Jens Wolff

Publications (2)15.07 Total impact

• Article: Endotoxin-induced gene expression differences in the brain and effects of iNOS inhibition and norepinephrine.

  Stephanie Wolff, Sabine Klatt, Jens C Wolff, Jochen Wilhelm, Ludger Fink, Manfred Kaps, Bernhard Rosengarten
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  ABSTRACT: We studied gene expression differences in brain homogenate, hippocampus, somatosensory cortex and cerebellum of rats suffering from sepsis-associated delirium and analyzed the effects of norepinephrine and 1,400 W (specific inhibitor of the inducible nitric-oxide synthase). We applied microarray screenings to rat brain homogenate 1, 3 and 4.5 h after lipopolysaccharide (LPS, 5 mg/kg) or 0.9% NaCl treatment. Therapy groups were analyzed after 4.5 h. Validations and compartment specific investigations were carried out by real-time PCR. Most striking gene expression differences were seen 4.5 h after LPS administration, especially within the hippocampus (chemokines and endothelial cell-specific molecule 1). Norepinephrine resulted in a discrete chemokine up-regulation, while 1,400 W had hardly any effect. Strongest gene regulations were found within the hippocampus. Norepinephrine showed a tendency of having a proinflammatory influence, while 1,400 W had no clear-cut effect onto the gene expression level.
  European Journal of Intensive Care Medicine 02/2009; 35(4):730-9. · 5.17 Impact Factor
• Article: Lack of NB1 GP (CD177/HNA-2a) gene transcription in NB1 GP- neutrophils from NB1 GP-expressing individuals and association of low expression with NB1 gene polymorphisms.

  Jens Wolff, Cornelia Brendel, Ludger Fink, Rainer M Bohle, Karin Kissel, Juergen Bux
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  ABSTRACT: The human neutrophil NB1 glycoprotein (NB1 GP, HNA-2a, CD177) has gained clinical importance for being involved in pulmonary transfusion reactions and immune neutropenias. The NB1 GP shows the unique feature of being expressed only on a neutrophil subpopulation. Recently, we identified splicing defects responsible for an NB1 GP deficiency. In this study, we have investigated the molecular basis of the heterogeneous expression of NB1 GP by separating the 2 neutrophil subpopulations using immunofluorescence followed by single-cell picking or by fluorescence-activated cell sorter. We found a lack of NB1 mRNA in the NB1 GP- cells that remained constant even after granulocyte colony-stimulating factor (G-CSF) administration. Comparing the cDNA sequences of donors with a large (> 60%) and those with a small (< 40%) NB1 GP-expressing subpopulation, we found 6 polymorphisms. Of the 6, 3 were significantly associated with a small NB1 GP-expressing subpopulation, indicating a genetic basis for NB1 GP nonexpression.
  Blood 07/2003; 102(2):731-3. · 9.90 Impact Factor