EFFECT OF TRIIODOTHYRONINE ON NITRIC-OXIDE PRODUCTION IN MESANGIAL CELLS AND RENAL TUBULAR EPITHELIAL-CELLS

Citation
H. Trachtman et al., EFFECT OF TRIIODOTHYRONINE ON NITRIC-OXIDE PRODUCTION IN MESANGIAL CELLS AND RENAL TUBULAR EPITHELIAL-CELLS, Research communications in molecular pathology and pharmacology, 93(1), 1996, pp. 69-78
Citations number
29
Categorie Soggetti
Pharmacology & Pharmacy",Pathology,Biology
ISSN journal
10780297
Volume
93
Issue
1
Year of publication
1996
Pages
69 - 78
Database
ISI
SICI code
1078-0297(1996)93:1<69:EOTONP>2.0.ZU;2-O
Abstract
Nitric oxide (NO) is a signalling molecule that is produced by mesangi al cells and renal tubular epithelial (RTE) cells. It plays a role in the regulation of glomerular and tubular function. In renal cells, NO is synthesized by the inducible isoform of the enzyme nitric oxide syn thase (NOS). Thyroid hormone modulates the activity of neuronal NOS; t herefore, we examined whether triiodothyronine (T-3) stimulated the ac tivity of inducible iNOS in mesangial cells, LLC-PK1 cells (analogue o f the proximal tubule) and MDCK cells (analogue of the distal tubule). T-3 (concentration range: 10(-10) - 10(-7) M) had no effect on NO syn thesis or iNOS protein expression by the three renal cell types. In ad dition, T-3 did not modulate NO production in RAW 264.7 cells, a murin e macrophage cell line, confirming that the hormone had no effect on i NOS activity. We conclude that, unlike its effect on neuronal NOS, T-3 does not regulate iNOS activity in mesangial cells, RTE cells, or mac rophages. and that the effects of T-3 on renal cell growth and functio n are not mediated by inducible increases in NO synthesis.