Exposure of cultured rat mesangial cells to ET-1 increased preproET-1 mRNA expression to 465% of control values (p<0.01), an effect mediated by the ETB receptor subtype.
In rat mesangial cells, autoinduction of ET-1 occurs through the ETB receptor subtype via increases in both preproET-1 transcription and mRNA stability.
p-value: p=<0.01
Autoinduction of endothelin-1 (ET-1) has been suggested to be involved in the profound and long-lasting effects of ET-1. We examined mechanisms that underlie autoinduction of ET-1 in cultured rat glomerular mesangial cells. Incubation of mesangial cells with ET-1 resulted in an immediate and dose-dependent stimulation of preproET-1 mRNA expression as assessed by polymerase chain reaction coupled with reverse transcription. Within 1 h of exposure to ET-1 (10(-7) M), preproET-1 mRNA expression was increased to a maximal level of 465 +/- 43% of the control value (p 10(-9) M abolished ET-1 stimulation of preproET-1 mRNA (p < 0.001), whereas an ETA-specific antagonist, BQ123, was without effects (up to 10(-5) M). The ETB agonist, sarafotoxin S6c (10(-7) M), significantly stimulated preproET-1 mRNA expression to 201 +/- 14% above controls (p < 0.01), and effect that was lessened significantly by RES701-1 (p < 0.05). RES701-1 abolished the ET-1-induced production of the ET-1 peptide (p < 0.001). Taken together, we demonstrates that in mesangial cells, autoinduction of ET-1 occurs through the ETB receptor subtype via increases in both preproET-1 transcription and mRNA stability.
Iwasaki et al. (Wed,) reported a other. Endothelin-1 (ET-1) vs. Control (non-stimulated cells) was evaluated on preproET-1 mRNA expression (p=<0.01). Exposure of cultured rat mesangial cells to ET-1 increased preproET-1 mRNA expression to 465% of control values (p<0.01), an effect mediated by the ETB receptor subtype.