## Abstract Since NO production by NOS‐2 made by astrocytes activated by proinflammatory cytokines contributes to the killing of neurons in variously damaged human brains, knowing the mechanisms responsible for NOS‐2 expression should contribute to developing effective therapeutics. The expression
Nitric oxide synthase: expression of the endothelial, Ca2+/calmodulin-dependent isoform in human B and T lymphocytes
✍ Scribed by Norbert Reiling; Rolf Kröncke; Artur J. Ulmer; Johannes Gerdes; Hans-Dieter Flad; Sunna Hauschildt
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 660 KB
- Volume
- 26
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
✦ Synopsis
Nitric oxide (NO) is a pleiotropic mediator of a variety of cellular processes such as vasorelaxation, neurotransmission, and cytotoxicity. We studied the expression of the human endothelial, CaZ+/calmodulin-dependent NO synthase (NOS) isoform (ecNOS) in highly purified human lymphocytes from peripheral blood and tonsillar tissue. ecNOS mRNA was detected in IgD' or IgD-B cells, peripheral blood and tonsillar T cells. Upon stimulation, ecNOS mRNA expression decreased in all these lymphocyte subpopulations. Germinal center T cells and follicular dendritic cells did not express ecNOS mRNA either in an unstimulated or in a stimulated state. ecNOS expression by human lymphocytes was further substantiated by its mRNA detection in lymphoid cell lines such as Raji, Daudi, and Jurkat. By the use of a specific monoclonal antibody, ecNOS was shown to be present in T cells from peripheral blood and in various germinal center cells of frozen tonsillar sections. These data are the first to demonstrate the expression of the endothelial ecNOS at mRNA and protein level in human lymphocytes.
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