Objective. To determine the presence of mesenchymal progenitor cells (MPCs) in human articular cartilage.Methods. Primary cell cultures established from normal and osteoarthritic (OA) human knee articular cartilage were analyzed for the expression of CD105 and CD166, cell surface markers whose coexpression defines mesenchymal stem cells (MSCs) in bone marrow and perichondrium. The potential of cartilage cells to differentiate to adipogenic, osteogenic, and chondrogenic lineages was analyzed after immunomagnetic selection for CD105؉/CD166؉ cells and was compared with bone marrow-derived MSCs (BM-MSCs).Results. Up to 95% of isolated cartilage cells were CD105؉ and ϳ5% were CD166؉. Conclusion. These findings indicate that multipotential MPCs are present in adult human articular cartilage and that their frequency is increased in OA cartilage. This observation has implications for understanding the intrinsic repair capacity of articular cartilage and raises the possibility that these progenitor cells might be involved in the pathogenesis of arthritis.

Expression of group IIA secretory phospholipase A 2 (sPLA 2 -IIA) is documented in the cerebral cortex (CTX) after ischemia, suggesting that sPLA 2 -IIA is associated with neurodegeneration. However, how sPLA 2 -IIA is involved in the neurodegeneration remains obscure. To clarify the pathologic role of sPLA 2 -IIA, we examined its neurotoxicity in rats that had the middle cerebral artery occluded and in primary cultures of cortical neurons. After occlusion, sPLA 2 activity was increased in the CTX. An sPLA 2 inhibitor, indoxam, significantly ameliorated not only the elevated activity of the sPLA 2 but also the neurodegeneration in the CTX. The neuroprotective effect of indoxam was observed even when it was administered after occlusion. In primary cultures, sPLA 2 -IIA caused marked neuronal cell death. Morphologic and ultrastructural characteristics of neuronal cell death by sPLA 2 -IIA were apoptotic, as evidenced by condensed chromatin and fragmented DNA. Before apoptosis, sPLA 2 -IIA liberated arachidonic acid (AA) and generated prostaglandin D 2 (PGD 2 ), an AA metabolite, from neurons. Indoxam significantly suppressed not only AA release, but also PGD 2 generation. Indoxam prevented neurons from sPLA 2 -IIA-induced neuronal cell death. The neuroprotective effect of indoxam was observed even when it was administered after sPLA 2 -IIA treatment. Furthermore, a cyclooxygenase-2 inhibitor significantly prevented neurons from sPLA 2 -IIA-induced PGD 2 generation and neuronal cell death. In conclusion, sPLA 2 -IIA induces neuronal cell death via apoptosis, which might be associated with AA metabolites, especially PGD 2 . Furthermore, sPLA 2 contributes to neurodegeneration in the ischemic brain, highlighting the therapeutic potential of sPLA 2 -IIA inhibitors for stroke.

The 29-kDa amino-terminal fibronectin fragment (FN-f) has a potent chondrolytic effect and is thought to be involved in cartilage degradation in arthritis. However, little is known about signal transduction pathways that are activated by FN-f. Here we demonstrated that

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