cell migration
to cardiomyocytes is regulated by AIF-1 expression. We observed significant
migration of B cells to hyperglycemic GFP-tagged AIF-1 transfected H9C2
cells compared to control cells transfected with an empty vector. Interestingly,
Adenovirus AIF-1 overexpression promoted B cell homing to diabetic heart
tissues, reduced inflammation and pathological remodeling. These effects of
AIF-1 overexpression on the diabetes-induced cardiac dilatation and function
are independent of AIF-1 effects on hyperglycemia since blood glucose levels
are similar in diabetic WT mice with or without AIF-1 overexpression. This
study suggests that diabetes attenuates AIF-1 expression, and this in turn,
prevents B cell homing to diabetic heart tissues which in trun results in an
increase of cardiac inflammation that leads to DCM.
Khadija Rafiq has her expertise in Immunology
and Cellular Biology. Over the past several years
she has been investigating how the immune
system affects cardiac myocyte growth and
cardiac function with a focus on signaling mol-
ecules that are activated by inflammatory pro-
teases. Her research interest focuses on eluci-
dating the role of inflammatory serine proteases
in the development of diabetic cardiomyopathy.
It is well known that inflammation plays a role
in the development of diabetic cardiomyopathy.
The goals of her research are to identify novel
signaling mechanisms that control cardiac cell
growth and apoptosis.
Khadija.rafiq@jefferson.eduBIOGRAPHY
Khadija Rafiq et al., Virol Res J 2018, Volume 2