Intense light as anticoagulant therapy in humans

Blood coagulation is central to myocardial ischemia and
reperfusion (IR) injury. Studies on the light elicited circadian rhythm protein
Period 2 (PER2) using whole body Per2-/- mice found deficient
platelet function and reduced clotting which would be
expected to protect from myocardial IR-injury. In contrast, intense light
induction of PER2 protected from myocardial IR-injury while Per2
deficiency was detrimental. Based on these conflicting data, we sought to
evaluate the role of platelet specific PER2 in coagulation and myocardial ischemia
and reperfusion injury. We demonstrated that platelets from mice with tissue-specific deletion
of Per2 in the megakaryocyte lineage (Per2loxP/loxP-PF4-CRE)
significantly clot faster than platelets from control mice. We further found
increases in infarct sizes or plasma troponin levels in Per2loxP/loxP-PF4-CRE
mice when compared to controls. As intense light increases PER2 protein in
human tissues, we also performed translational studies and tested the effects
of intense light therapy on coagulation in healthy human subjects. Our human
studies revealed that intense light therapy repressed procoagulant pathways in
human plasma samples and significantly reduced the clot rate. Based on these
results we conclude that intense light elicited PER2 has an inhibitory function
on platelet aggregation in mice. Further, we suggest intense light as a novel
therapy to prevent or treat clotting in a clinical setting.