Yuji Yamanishi

TL;DR: It is found that activation of HIF-1alpha is essential for myeloid cell infiltration and activation in vivo through a mechanism independent of VEGF, and its direct regulation of survival and function in the inflammatory microenvironment is demonstrated.

TL;DR: The microdissection findings suggest that p53 mutations are induced in RA synovial tissues by inflammatory oxidative stress, and this process provides some of the mutant clones with a selective growth advantage.

TL;DR: Real-time PCR demonstrated that TGF-β significantly increased aggrecanase-1 gene expression in FLS, and aggreCanase-2 protein may be regulated by a post-translational mechanism in OA and RA ST, which can contribute to cartilage degradation in RA and OA.

TL;DR: Elucidation of gene mutations and detailed signal transduction pathways that are specific to RA as well as mechanisms of action of matrix-degrading enzymes may lead to development of a novel therapy for RA.

TL;DR: P53 expression occurs during inflammation and acts to suppress local inflammatory responses, and the loss of p53 function in synoviocytes or other cells in the joint because of dominant-negative mutations might contribute to invasion and destruction of the joint in this disease.