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Complement-Induced Post-Translational Regulation of Tgf-ß Signaling on Endothelial Cells

Record Type:	Electronic resources : Monograph/item
Title/Author:	Complement-Induced Post-Translational Regulation of Tgf-ß Signaling on Endothelial Cells/
Author:	Liu, Kevin.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 202,
Description:	58 p
Notes:	Source: Dissertations Abstracts International, Volume: 83-05, Section: B
Contained By:	Dissertations Abstracts International83-05B
Subject:	Medicine -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28318851
ISBN:	9798492731151

Complement-Induced Post-Translational Regulation of Tgf-ß Signaling on Endothelial Cells
Liu, Kevin.

Complement-Induced Post-Translational Regulation of Tgf-ß Signaling on Endothelial Cells - Ann Arbor : ProQuest Dissertations & Theses, 202 - 58 p

Source: Dissertations Abstracts International, Volume: 83-05, Section: B

Thesis (M.D.)--Yale University, 2021

This item must not be sold to any third party vendors

Cardiac allograft vasculopathy (CAV) is a complex vaso-occlusive complication of heart transplantation currently identified as a major limiting factor to long-term survival in those who receive a cardiac transplant. In CAV, neointimal lesions form in graft vessels leading to ischemic complications and ultimately allograft loss. CAV is medically untreatable and affects ~50% of heart transplant patients. Endothelial cells (ECs) are a critical site where CAV lesions form, and antibodies produced by the recipient that bind to donor HLA molecules on graft endothelium (donor specific antibodies) have been identified as a key mediator in this process. Recent studies have further identified a role for antibody-mediated complement fixation, specifically in determining pro-inflammatory signaling changes induced through this process. The laboratory of my mentor, Dr. Jane-wit, studies complement-mediated signaling in ECs and has previously identified a signaling pathway implicated in CAV. In an unbiased assay to identify new components of this pathway, I unexpectedly found that TGF-s signaling molecules, canonically understood to be anti-inflammatory, were involved in complement-induced EC activation. During my thesis I defined a novel function for proteasomes as cellular chaperones to activate TGF-s signaling in response to complement activation. My thesis studies identify a pathologic role for endothelial TGF-s signaling in CAV

ISBN: 9798492731151Subjects--Topical Terms:

1092511
Medicine
Subjects--Index Terms:

Cardiac allograft vasculopath

Complement-Induced Post-Translational Regulation of Tgf-ß Signaling on Endothelial Cells
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