alexa Mechanisms Of Endothelial Regeneration And Resolution Of Inflammatory Injury
ISSN: 2157-7552

Journal of Tissue Science & Engineering
Open Access

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Global Congress on Tissue Engineering, Regenerative & Precision Medicine
December 1-2, 2016 | San Antonio, USA

Youyang Zhao
University of Illinois at Chicago, USA
Posters & Accepted Abstracts: J Tissue Sci Eng
DOI: 10.4172/2157-7552.C1.031
Abstract
Acute lung injury (ALI) and its severe form acute respiratory distress syndrome (ARDS) are complex, multi-factorial syndromes which manifest themselves by leaky lung microvessels, protein rich edema and hypoxemia. Despite recent advances on the understanding of the underlying mechanisms, there are currently no effective pharmacological or cell-based treatment of the disease with a mortality rate as high as 40%. Given that recent studies from both human and animal studies has demonstrated the key role of microvascular leakage in determining the outcome of sepsis and associated ARDS, targeting microvascular leakage repair mechanisms represents a novel, effective therapeutic approach for the prevention and treatment of ALI/ARDS. Employing genetic lineage tracing, we have demonstrated that resident endothelial cell proliferation is essential for endothelial regeneration following sepsis challenge. We have defined the crucial role of the Forkhead transcription factor FoxM1 in mediating the intrinsic endothelial regeneration program and delineated the signaling pathway mediated by the p110 gamma isoform of PI3K in mediating endothelial regeneration and vascular repair and resolution of inflammatory injury. We also identified endothelial FoxM1 as the endogenous mediator of the adult stem cell-elicited paracrine effects on protecting from acute lung injury. Our studies suggest that targeting the intrinsic FoxM1-dependent endothelial regeneration program is an effective therapeutic strategy for reversing lung microvessel leakiness and improving survival of sepsis and ARDS patients.
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