Heart-Infiltrating Prominin-1 ⁺ /CD133 ⁺ Progenitor Cells Represent the Cellular Source of Transforming Growth Factor β–Mediated Cardiac Fibrosis in Experimental Autoimmune Myocarditis

Abstract

Rationale: Myocardial fibrosis is a hallmark of inflammation-triggered end-stage heart disease, a common cause of heart failure in young patients. Objective: We used CD4 ؉ T-cell-mediated experimental autoimmune myocarditis model to determine the parameters regulating cardiac fibrosis in inflammatory heart disease.

Regeneration of skeletal muscle

“…Being a circulating cell population, these CD133+ cells present an interesting cell pool that could be targeted to home to the site of injury and contribute to muscle repair. The ability of these cells to home and respond to injury has been reported in a number of studies, particularly in ischemic injury of the heart (Kania et al 2009;Kubo et al 2008;Voo et al 2008;Navarro-Sobrino et al 2010). Torrente et al (2004) have shown that the direct injection of CD133+ cells into dystrophic muscle improves skeletal muscle structure and replenishes the satellite cell pool, leading to a successful phase I clinical trial of autologous CD133+ cell injection in eight individuals with Duchenne muscular dystrophy .…”

Myeloid Differentiation Factor-88/Interleukin-1 Signaling Controls Cardiac Fibrosis and Heart Failure Progression in Inflammatory Dilated Cardiomyopathy

“…23 We therefore created chimeric mice to address the specific role of BM-derived cells in heart failure progression and tissue fibrosis. All chimeric mice were immunized with bmDCs, and for fibrosis development, animals were challenged with MyHC-␣/CFA.…”

Involvement of endothelial progenitor cells in the formation of plexiform lesions in broiler chickens: possible role of local immune/inflammatory response

“…These results raise a possibility that there is an intrinsic relationship between the two morphologically different cell types in the PLs. Indeed, it has been reported that CD133 + progenitors can differentiate into both fibroblasts and monocytes/macrophages in inflamed tissue (Kania et al, 2009). Therefore, it is very likely that there is a process of EPC-to-macrophage transition during the maturing of PLs.…”