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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.edu

BIOGRAPHY

Khadija Rafiq et al., Virol Res J 2018, Volume 2