ABSTRACT. This study aimed to investigate the effects of mitochondrial ATP-sensitive potassium (MitoK ATP ) channel opening on the translocation of protein kinase C epsilon (PKCε). In addition, we aimed to determine the relationship between PKCε translocation and the production of reactive oxygen species (ROS). PKCε protein expression in cultured adult rat ventricular myocytes was investigated by immunofluorescence and Western blotting. Diazoxide (DZ), a selective MitoK ATP channel activator, caused a significant translocation to myofibrillar-like structures in cultured adult rat ventricular myocytes. N-2-Mercaptopropionylglycine, a free radical scavenger, could partially inhibit the translocation of PKCε induced by DZ. By contrast, chelerythrine, a selective PKC inhibitor, could completely block the translocation of PKCε induced by DZ. The opening of MitoK ATP channels might activate and cause PKCε to translocate into myofibrillar-like structures. PKCε activation occurred downstream of the MitoK ATP channel, possibly as a result of ROS production that 4517 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 13 (2): 4516-4522 (2014) MitoK ATP channels and PKCε translocation occurred after the MitoK ATP channels opened.

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Introduction Degenerative disc disease (DDD) is a prevalent musculoskeletal disorder and is the major cause of low back pain. But our comprehension about development of the intervertebral disc (IVD) and pathogenesis of disc degeneration is unclear, which is an obstacle for appropriate therapies. Materials and Methods Recently, some reports identified stem/progenitor cells within particular IVD niches and cartilage endplate. These cells together with mesenchymal stem cells are recruited to nucleus pulposus (NP) and annulus fibrosus (AF) to generate regenerative functions in a healthy IVD. The possibility of stimulating these stem cells holds promise for future therapy for DDD. But factors which recruit stem cells to NP and AF are unknown. There are increasing evidences that N-acetylated proline-glycine-proline (N-AC-PGP), which is a degradation fragment of collagen, plays an important role in inflammatory cell recruitment. But whether it presents in IVD and whether it is a chemokine of stem cell have remained elusive. Results In this study, we demonstrated the presence of N-AC-PGP in IVD and found the correlation between its content in IVD and degeneration grade of IVD. Then we described the generation pathway of N-AC-PGP in IVD. At last, we demonstrated that N-AC-PGP can recruit cartilage endplate stem cells (CESC) by binding with CXC receptors 2 on CESC. Conclusion These findings reveal a possible regeneration mechanism in IVD, which depends on the chemotaxis of N-AC-PGP for CESC and indicate a new therapy by using N-AC-PGP to stimulate stem cells in IVD. Disclosure of Interest None declared