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However, the mechanisms triggered by L\u2010PDT on the tumor vasculature are still debated. In pericyte and endothelial cell co\u2010cultures, we show that pericytes exhibit enhanced sensitivity towards L\u2010PDT compared to endothelial cells, displaying actin stress fibers and cellular contraction via Rho\/ROCK kinase signaling myosin light chain and focal adhesion kinase phosphorylation (MLC\u2010P, FAK\u2010P). We then confirm, in two separate MPM models, in mice the phosphorylation of the MLC in pericytes specifically following L\u2010PDT. Furthermore, while L\u2010PDT does not affect tumor vascular density or diameter, we show that it enhances tumor vascular pericyte coverage, leads to a drop in tumor interstitial fluid pressure and enhances the transport of FITC\u2010dextran throughout tumors. In conclusion, L\u2010PDT has the potential to stabilize the tumor vascular bed which improves vascular transport. The mechanism described in the present study may help translate and optimize this approach in patients. Lasers Surg. 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