Details

Autor(en) / Beteiligte

• Schena, Giana J
• Kubo, Hajime
• Feldsott, Eric
• Berretta, Remus
• Mohsin, Sadia
• Houser, Steven R

Titel

Abstract 554: Mechanism of Action for the Beneficial Effects of Cortical Bone Stem Cells on the Heart After Myocardial Infarction

Ist Teil von

• Circulation research, 2018-08, Vol.123 (Suppl_1)

Erscheinungsjahr

2018

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• Abstract only Rationale: Myocardial infarction (MI) causes the death of a portion of the heart and can lead to adverse remodeling that results in poor cardiac pump function and heart failure. We have previously shown that a novel stem cell type, cortical bone stem cells (CBSCs), causes improved repair of cardiac tissue after MI. When injected into the infarct border zone in both mouse and pig hearts, CBSCs reduced infarct size and induced neovascularization via a largely paracrine manner. Objectives: This study investigates the mechanism involved in the angiogenesis alterations implemented by CBSCs, in particular the wound-healing of endothelial cells. Our goal was to comprehend how mCBSCs affected cardiac repair in an inflammatory environment. Methods and Results: We performed scratch assays and tubule formation (TF) assays on human umbilical vein endothelial cells (HUVECs) and cardiac endothelial cells (CECs) in mCBSC CM and media controls, and in the presence of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α. Both HUVECs and CECs show reduced cell migration and reduced TF. TF was rescued when the cells were plated on Matrigel. We investigated the angiogenesis-related cytokines present within both the mCBSC CM and CM-treated HUVECs and CECs via angiogenesis dot blots. We discovered a significant increase of CXCL-10 and Endostatin/Collagen XVIII relative to murine embryonic fibroblast CM. Conclusions: Our findings show that part of the mechanism underlying the wound-healing and neovascularization induced by CBSCs post-MI involves secretion of angiogenesis-related cytokines which alter the behavior of cardiac endothelial cells.