A cardiac developmental defect prevents thyroid hormone induced tachycardia in the syndrome of resistance to thyroid hormone alpha

Purpose: the objective of this study was to determine cardiac gene expression profile in the mice heart of mutated thyroid receptor alpha 1 (TRα1R384C+/m) male offspring of control dams as well as of dams treated with 3,3',5-triiodo-L-thyronine (T3) from embryonic day 12.5 to 18.5 Methods: wildtype females were mated to heterozygous TRα1R384C+/m males to obtain TRα1R384C+/+ or TRα1R384C+/m offspring. Dams were treated from embryonic day 12.5 to 18.5 with T3 via drinking water (0.5 mg/L), while the drinking water of control dams only contained 0.01% BSA. Offspring were NEVER treated and analyzed at 4 to 5 months.

研究目的：本研究旨在明确对照组孕鼠及自胚胎第12.5天至18.5天经3,3',5-三碘-L-甲状腺原氨酸（3,3',5-triiodo-L-thyronine, T3）处理的孕鼠所产的突变型甲状腺受体α1（mutated thyroid receptor alpha 1, TRα1R384C+/m）雄性子代小鼠的心脏基因表达谱。实验方法：将野生型雌鼠与杂合子TRα1R384C+/m雄鼠交配，以获得TRα1R384C+/+或TRα1R384C+/m子代小鼠。孕鼠自胚胎第12.5天至18.5天通过饮用水给予T3（浓度为0.5 mg/L），对照组孕鼠的饮用水仅添加0.01%牛血清白蛋白（Bovine Serum Albumin, BSA）。子代小鼠未接受任何干预，于4至5月龄时开展相关分析。