|  Help  |  About  |  Contact Us

Publication : Nitric oxide synthase-2 and expression of perforin in uterine NK cells.

First Author  Burnett TG Year  2000
Journal  J Immunol Volume  164
Issue  10 Pages  5245-50
PubMed ID  10799885 Mgi Jnum  J:112258
Mgi Id  MGI:3655922 Doi  10.4049/jimmunol.164.10.5245
Citation  Burnett TG, et al. (2000) Nitric oxide synthase-2 and expression of perforin in uterine NK cells. J Immunol 164(10):5245-50
abstractText  In human, mouse, and rat pregnancy, maternal NK cells accumulate and differentiate at implantation sites. These cells, termed uterine NK (uNK) cells, express NO synthase (NOS)-2 and develop cytolytic molecules such as perforin and granzymes during differentiation in situ. In this study, relationships between expression of the NOS-2 gene, uNK cell population density and tissue distribution, and synthesis of perforin were investigated. Uteri from wild-type (WT) and NOS-2-/- mice were collected at gestation days (g.d.) 8, 10, 12, 14, and 16 (n, >2/g.d.). Histochemical staining failed to reveal any differences between the population densities or tissue distributions of uNK cells in WT and NOS-2-/- uteri at any stage of gestation. By contrast, immunohistochemical staining with anti-perforin Abs demonstrated significantly fewer perforin-positive uNK cells in two uterine compartments of NOS-2-/- mice in comparison to the same compartments in WT mouse uteri. Perforin-positive uNK cells were reduced in NOS-2-/- metrial glands at g.d. 8, 10, and 12 and in decidua basalis at g.d. 12 (p < 0.05). Analysis of perforin protein by immunoblotting confirmed this observation. Northern blot hybridization studies showed that loss of perforin protein in NOS-2-/- mice was accompanied by decreased steady-state levels of perforin mRNA. These results demonstrate that migration of uNK cells into the uterus, selection of residency sites, and proliferation in situ are independent of NOS-2. By contrast, their differentiation, including transcription and translation of the cytotoxic molecule perforin, was shown to rely on normal expression of the NOS-2 gene.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

2 Authors

3 Bio Entities

Trail: Publication

0 Expression