Dysregulation of the Nadase CD38 impairs articular chondrocyte homeostasis

Deletion of IFT80 Impairs Epiphyseal and Articular Cartilage Formation Due to Disruption of Chondrocyte Differentiation

Intraflagellar transport proteins (IFT) play important roles in cilia formation and organ development. Partial loss of IFT80 function leads Jeune asphyxiating thoracic dystrophy (JATD) or short-rib polydactyly (SRP) syndrome type III, displaying narrow thoracic cavity and multiple cartilage anomalies. However, it is unknown how IFT80 regulates cartilage formation. To define the role and mechani...

Articular chondrocyte network mediated by gap junctions: role in metabolic cartilage homeostasis.

OBJECTIVE This study investigated whether chondrocytes within the cartilage matrix have the capacity to communicate through intercellular connections mediated by voltage-gated gap junction (GJ) channels. METHODS Frozen cartilage samples were used for immunofluorescence and immunohistochemistry assays. Samples were embedded in cacodylate buffer before dehydration for scanning electron microsco...

Design, synthesis and SAR studies of NAD analogues as potent inhibitors towards CD38 NADase.

Nicotinamide adenine dinucleotide (NAD), one of the most important coenzymes in the cells, is a substrate of the signaling enzyme CD38, by which NAD is converted to a second messenger, cyclic ADP-ribose, which releases calcium from intracellular calcium stores. Starting with 2'-deoxy-2'-fluoroarabinosyl-β-nicotinamide adenine dinucleotide (ara-F NAD), a series of NAD analogues were synthesized ...

Articular Chondrocyte Mechanics at Different Loading Rates

INTRODUCTION Mechanical impact loading is known to cause cell death and to lead to the onset and progression of osteoarthritis [1]. In order to understand why in-situ cells die readily following impact loading but remain unaffected when the same load is applied at a slow rate, we used a Finite Element model of articular cartilage and chondrocytes to study the in-situ cell mechanics, which canno...

Chondrocyte multiplication in osteoarthritic articular cartilage.