Angiogenesis as a Survival Mechanism in Heartworm Disease: The Role of Fructose-Bisphosphate Aldolase and Actin from Dirofilaria immitis in an In Vitro Endothelial Model

Angiogenesis as a Survival Mechanism in Heartworm Disease: The Role of Fructose-Bisphosphate Aldolase and Actin from Dirofilaria immitis in an In Vitro Endothelial Model

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Heartworm disease, caused by Dirofilaria immitis, is a vector-borne zoonotic disease, (mainly affecting canids and felids) causing chronic vascular and pulmonary pathology in its early stages, which worsens with parasite load and/or death of adult worms in the pulmonary artery or right heart cavity, and can be fatal to the host.Angiogenesis is a mechanism by which new blood vessels are formed from existing ones.The aim of this work was to study the effect of two molecules of the D.immitis excretory/secretory antigen (DiES) on the angiogenic process, taking Ball - Glove First Base - Junior into account that this antigen is able to interact with this process and use it as a survival mechanism.

For this purpose, an in vitro model of endothelial cells was used and treated with two recombinant proteins, i.e., actin (Act) and fructose-bisphosphate aldolase (FBAL) proteins belonging to DiES, and both pro- and antiangiogenic molecules were analyzed, as well as the cellular processes of cell proliferation, migration, and pseudocapillary formation.Act and FBAL proteins, together with vascular endothelial growth factor (VEGF-A), as an angiogenic precursor, are able to stimulate the production of proangiogenic factors as well as cellular processes of proliferation, migration, and pseudocapillary 8 Piece Modular Sectional formation.

This implies that these molecules could be produced by D.immitis to facilitate its survival, and the relationship between parasite and canine host would be further elaborated.