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15. Correction: The Dkk3 gene encodes a vital intracellular regulator of cell proliferation

Author

Leonard, Jack L., primary, Leonard, Deborah M., additional, Wolfe, Scot A., additional, Liu, Jilin, additional, Rivera, Jaime, additional, Yang, Michelle, additional, Leonard, Ryan T., additional, Johnson, Jacob P. S., additional, Kumar, Prashant, additional, Liebmann, Kate L., additional, Tutto, Amanda A., additional, Mou, Zhongming, additional, and Simin, Karl J., additional

Published
2017
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16. The Dkk3 gene encodes a vital intracellular regulator of cell proliferation

Author

Leonard, Jack L., primary, Leonard, Deborah M., additional, Wolfe, Scot A., additional, Liu, Jilin, additional, Rivera, Jaime, additional, Yang, Michelle, additional, Leonard, Ryan T., additional, Johnson, Jacob P. S., additional, Kumar, Prashant, additional, Liebmann, Kate L., additional, Tutto, Amanda A., additional, Mou, Zhongming, additional, and Simin, Karl J., additional

Published
2017
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46. Placental 5Deiodinase Activity and Fetal Thyroid Hormone Economy Are Unaffected by Selenium Deficiency in the Rat

Author

CHANOINE, JEAN-PIERRE, ALEX, SHARON, STONE, SCOTT, FANG, SHIH LIEH, VERONIKIS, IRINI, LEONARD, JACK L., and BRAVERMAN, LEWIS E.

Abstract

In adult male rats, selenium deficiency results in a near complete loss in the selenoprotein 5'-deiodinase in the liver, resulting in decreased peripheral deiodination of thyroxine (T4) and increased serum T4 concentrations. Serum 3,5,3'-triiodothyronine concentrations are normal or slightly decreased, and serum 3,3',5'-triiodothyronine concentrations are normal or slightly increased in selenium-deficient rats. We now report the effects of selenium deficiency on maternal and fetal thyroid hormone economy and on placenta 5-deiodinase activity in the rat. Weanling female rats were fed either a selenium-deficient or selenium-supplemented diet for 4 wk before mating and then throughout gestation. Rats were killed at 21 d of gestation. Selenium deficiency was confirmed by a 95 and 94 decrease in glutathione peroxidase and a 84 and 56 decrease in liver type I outer ring 5' deiodinase activity in the mother and the fetus, respectively. In contrast to the increase in circulating T4 observed in selenium-deficient male and nonpregnant female adult rats, serum T4 was not affected by selenium deficiency in pregnant rats, but there was a 3-fold increase in serum 3,3',5'-triiodothyronine concentrations associated with a 70 decrease in maternal brain type II outer ring 5' deiodinase activity. Maternal serum 3,5,3'-triiodothyronine concentrations were decreased by 21. Placental 5-deiodinase activity was unaffected by selenium deficiency. In the fetus, serum T4, 3,3',5'-triiodothyronine, and TSH concentrations were not affected by selenium deficiency. These data suggest that placental 5-deiodinase is not a selenoenzyme and that the failure of selenium deficiency to increase serum T4 concentrations in the mother as well as the minor role played by liver type I outer ring 5' deiodinase in the fetus results in the protection of fetal thyroid hormone economy against the potentially deleterious effects of selenium deficiency.

Published
1993

47. THE ROLE OF PROTEIN KINASE C IN LIPOPOLYSACCHARIDEINDUCED MYOCARDIAL DEPRESSION IN GUINEA PIGS

Author

Heard, Stephen O., Toth, Ildiko E., Perkins, Michael W., and Leonard, Jack L.

Abstract

The effect of lipopolysaccharide (LPS) on cardiac protein kinase C (PKC) activation and cardiac depression was evaluated. Guinea pigs (n = 44) received intraperitoneal injections of saline or Escherichia coli LPS (2 mg/kg). Left atria were harvested 16 h later and suspended in oxygenated low calcium (1 mM) (n = 24) or high calcium (5 mM) (n = 20) 30°C Krebs-Henseleit buffer. Atria were treated with H-7 (n = 23), a PKC inhibitor, or vehicle (n = 21). Contractile responses to changes in preload and stimulating frequency, in the resting and potentiated states, and to escalating doses of phenylephrine were measured. PKC activation in ventricular muscle was also determined. LPS activated ventricular PKC (p< .05) but treatment with H-7 failed to reverse LPS-induced atrial dysfunction in the low calcium buffer. Contractile function in the potentiated state indicated that LPS appears to interfere with calcium release from the sarcoplasmic reticulum (SR). The contractile response to phenylephrine was markedly attenuated in atria harvested from endotoxic animals. These data indicate that LPS-induced cardiac depression is mediated, in part, by alterations in SR calcium release. LPS activates cardiac PKC but a causal relationship among LPS, PKC, and cardiac dysfunction remains to be established.

Published
1994

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