TY  - JOUR
A1  - García-Fernández, Patricia
A1  - Reinhold, Colette
A1  - Üçeyler, Nurcan
A1  - Sommer, Claudia
T1  - Local inflammatory mediators involved in neuropathic pain
JF  - International Journal of Molecular Sciences
N2  - Polyneuropathy (PNP) is a term to describe diseases of the peripheral nervous system, 50% of which present with neuropathic pain. In some types of PNP, pain is restricted to the skin distally in the leg, suggesting a local regulatory process leading to pain. In this study, we proposed a pro-inflammatory pathway mediated by NF-κB that might be involved in the development of pain in patients with painful PNP. To test this hypothesis, we have collected nerve and skin samples from patients with different etiologies and levels of pain. We performed RT-qPCR to analyze the gene expression of the proposed inflammatory pathway components in sural nerve and in distal and proximal skin samples. In sural nerve, we showed a correlation of TLR4 and TNFα to neuropathic pain, and an upregulation of TNFα in patients with severe pain. Patients with an inflammatory PNP also presented a lower expression of TRPV1 and SIRT1. In distal skin, we found a reduced expression of TLR4 and miR-146-5p, in comparison to proximal skin. Our findings thus support our hypothesis of local inflammatory processes involved in pain in PNP, and further show disturbed anti-inflammatory pathways involving TRPV1 and SIRT1 in inflammatory PNP.
KW  - polyneuropathy
KW  - pain
KW  - inflammation
KW  - NF-κB
KW  - TNFα
Y1  - 2023
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-313613
SN  - 1422-0067
VL  - 24
IS  - 9
ER  - 
TY  - JOUR
A1  - Meierjohann, Svenja
T1  - Hypoxia independent drivers of melanoma angiogenesis
JF  - Frontiers in Oncology
N2  - Tumor angiogenesis is a process which is traditionally regarded as the tumor’s response to low nutrient supply occurring under hypoxic conditions. However, hypoxia is not a pre-requisite for angiogenesis. The fact that even single tumor cells or small tumor cell aggregates are capable of attracting blood vessels reveals the early metastatic capability of tumor cells. This review sheds light on the hypoxia-independent mechanisms of tumor angiogenesis in melanoma.
KW  - melanoma
KW  - angiogenesis
KW  - hypoxia-independent
KW  - reactive oxygen species
KW  - NF-κB
Y1  - 2015
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-125586
VL  - 5
IS  - 120
ER  - 
TY  - JOUR
A1  - Serfling, Edgar
A1  - Avots, Andris
A1  - Klein-Hessling, Stefan
A1  - Rudolf, Ronald
A1  - Vaeth, Martin
A1  - Berberich-Siebelt, Friederike
T1  - NFATc1/alphaA: The other Face of NFAT Factors in Lymphocytes
N2  - In effector T and B cells immune receptor signals induce within minutes a rise of intracellular Ca++, the activation of the phosphatase calcineurin and the translocation of NFAT transcription factors from cytosol to nucleus. In addition to this first wave of NFAT activation, in a second step the occurrence of NFATc1/αA, a short isoform of NFATc1, is strongly induced. Upon primary stimulation of lymphocytes the induction of NFATc1/αA takes place during the G1 phase of cell cycle. Due to an auto-regulatory feedback circuit high levels of NFATc1/αA are kept constant during persistent immune receptor stimulation. Contrary to NFATc2 and further NFATc proteins which dampen lymphocyte proliferation, induce anergy and enhance activation induced cell death (AICD), NFATc1/αA supports antigenmediated proliferation and protects lymphocytes against rapid AICD. Whereas high concentrations of NFATc1/αA can also lead to apoptosis, in collaboration with NF-κB-inducing co-stimulatory signals they support the survival of mature lymphocytes in late phases after their activation. However, if dysregulated, NFATc1/αA appears to contribute to lymphoma genesis and – as we assume – to further disorders of the lymphoid system. While the molecular details of NFATc1/αA action and its contribution to lymphoid disorders have to be investigated, NFATc1/αA differs in its generation and function markedly from all the other NFAT proteins which are expressed in lymphoid cells. Therefore, it represents a prime target for causal therapies of immune disorders in future.
KW  - Medizin
KW  - Activation induced cell death/AICD
KW  - Anergy
KW  - Apoptosis
KW  - Calcineurin
KW  - NFATc
KW  - NFATc1/αA
KW  - NF-κB
KW  - Proliferation
Y1  - 2012
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-75748
ER  -