A paper from Emanuela Tolosano’s lab in collaboration with Silvio Aime’s group described a new method to measure iron absorption in mice.

The  study of iron metabolism is essential in nutritional sciences as iron deficiency represents a serious health problem worldwide. The mouse is utilized as a unique and powerful model for the identification and characterization of genes involved in iron metabolism and for the study of iron disorders. Thus, sophisticated and sensitive techniques have been developed to study iron metabolism in this animal model. In this work, V. Fiorito and S. Geninatti Crich developed a method to measure iron absorption in mice using inductively coupled plasma mass spectrometry (ICP-MS) to detect ⁵⁷Fe in tissues after its oral administration. This represents a sensitive, safe, and reliable alternative to radioisotope-based methods. 

A paper from Silvia Deaglio’s lab describes a novel autocrine loop that creates   favorable microenvironmental conditions for growth and survival of chronic  lymphocytic leukemia (CLL) cells.

Recent studies have shown that the tumor microenvironment is marked by increased levels of extracellular ATP, as well as by upregulation of the ecto-enzymes that metabolize it. The final consequence is an increase in local concentrations of adenosine (ADO), a powerful cytoprotective molecule with immunosuppressive effects. In this study, Serra and colleagues show that a subset of chronic lymphocytic leukemia (CLL) patients express both CD39 and CD73, the two enzymes that catalyze production of ADO from ATP. In the lymph node compartment, CD39+/CD73+ cells display a para-immunoblast morphology and are confined to CLL proliferation centers and to perivascular areas, where recirculation to and from lymphoid organs occurs. As expected, CD39+/CD73+ CLL cells catalyze the conversion of ATP to ADO. Once released in the extracellular milieu, ADO activates purinergic A2A receptors, highly expressed by resting and proliferating CLL cells. Activation of ADO receptors increases cytoplasmic cAMP levels, inhibiting chemotaxis and limiting spontaneous and/or drug-induced apoptosis of CLL cells. These data are consistent with the existence of an autocrine adenosinergic loop, which supports engraftment of leukemic cells in growth-favorable niches, while simultaneously protecting from the action of chemotherapeutic agents.

A paper from Giovanni Camussi and Benedetta Bussolati’s lab described the cystogenic potential of CD133+ progenitor cells of human polycystic kidneys.

In autosomal dominant polycystic kidney disease, cysts arise focally and disrupt normal renal tissue leading to renal failure. In this paper, Raquel Carvalhosa shows that cyst-lining cells express the stem cell marker CD133. CD133+ progenitor cells isolated from polycystic kidney, carrying mutations of PKD genes, showed a dedifferentiated phenotype similar to CD133+ progenitor cells from normal kidney, previously described in the lab. However, these cells were more proliferative and presented a defective epithelial differentiation phenotype with respect to normal renal CD133+ cells as they were not able to express all tubular epithelial cell markers when cultured in epithelial differentiation medium. Polycystic CD133+ cells, in contrast to normal renal CD133+ cells, formed cysts in vitro in a three-dimensional culture system and in vivo when injected subcutaneously within Matrigel in SCID mice. These results indicate that polycystic CD133+ cells retain a dedifferentiated phenotype and the ability to generate cysts.