Giemsa's stain changes melanin from brown to green. Path499-SuppFigLegends.docWord document, 33 KBįigure S1. Copyright © 2017 Pathological Society of Great Britain and Ireland. This PGD 2 acts as a negative regulator of the tumorigenic changes in tumor ECs. These observations suggest that tumor cell-derived inflammatory cytokines increase L-PGDS expression and subsequent PGD 2 production in the tumor ECs. Morphological and in vivo studies showed that endothelial L-PGDS deficiency resulted in functional changes of tumor ECs such as accelerated vascular hyperpermeability, angiogenesis, and endothelial-to-mesenchymal transition (EndMT) in tumors, which in turn reduced tumor cell apoptosis. Systemic or EC-specific deficiency of L-PGDS accelerated the growth of melanoma in mice, whereas treatment with an agonist of the PGD 2 receptor, DP1 (BW245C, 0.1 mg/kg, injected intraperitoneally twice daily), attenuated it.
We also investigated the contribution of L-PGDS–PGD 2 to tumor growth and vascularization.
In vitro experiments showed that stimulation with tumor cell-derived IL-1 and TNF-α increased L-PGDS mRNA expression and its product prostaglandin D 2 (PGD 2) in human normal ECs. In situ hybridization also showed L-PGDS (PTGDS) mRNA expression in the ECs of human melanoma and oral squamous cell carcinoma. Immunostaining of mouse melanoma revealed expression of L-PGDS protein in the ECs. Here, we found a marked increase in lipocalin-type prostaglandin D synthase (L-PGDS) mRNA ( Ptgds) expression in ECs isolated from mouse melanoma. They have abnormal characteristics compared to the ECs in normal tissues. Endothelial cells (ECs) are a key component of the tumor microenvironment.
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