VIP treatment prevents embryo resorption by modulating efferocytosis and activation profile of maternal macrophages in the CBAxDBA resorption prone model.

Successful embryo implantation occurs followed by a local pro-inflammatory response subsequently shifted toward a tolerogenic one. VIP (vasoactive intestinal peptide) has embryotrofic, anti-inflammatory and tolerogenic effects. In this sense, we investigated whether the in vivo treatment with VIP contributes to an immunosuppressant local microenvironment associated with an improved pregnancy outcome in the CBA/J × DBA/2 resorption prone model.

Extracellular histones reduce survival and angiogenic responses of late outgrowth progenitor and mature endothelial cells.

Unlabelled: ESSENTIALS: Extracellular histones are highly augmented in sites of neovessel formation, such as regeneration tissues. We studied histone effect on survival and angiogenic activity of mature and progenitor endothelial cells. Extracellular histones trigger apoptosis and pyroptosis and reduce angiogenesis in vivo and in vitro.

Galectins in the regulation of platelet biology.

Platelets are anucleated blood cells derived from megakaryocytes, and although they are essential for proper hemostasis, their function extends to physiologic processes such as tissue repair, wound remodeling, and antimicrobial host defense, or pathologic conditions such as thrombosis, atherosclerosis, chronic inflammatory diseases, and cancer. Recently, we demonstrated that two structurally divergent members of the galectin family, galectin-1 and galectin-8, are potent platelet agonists. The emergence of galectins as soluble mediators capable of triggering platelet activation opens a new field of research that will provide further insights into the mechanisms linking inflammatory responses to thrombus formation and could expand our view of the role of platelets much beyond hemostasis to their pathophysiologic role during inflammation and cancer.

Acidic preconditioning improves the proangiogenic responses of endothelial colony forming cells.

Objective: Acidosis is present in several pathological conditions where vasculogenesis takes place including ischemia, tumor growth and wound healing. We have previously demonstrated that acidosis induces human CD34+ cell apoptosis. Considering that endothelial colony-forming cells (ECFC) are a subpopulation of CD34+ cells and key players in vasculogenesis, in the present study we investigated the effect of acidosis on the survival and functionality of ECFC.

Galectins: new agonists of platelet activation.

Platelet activation at sites of vascular injury leads to the formation of a hemostatic plug and is crucial for hemostasis. However, uncontrolled platelet activation may lead to the formation of occlusive thrombi. Several soluble or matricellular proteins can activate platelets.

Binding of galectin-1 to αIIbβ₃ integrin triggers "outside-in" signals, stimulates platelet activation, and controls primary hemostasis.

Understanding noncanonical mechanisms of platelet activation represents an important challenge for the identification of novel therapeutic targets in bleeding disorders, thrombosis, and cancer. We previously reported that galectin-1 (Gal-1), a β-galactoside-binding protein, triggers platelet activation in vitro. Here we investigated the molecular mechanisms underlying this function and the physiological relevance of endogenous Gal-1 in hemostasis.

Chemokine receptor CCR1 disruption limits renal damage in a murine model of hemolytic uremic syndrome.

Shiga toxin (Stx)-producing Escherichia coli is the main etiological agent that causes hemolytic uremic syndrome (HUS), a microangiopathic disease characterized by hemolytic anemia, thrombocytopenia, and acute renal failure. Although direct cytotoxic effects on endothelial cells by Stx are the primary pathogenic event, there is evidence that indicates the inflammatory response mediated by polymorphonuclear neutrophils and monocytes as the key event during HUS development. Because the chemokine receptor CCR1 participates in the pathogenesis of several renal diseases by orchestrating myeloid cell kidney infiltration, we specifically addressed the contribution of CCR1 in a murine model of HUS.