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FSTL-1 secreted by mesenchymal stem cells increases cell viability of human aortic endothelial cells under hypoxic stress

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Date Issued:
2012
Summary:
Human mesenchymal stem cells (MSCs) are being evaluated for the treatment of a broad array of diseases due to their ability to secrete a variety of therapeutically beneficial paracrine-acting factors. For example, MSC conditioned media (MSC-CM) has been shown to inhibit hypoxia-induced apoptosis in human aortic endothelial cells (HAECs) via activation of the P13-AKT pathway. However, the factors secreted by MSCs responsible for this effect have yet to be identified. Recent studies have shown that the glycoprotein Follistatin-like 1 (FSTL1) activates the P13-AKT pathway by binding to the receptor disco-interacting protein (DIP2A) expressed on the surface of cells. Based on our data indicating that MSCs constitutively secrete high quantities of FSTL1, we hypothesize that this protein principally mediates the anti-apoptopic effect of MSC-CM on HAECs. Loss-of-function studies employing siRNA-mediated knockdown of the protein and neutralizing antibodies will be used to assess the role of FSTL1 in growth and survival of HAECs following exposure to hypoxic stress.
Title: FSTL-1 secreted by mesenchymal stem cells increases cell viability of human aortic endothelial cells under hypoxic stress.
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Name(s): Eid, Nibal.
Harriet L. Wilkes Honors College
Type of Resource: text
Genre: Thesis
Issuance: multipart monograph
Date Issued: 2012
Publisher: Florida Atlantic University
Physical Form: electronic
electronic resource
Extent: vi, 14 p. : ill. (some col.)
Language(s): English
Summary: Human mesenchymal stem cells (MSCs) are being evaluated for the treatment of a broad array of diseases due to their ability to secrete a variety of therapeutically beneficial paracrine-acting factors. For example, MSC conditioned media (MSC-CM) has been shown to inhibit hypoxia-induced apoptosis in human aortic endothelial cells (HAECs) via activation of the P13-AKT pathway. However, the factors secreted by MSCs responsible for this effect have yet to be identified. Recent studies have shown that the glycoprotein Follistatin-like 1 (FSTL1) activates the P13-AKT pathway by binding to the receptor disco-interacting protein (DIP2A) expressed on the surface of cells. Based on our data indicating that MSCs constitutively secrete high quantities of FSTL1, we hypothesize that this protein principally mediates the anti-apoptopic effect of MSC-CM on HAECs. Loss-of-function studies employing siRNA-mediated knockdown of the protein and neutralizing antibodies will be used to assess the role of FSTL1 in growth and survival of HAECs following exposure to hypoxic stress.
Identifier: 818344720 (oclc), 3359296 (digitool), FADT3359296 (IID), fau:1424 (fedora)
Note(s): by Nibal Eid.
Thesis (B.A.)--Florida Atlantic University, Honors College, 2012.
Includes bibliography.
Electronic reproduction. Boca Raton, Fla., 2012. Mode of access: World Wide Web.
Subject(s): Stem cells -- Transplantation
Molecular biology
Gene therapy
Coronary heart disease -- Prevention
Stress (Physiology)
Held by: FBoU FAUER
Persistent Link to This Record: http://purl.flvc.org/FAU/3359296
Use and Reproduction: Copyright © is held by the author, with permission granted to Florida Atlantic University to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder.
Host Institution: FAU

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