immunology-2018-scientifictracks

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Immunology 2018
J u l y 0 5 - 0 7 , 2 0 1 8
V i e n n a , A u s t r i a
Page 56
Journal of Clinical Immunology and Allergy
ISSN 2471-304X
1 5 t h I n t e r n a t i o n a l C o n f e r e n c e o n
Immunology
Calcific aortic valve disease (CAVD) is one of the most prevalent
cardiovascular diseases in the elderly and is becoming an increasingly
important health issue with the emerging longevity. Chronic inflammation and
progressive calcification of the aortic valve leaflets cause valvular dysfunction
and heart failure. Currently, pharmacological intervention of CAVD progression
is unavailable and the interaction between the pro-inflammatory and pro-
osteogenic mechanisms in aortic valve calcification is poorly understood.
Aortic valve interstitial cells (AVICs) are actively involved in valvular
calcification. Our studies found that human AVICs express osteogenic proteins
(including BMP-2 and TGF-β1) in response to stimulation of Toll-like receptor
(TLR) 2, 3 or 4. Further, the TLR-mediated osteogenic response in human AVICs
leads to pro-osteogenic reprogramming characterized by the expression of
Runx2 and alkaline phosphatase, and formation of calcium deposits. These
studies uncovered a novel mechanistic role of the AVIC innate immunity in
aortic valve calcification. Our recent work identified several endogenous
factors that can elicit the osteogenic responses in human AVICs through TLRs,
including oxidized low-density lipoprotein, biglycan and matrilin 2. While these
endogenous factors utilize distinct TLRs, they induce the osteogenic responses
through common signalling pathways, mainly the NF-κB and ERK1/2 pathways.
Our findings demonstrate that damage-associated molecular patterns are
capable of inducing the osteogenic responses in human AVICs and that the
innate immune receptors have novel functions in modulating the osteogenic
responses in human aortic valve cells. These findings suggest that AVIC TLRs
may play an important role in the pathogenesis of CAVD and that modulation
of the common signalling pathways utilized by TLRs may have therapeutic
potential for suppression of CAVD progression.
Biography
Xianzhong Meng has been graduated from Harbin Medical
University, Harbin, China in 1978. He received MS in 1981
and PhD in 1985 from the same university. He then received
Postdoctoral training at Cleveland Clinic, Cleveland, USA. He
became an Investigator in the Cardiothoracic Inflammtion
Research Laboratory, Department of Surgery, University of
Colorado Denver in 1990. He is currently a Tenured Professor
in the Department of Surgery and the Director of Cardiothoracic
Inflammation Research Program at University of Colorado
Denver. His current research focusses on the impact of aging
on myocardial ischemia/reperfusion injury and the molecular
mechanism of heart valve calcification. His research is
supported continuously by NIH grants. He is the author/co-
author of over 160 papers published in peer-reviewed journals,
and he has given over 100 presentations, invited lectures
and seminars in universities, professional societies, and
international conferences.
Valvular interstitial cell innate immunity in the
pathobiology of calcific aortic valve disease
Xianzhong Meng, Lihua Ao and David A Fullerton
University of Colorado Denver, USA
Xianzhong Meng et al., Insights Allergy Asthma Bronchitis 2018, Volume: 4
DOI: 10.21767/2471-304X-C1-002