Authors:

Alyssa Smith

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About Paper:

In-utero hypothyroidism adversely affects fetal growth and maturation, however, the exact molecular mechanisms by which this occurs are unknown. The objective of this study was to examine the organ-specific effects of fetal hypothyroidism on the regulation of cell cycle progression in the late gestation porcine fetus. Eight pregnant gilts were dosed with either methimazole (MMI) or an equivalent negative control (CON) during days 85-106 out of 114 days of gestation. After the treatment period, the gilts were humanely euthanized, and tissue samples taken from two male and two female fetuses from each gilt (n = 32). Complete hypothyroidism of the MMI fetuses was confirmed via ELISA assay, and total RNA was then extracted from eight different tissues, including heart, ileum, kidney, lung, liver, muscle, spleen, and thymus. RNA was reverse transcribed to allow for analysis of the expression of three cell cycle promoters (CDK1, CDK2, and CDK4) and one cell cycle inhibitor (CDKN1A) by qPCR. The relative expression of these genes was compared between the MMI and CON groups, and initial results showed that each tissue experienced at least one significant up- or downregulation in the expression of the aforementioned genes as a result of treatment with MMI. Many changes in gene expression were observed in the muscle, which had significant downregulations of CDK1, CDK2, and CDK4. These findings indicate the occurrence of organ-specific disruptions in cell cycle progression as a result of in-utero hypothyroidism, which could be responsible for some of the detrimental effects of hypothyroidism on fetal development.

Source:

Purdue University / 2023

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Co-authors:

Alyssa Smith