RESUMEN
Thyroid hormones play an important role in the development and function of the cardiac myocyte. Dysregulation of the thyroid hormone milieu affects the fetal cardiac cells via complex molecular mechanisms, either by altering gene expression or directly by affecting post-translational processes. This review offers a comprehensive summary of the effects of thyroid hormones on the developing cardiovascular system and its adaptation. Furthermore, we will highlight the gaps in knowledge and provide suggestions for future research.
Asunto(s)
Glándula Tiroides , Hormonas Tiroideas , Humanos , Recién Nacido , Feto , CorazónRESUMEN
Abnormal adrenal findings such as hemorrhage or calcifications in the neonate can stem from a variety of etiologies. Clinical presentation can vary significantly based on the degree of hemorrhage or the associated condition. Thorough work-up is important to rule out critical underlying conditions as well as adrenal insufficiency.
RESUMEN
The present study tests the hypothesis that hyperoxia results in increased tyrosine phosphorylation of apoptotic proteins Bcl-2, Bcl-xl, Bax & Bad in the mitochondrial fraction of the cerebral cortex of newborn piglets. Twelve newborn piglets were divided into normoxic [Nx, n = 6], exposed to a FiO(2) of 0.21 for 1 h and hyperoxic [Hyx, n = 6], exposed to FiO(2) of 1.0 for 1 h. PaO(2) in Hyx group was maintained at 400 mmHg while the Nx group was kept at 80 to 100 mmHg. The density (O.D.x mm(2)) of phosphorylated Bcl2 protein on westernblot was 19.3 +/- 3.6 in Nx and 41.5 +/- 18.3 in Hyx, (P < 0.05). The density of phosphorylated Bcl-xl protein density was 26.9 +/- 7.0 in Nx and 47.9 +/- 2.5 in Hyx, (P < 0.05). Phosphorylated Bax density was 43.5 +/- 5.0 in Nx and 43.3 +/- 5.2 in Hyx. Phosphorylated Bad density was 23.6 +/- 3.9 in Nx, 24.4 +/- 4.7 in Hyx. The data show that during hyperoxia there is a significant increase in tyrosine phosphorylation of Bcl2 and Bcl-xl, while the phosphorylation of proapototic proteins Bax & Bad was not altered. We conclude that hyperoxia leads to post translational modification of anti apoptotic proteins Bcl2 and Bcl-xl in cerebral cortical mitochondria. We propose that phosphorylation of Bcl2 will result in loss of its antiapoptotic potential by preventing its dimerization with Bax leading to activation of the caspase pathway and subsequent neuronal death in the cerebral cortex of the newborn piglets.