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3 results on '"Niederberger E"'

1. Inhibitor kappa B kinase Beta dependent cytokine upregulation in nociceptive neurons contributes to nociceptive hypersensitivity after sciatic nerve injury.

Author

Kanngiesser M, Häussler A, Myrczek T, Küsener N, Lim HY, Geisslinger G, Niederberger E, and Tegeder I

Abstract

Inhibitor kappa B kinase (IKK)-mediated nuclear factor-kappa B (NF-[kappa]B) activation is a major pathway for transcriptional control of various pro-inflammatory factors. We here assessed whether activation of this pathway specifically in primary nociceptive neurons of the dorsal root ganglia (DRG) contributes to the development of nociceptive hypersensitivity. Mice carrying a cre-loxP-mediated deletion of inhibitor kappa B kinase beta (IKK[beta]) in DRG neurons were protected from nerve injury-evoked allodynia and hyperalgesia. This effect was mimicked by systemic treatment with an IKK[beta] inhibitor but was not observed upon specific inhibition of IKK[beta] in the spinal cord, suggesting a specific role of IKK[beta] in the peripheral neurons. The deletion of IKK[beta] in DRG neurons did not affect constitutive neuronal NF-[kappa]B activity, but reduced nerve injury-evoked NF-[kappa]B stimulation in the DRG and was associated with reduced upregulation of interleukin-16, monocyte chemoattractant protein-1/chemokine (CC motif) ligand 2 (MCP-1/CCL2), and tumor necrosis factor alpha (TNF[alpha]) in the DRG. These cytokines evoked a rapid rise of intracellular calcium in subsets of primary DRG neurons. The results suggest that IKK[beta]-mediated NF-[kappa]B stimulation in injured primary sensory neurons promotes cytokine and chemokine production and contributes thereby to the development of chronic pain. PERSPECTIVE: Inhibitors of IKK that do not pass the blood-brain barrier and act only in the periphery might be useful for reduction of the pro-inflammatory response in peripheral DRG neurons and reduce thereby nerve injury-evoked pain without affecting neuroprotective effects of NF-[kappa]B in the central nervous system. [ABSTRACT FROM AUTHOR]

Published
2012

2. The Non-Canonical IκB Kinases IKK and TBK1 as Potential Targets for the Development of Novel Therapeutic Drugs

Author

Niederberger, E., V. Moser, C., L. Kynast, K., and Geisslinger, G.

Abstract

IκB kinase epsilon (IKK) and TANK-binding kinase 1 (TBK1) are two non-canonical IKKs which are involved in interferon regulatory factor (IRF) as well as nuclear factor kappaB (NF-κB) signaling cascades. Both kinases have already been linked to the pathophysiology of several diseases and therefore been suggested as potential promising targets for the development of therapeutic drugs. In this review, we summarize the roles of IKK and TBK1 in different diseases and outline therapeutic options for modulation of these kinases.

Published
2013

3. Maillard Reaction Products Modulating the Growth of Human Tumor Cells in Vitro

Author

Marko, D., Habermeyer, M., Kemeny, M., Weyand, U., Niederberger, E., Frank, O., and Hofmann, T.

Abstract

We investigated the effect of a series of Maillard reaction products formed from carbohydrates under household heating conditions on the growth of human tumor cells in vitro. 4-Hydroxy-5-methyl-3-(2H)-furanone (1) was found to potently enhance the proliferation of human tumor cells. In contrast, the Maillard-type chromophores 2-(2-furyl)methylidene-4-hydroxy-5-methyl-2H-furan-3-one (2), 4-(2-furyl)-7-[(2-furyl)methylidene]-2-hydroxy-2H,7H,8aH-pyrano[2,3-b]pyran-3-one (6), and 3-hydroxy-4[(E)-(2-furyl)methylidene]methyl-3-cyclopentene-1,2 dione (13) inhibited the growth of human tumor cells in vitro in the low micromolar range. GXF251L cells (gastric carcinoma), synchronized by serum deprivation, were retained in the G1-phase of the cell cycle after treatment with 2, 6, or 13 for 24 h. Concomitantly, a distinct sub-G1 peak was observed, indicative for apoptosis induction. DNA fragmentation was further investigated by ELISA using antibodies raised against histones and DNA. 2 induced a significant increase of fragmented DNA at concentrations ≥30 μM. After treatment with compound 6, DNA fragmentation was observed at a higher concentration range (≥50 μM), whereas incubation with 13 resulted in a marked DNA fragmentation already at 20 μM. On the protein level, the activation of caspase 3, as an early marker for apoptosis induction, was determined. The results were almost identical to those obtained in the DNA fragmentation ELISA. In summary, Maillard reaction products potently modulating the growth of human tumor cells were identified. The Maillard-type chromophores 2, 6, and 13 were found to interfere with the proliferation of gastric carcinoma cells, causing cell cycle arrest and apoptosis induction.

Published
2003

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