Abstract
Adrenalectomy leads to the decline in the levels of renal Na-K-adenosinetriphosphatase (Na-K-ATPase) α- and β-subunit protein and mRNA. Both α- and β-mRNA, however, return to the control level within 1 h after corticosterone administration. Whether or not glucocorticoid acts directly on a specific segment of nephron to upregulate Na-K-ATPase has not been determined. Studies were undertaken in an attempt to elucidate this problem. Using primary cultures of renal proximal tubules, we found that 24-h treatment with dexamethasone augmented Na-K-ATPase activity and induced coordinate increase of α- and β-protein and mRNA abundance dependent on the doses in the range of 10-8 to 10-6 M. We further demonstrated that 24-h incubation of dexamethasone (10-7 M) enhanced Na-K-ATPase activity by 58 ± 14%, α- and β-protein abundance by 70 ± 18 and 51 ± 10%, and α- and β-mRNA levels by 87 ± 12 and 62 ± 11%, respectively. The time course studies revealed that significant increase of Na-K-ATPase activity and α- and β-protein abundance was reached within 8 h, and enhancement of α- and β-mRNA abundance was reached within 4 h of dexamethasone treatment. Pretreatment of cultured proximal tubule cells with cycloheximide (20 μg/ml) completely inhibited dexamethasone-induced increase of Na-K-ATPase α- and β-mRNA. Our results indicate that dexamethasone upregulates Na-K-ATPase in proximal tubule cells via pretranslational mechanisms, which may be mediated by proteins.
| Original language | English |
|---|---|
| Journal | American Journal of Physiology - Renal Fluid and Electrolyte Physiology |
| Volume | 268 |
| Issue number | 5 37-5 |
| Publication status | Published - May 1995 |
| Externally published | Yes |
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Keywords
- Glucocorticoids
- Primary culture
- Proximal tubule
- Sodium-potassium-adenosinetriphosphatase
ASJC Scopus subject areas
- Physiology
- Agricultural and Biological Sciences(all)
Cite this
Glucocorticoid upregulates Na-K-ATPase α- and β-mRNA via an indirect mechanism in proximal tubule cell primary cultures. / Lee, Yi Chao; Lin, Hsi Hui; Tang, Ming Jer.
In: American Journal of Physiology - Renal Fluid and Electrolyte Physiology, Vol. 268, No. 5 37-5, 05.1995.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Glucocorticoid upregulates Na-K-ATPase α- and β-mRNA via an indirect mechanism in proximal tubule cell primary cultures
AU - Lee, Yi Chao
AU - Lin, Hsi Hui
AU - Tang, Ming Jer
PY - 1995/5
Y1 - 1995/5
N2 - Adrenalectomy leads to the decline in the levels of renal Na-K-adenosinetriphosphatase (Na-K-ATPase) α- and β-subunit protein and mRNA. Both α- and β-mRNA, however, return to the control level within 1 h after corticosterone administration. Whether or not glucocorticoid acts directly on a specific segment of nephron to upregulate Na-K-ATPase has not been determined. Studies were undertaken in an attempt to elucidate this problem. Using primary cultures of renal proximal tubules, we found that 24-h treatment with dexamethasone augmented Na-K-ATPase activity and induced coordinate increase of α- and β-protein and mRNA abundance dependent on the doses in the range of 10-8 to 10-6 M. We further demonstrated that 24-h incubation of dexamethasone (10-7 M) enhanced Na-K-ATPase activity by 58 ± 14%, α- and β-protein abundance by 70 ± 18 and 51 ± 10%, and α- and β-mRNA levels by 87 ± 12 and 62 ± 11%, respectively. The time course studies revealed that significant increase of Na-K-ATPase activity and α- and β-protein abundance was reached within 8 h, and enhancement of α- and β-mRNA abundance was reached within 4 h of dexamethasone treatment. Pretreatment of cultured proximal tubule cells with cycloheximide (20 μg/ml) completely inhibited dexamethasone-induced increase of Na-K-ATPase α- and β-mRNA. Our results indicate that dexamethasone upregulates Na-K-ATPase in proximal tubule cells via pretranslational mechanisms, which may be mediated by proteins.
AB - Adrenalectomy leads to the decline in the levels of renal Na-K-adenosinetriphosphatase (Na-K-ATPase) α- and β-subunit protein and mRNA. Both α- and β-mRNA, however, return to the control level within 1 h after corticosterone administration. Whether or not glucocorticoid acts directly on a specific segment of nephron to upregulate Na-K-ATPase has not been determined. Studies were undertaken in an attempt to elucidate this problem. Using primary cultures of renal proximal tubules, we found that 24-h treatment with dexamethasone augmented Na-K-ATPase activity and induced coordinate increase of α- and β-protein and mRNA abundance dependent on the doses in the range of 10-8 to 10-6 M. We further demonstrated that 24-h incubation of dexamethasone (10-7 M) enhanced Na-K-ATPase activity by 58 ± 14%, α- and β-protein abundance by 70 ± 18 and 51 ± 10%, and α- and β-mRNA levels by 87 ± 12 and 62 ± 11%, respectively. The time course studies revealed that significant increase of Na-K-ATPase activity and α- and β-protein abundance was reached within 8 h, and enhancement of α- and β-mRNA abundance was reached within 4 h of dexamethasone treatment. Pretreatment of cultured proximal tubule cells with cycloheximide (20 μg/ml) completely inhibited dexamethasone-induced increase of Na-K-ATPase α- and β-mRNA. Our results indicate that dexamethasone upregulates Na-K-ATPase in proximal tubule cells via pretranslational mechanisms, which may be mediated by proteins.
KW - Glucocorticoids
KW - Primary culture
KW - Proximal tubule
KW - Sodium-potassium-adenosinetriphosphatase
UR - http://www.scopus.com/inward/record.url?scp=0029002175&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029002175&partnerID=8YFLogxK
M3 - Article
C2 - 7771515
AN - SCOPUS:0029002175
VL - 268
JO - American Journal of Physiology - Renal Physiology
JF - American Journal of Physiology - Renal Physiology
SN - 1931-857X
IS - 5 37-5
ER -