Drs. Tania Rivera and Heather Tian awarded Japan College of Rheumatology Scholarships
Two fellows of the NYU Division of Rheumatology, Dr. Tania Rivera and Dr. Heather Tian, were awarded Japan College of Rheumatology Travel Scholarships. These prestigious awards supported their travel to the Japan College of Rheumatology annual meeting where they were invited to present their research. Dr. Rivera received the highest score for her abstract of any international fellow.
Autoimmune congenital heart block (CHB) occurs in children of anti-SSA/Ro-SSB/La-antibody-positive mothers. Previous studies suggested that the underlying mechanism of the disease is the fibrosis of the conduction system, and implicate hypoxia as an amplification factor. The role of the MMP2 in tissue remodeling and development of cardiac fibrosis has been studied in adults but never described in newborns. It has been reported that the transforming growth factor beta1 (TGFbeta1) induces secretion of MMP2 by fibroblasts during tissue regeneration. The aims of this study were to determine the levels of MMP2 and erythropoietin (as an indirect measurement of hypoxia) in cord bloods of children with autoimmune congenital heart block.
MMP2 is playing an important role in the development of autoimmune congenital heart block. The increase of MMP2 levels could reflect a response to injury, and could be involved in the pathological development of fibrosis in the fetal heart. These elevated levels are apparently not related to hypoxia.

The role of adenosine in anti-atherosclerosis has recently been investigated. We examined whether LXRs mediate the effect of adenosine on reverse cholesterol transport. LXRs are nuclear receptors that function as cholesterol sensors and play a central role in lipid homeostasis and anti-inflammation. In macrophages LXRs control the transcription of crucial genes in cholesterol efflux and its transport to the liver, including ABCA1. We found adenosine A2A receptor agonist inhibits foam cell formation and induce ABCA1 expression in human macrophage cell line.
The effects of adenosine on form cell formation and ABCA-1 expression were reversed in the presence of LXR antagonist. Our results suggest a mechanism for adenosine-mediated anti-atherosclerosis: Adenosine acts via LXRs to promote reverse cholesterol transport and abrogate foam cell formation. Crosstalk between LXRs and adenosine pathways may shed light on the regulation of inflammation and atherosclerosis.