fig3

Understanding how MSCs reverse radiation-induced fibrosis: HGF <i>vs.</i> TGF-B1

Figure 3. (A) “Target cell” mechanism of injury. Ionizing Radiation damages nuclear cell DNA. The cell responds by repairing itself successfully, whereas a faulty repair can result in survival with an unstable genome or apoptosis; (B) RIBE (radiation induced bystander effect)- Ionizing radiation damages any portion of the cell which can then release molecular compounds (DAMPS- damage associated macromolecular patterns) that act as “danger signals” to neighboring cells. These compounds may even cause chromatin changes in adjacent non-irradiated cells. The bystander cell responds by repairing itself successfully, whereas a faulty repair can result in survival with an unstable genome or apoptosis; (C) Ionizing radiation liberates matrix-embedded cytokines (TGF-β) that can then influence surrounding cells. Bystander cell behavior may then be “reprogrammed” by active TGF-β into undergoing apoptosis, EMT (epithelial to mesenchymal transformation), or mitotic arrest of the cell cycle at the G1 phase.

Plastic and Aesthetic Research
ISSN 2349-6150 (Online)   2347-9264 (Print)

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