The role of mitochondria in direct cell-to-cell connection dependent rescue of postischemic cardiomyoblasts

Pretreatment of therapeutic cells with poly(ADP-ribose) polymerase inhibitor enhances their efficacy in an in vitro model of cell-based therapy in myocardial infarct

“…Imaging a real myocardial infarct it may mean that areas with bigger oxidative damage could also be saved with such pretreated therapeutic cells. Regarding the exact mechanism of the therapeutic cells we assume based on our earlier observations (9,33) and on the results of others (8,36), that this beneficial effect could be related partly to cell-to-cell connections and partly to paracrine factors released from the therapeutic cells.…”

“…Another concern could be the fact that we used H9c2 cells as therapeutic cells. Our earlier experimental evidence showed that healthy H9c2 cells could save their oxidatively damaged neighbors from delayed death (33). Furthermore, since we obtained similar effectiveness with stem cells and H9c2 cells in that model, it reflects that multipotency of the grafted cells is not required for this type of rescue effect, widening the possible sources for cell therapy.…”

“…Based on our previous experiments (33), we used H9c2 cells as therapeutic cells which were added to the damaged cells 30 min after the start of simulated reperfusion and set a simulated ischemia so severe that the untreated therapeutic cells were not able to improve survival. The optimal time of simulated ischemia was set using time lapse video microscopy to follow the changes in the fluorescent intensity of calcein-AM/ethidium-homodimer-2 (EthD) viability staining (Fig.…”

Hyperacute Serum has Markedly Better Regenerative Efficacy than Platelet-Rich Plasma in a Human Bone Oxygen–Glucose Deprivation Model

“…Furthermore, bone samples were harvested from patients with end-stage OA, so the current results can reasonably be interpreted as relevant to OA. Avascular osteonecrosis or aseptic osteonecrosis is actually a bone infarction caused by bone loss after ischemia that eventually leads to severe OA, further supporting the pathogenic response to ischemia-like episodes as a suitable model for degenerative bone disease [50][51][52].…”

Bioenergetic-active materials enhance tissue regeneration by modulating cellular metabolic state

“…It has been suggested that engineering the modulation of oxidative metabolism to increase cellular ATP levels could help address the high energetic requirements associated with enhanced anabolic biosynthesis, mitosis, and migration involved in tissue repair/regeneration (5). Recent progress in cellular bioenergetics (CBE) has highlighted the potential of approaches that allow the delivery of bioenergy for therapeutic purposes (6)(7)(8)(9)(10); however, these applications only provide benefits in in vitro models or relatively thin superficial tissues such as skin when continuously administered. To date, a three-dimensional (3D) scaffold with long-term bioenergetics effects that can stimulate the repair of critical size defects in complex tissues such as bone remains elusive.…”