Biomedical subjects

L G Petersen

Publications and source records attributed to L G Petersen.

9 recordsLinked to original sources

PubMed2006

IL-1beta-induced pro-apoptotic signalling is facilitated by NCAM/FGF receptor signalling and inhibited by the C3d ligand in the INS-1E rat beta cell line.

AIMS/HYPOTHESIS: IL-1beta released from immune cells induces beta cell pro-apoptotic signalling via mitogen-activated protein kinases (MAPKs) and nuclear factor-kappaB (NF-kappaB). In neurons, the neural cell adhesion molecule (NCAM) signals to several elements involved in IL-1beta-induced pro-apoptotic signalling in beta cells. Pancreatic beta cells express NCAM, but its biological effects in these cells are unclear. The aim of this study was to investigate whether there is cross-talk between NCAM signalling and cytokine-induced pro-apoptotic signalling. MATERIALS AND METHODS: Western blotting was used to investigate levels of NCAM and inducible nitric oxide synthase, phosphorylation of Src and MAPKs, and cleavage of caspase-3. MAPK activity was investigated with an in vitro kinase assay. Apoptosis was detected by cleaved caspase-3 and a Cell Death Detection ELISA(plus) assay. NCAM-induced fibroblast growth factor receptor (FGFR) activation was investigated in NCAM(-/-) Trex293 cells where FGFR phosphorylation was measured by Western blotting after NCAM transfection. RESULTS: Pre-exposure of INS-1E cells to the FGFR-inhibitor SU5402, but not to the Src-inhibitor PP2, dose-dependently inhibited IL-1beta-mediated MAPK activity. A synthetic peptide, C3d, reported to bind NCAM, did not activate MAPK or Akt as reported in neurons but inhibited IL-1beta-induced MAPK activity, thereby mimicking the effect of SU5402. Furthermore, C3d inhibited NCAM-induced FGFR phosphorylation and apoptosis induced by IL-1beta plus IFN-gamma, but did not affect IL-1beta-induced NF-kappaB signalling. CONCLUSIONS/INTERPRETATION: We suggest that NCAM signalling through FGFR is required for efficient IL-1beta pro-apoptotic signalling by facilitating IL-1beta-induced MAPK activation downstream of the NF-kappaB-MAPK branching point. Further, these data identify a novel function of C3d as an inhibitor of NCAM-induced FGFR activity and of IL-1beta-induced MAPK activation in beta cells.

Animals↗

PubMed1998

The effect of musculus extensor digitorum brevis transfer for chronic lateral ankle instability.

Thirty-eight patients who had undergone surgery for instability of their ankles between 1980 and 1994 answered questionnaires regarding the results. In 32 of the 38 patients, clinical examinations were performed including practice on a balancing board, circle-running tests, and active and passive electromyographic measurements on the musculus extensor digitorum brevis (MEDB). The questionnaires showed that 90% of the patients with a median observation time of 9 years (range, 16 months-14 years) were content with the results of their operations, and the number of painful distortions of the ankle were reduced considerably in 96% of the patients. Within the group of active sportspersons with more than 4 hours of weekly exercise, 42% returned to their previous levels of sports activity. The tendency to have ankle pain disappeared in 90% of the patients. At the clinical examination, the time spent on the balancing board was reduced by 25% for the operated foot. When the patient ran in a circle with the operated leg toward the center, as compared with running with the nonoperated leg toward the center, the time was enhanced by 8%. We found electromyographic activity in the MEDB during active movement of the toes and with passive supination of the talocrural joint but not during passive pronation of the foot. The MEDB transfer procedure not only strengthens the lateral ligaments but also seems to add proprioceptive protection to the ankle to prevent distortions.

Adolescent↗

PubMed1994