Long-term benefit of intracardiac delivery of autologous granulocyte–colony-stimulating factor-mobilized blood CD34+ cells containing cardiac progenitors on regional heart structure and function after myocardial infarct

Activation of Toll-like receptor 3 amplifies mesenchymal stem cell trophic factors and enhances therapeutic potency

“…Cultured CD34 ϩ progenitor cells are able to repair infarcted myocardium through trans-differentiation (83,85). Encouraging results from administration of autologous CD34 ϩ progenitor cells for cardiac repair have been documented in recent clinical trials (47,57). Their potential as functional cardiac progenitor cells is demonstrated here by robust expression of GATA4, Nkx2.5, and Mef2c as also demonstrated for c-kit ϩ cardiac progenitor cells (7).…”

“…In particular, CD34 ϩ progenitor cells, which can secrete trophic factors and differentiate into cardiomyocytes (84,85), have been used in clinical trials for cardiac repair (47,57). We used in situ immunostaining to quantify CD34 ϩ cardiac progenitor cells after therapy.…”

Disassociation Between Left Ventricular Mechanical and Electrical Properties in Ischemic Rat Heart After G-CSF Treatment

“…In recent years, G-CSF has been used for the repair of ischemic myocardium in both animal models and clinically. G-CSF mobilized progenitor cells can promote tissue differentiation and regeneration in infarcted hearts [2]. Furthermore, G-CSF can activate multiple signaling pathways in cardiac myocytes, and prevent left ventricular (LV) remodeling after myocardial infarction (MI) by decreasing cardiomyocyte death [3] and increasing the number of blood vessels [4], suggesting a direct action of G-CSF on the myocardium.…”

“…However, in cases of a large infarction or excessive host inflammatory response, sustained cytokine upregulation or a second wave of cytokine upregulation can occur, which corresponds to the chronic remodeling phase. As such, we administered G-CSF at either 60 min or 24 h post-MI to examine whether the actions of G-CSF on cardiac recovery were via direct (i.e., on signaling pathways [1,2]) or paracrine or mobilization [3] effects. …”

Activation of Vasculogenic Progenitor Cells by ent-16.ALPHA.,17-Dihydroxy-kauran-19-oic Acid

“…9) In addition, the mobilization of VPCs was increased by a granulocyte-colony stimulating factor and granulocyte monocyte-colony stimulating factor, and circulating VPCs were significantly increased. 8,[12][13][14] Even though the mobilization and activation of VPCs is a new strategy for the treatment of ischemic diseases, the characterization and development of a new agent that will stimulate/activate VPCs and enhance their regenerative potential is still in the early stages. Thus, the present study attempted to isolate a VPC activating agent from natural products and identify its mechanism of action.…”