Figure 7.

VT-dependent skin IR protection is associated with decreased inflammatory and enhanced wound healing processes. (A) In healthy quiescent tissues, Tie2 is found mainly on the microvascular endothelial cell membrane. (B) Following irradiation, neutrophil recruitment and cytokine production are evoked and erythema develops. Subclinical tissue damage builds and manifests as skin desquamation. When the broken skin attempts to repair, the wound’s granulation tissue angiogenesis may be impaired during wound healing. (C) Continuous VT treatment’s net effect on inflammation on the level of hemodynamics and neutrophil recruitment is a dampening one (lower degree of erythema and neutrophil presence), although how this is achieved beyond decreased MIP-2 levels on the grander scale of the cytokine network (taking into account elevated IL-6, for example) is uncertain. It is also unclear whether the dampened inflammation is from a radioprotective, radiomitigative, or a combinational effect. VT may render radioprotection partially through endothelial cell protection in irradiated skin, but the benefits may be delayed, manifesting only at the time of wound healing through increased clonogenic viability and angiogenic capacity, rather than during subclinical damage. Ultimately, VT treatment reduces the severity of normal tissue radiation damage.