Matrix Metalloproteinases and Tissue Inhibitors of Metalloproteinases in Echinoderms: Structure and Possible Functions.

Echinoderms are one of the most ancient groups of invertebrates. The study of their genomes has made it possible to conclude that these animals have a wide variety of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). The phylogenetic analysis shows that the MMPs and TIMPs underwent repeated duplication and active divergence after the separation of Ambulacraria (Echinodermata+Hemichordata) from the Chordata.

Tumor-Associated Macrophages as Potential Targets for Anti-Cancer Activity of Marine Invertebrate-Derived Compounds.

Tumor-associated macrophages (TAMs) are M2 phenotype dominant and promote tumor growth and metastasis. The new cancer treatment strategy includes TAM targeting and is aimed primarily at reprogramming TAMs toward the M1 phenotype or reducing the number and activity of M2 macrophages. Several marine invertebrate-derived drugs, combining efficacy and a low level of side effects, were approved for use in the cancer therapy.

Different Macrophage Type Triggering as Target of the Action of Biologically Active Substances from Marine Invertebrates.

Macrophages play a fundamental role in the immune system. Depending on the microenvironment stimuli, macrophages can acquire distinct phenotypes characterized with different sets of the markers of their functional activities. Polarization of macrophages towards M1 type (classical activation) is involved in inflammation and the related progression of diseases, while, in contrast, alternatively activated M2 macrophages are associated with the anti-inflammatory mechanisms.

[Apoptosis-modulating effect of prostaglandin E2 in coelomocytes of holothurian Eupentacta fraudatrix depends on the cell antioxidant enzyme status].

The effects of prostaglandin PGE2 on apoptosis and antioxidant enzyme activities were studied in two coelomocyte fractions of holothurian Eupentacta fraudatrix in vitro and in vivo. PGE2 (10(-8) - 10(-6) M) modulated apoptosis in a time- and concentration-dependent manner in both fractions studied in vitro. In vivo, PGE2 induced apoptosis at concentrations of 0.