| First Author | Tripathi A | Year | 2007 |
| Journal | Mol Immunol | Volume | 44 |
| Issue | 12 | Pages | 3185-94 |
| PubMed ID | 17336385 | Mgi Jnum | J:120814 |
| Mgi Id | MGI:3708041 | Doi | 10.1016/j.molimm.2007.01.024 |
| Citation | Tripathi A, et al. (2007) Production of nitric oxide by murine peritoneal macrophages in vitro on treatment with prolactin and growth hormone: Involvement of protein tyrosine kinases, Ca(++), and MAP kinase signal transduction pathways. Mol Immunol 44(12):3185-94 |
| abstractText | Prolactin (PRL) and growth hormone (GH) (somatotropin) have been known to possess immunomodulatory properties. In the present studies we have investigated the production of nitric oxide (NO) and TNF-alpha by murine peritoneal macrophages in vitro on treatment with PRL and GH and the signal transduction mechanism involved. It is observed that significantly enhanced production of NO is induced in macrophages on treatment with PRL and GH. It is further observed that protein tyrosine kinases, MAP kinases and Ca(++) channeling are involved in NO production by macrophages on in vitro treatment with PRL and GH. GH and PRL induced nitric oxide did not have any effect on the expression and production of TNF-alpha. PRL or GH induced TNF-alpha production by murine macrophages was insensitive in the presence of competitive inhibitor of NOS, l-NMMA. Similarly, there is no autocrine or paracrine effect of TNF-alpha on GH or PRL induced NO production and iNOS expression. |
