-
Mice experiencing a 3 hours of status epilepticus exhibit a rapid increase in expression of Dio2 and a decrease in the expression of Dio3 gene in hippocampus, amygdala and prefrontal cortex. Dio2 induction caused by SE accelerates production of T3 in different areas of the central nervous system and modifies the hippocampal gene expression profile, affecting the balance between adaptive and maladaptive mechanisms.
-
murine D2 knockout macrophages exhibited impaired phagocytosis and partially reduced cytokine response to stimulation with bacterial endotoxin. These effects are presumably due to reduced intracellular T3 availability.
-
Regulation of the expression and activity of the deiodinases constitutes a cell-autonomous, pre-receptor mechanism that controls crucial steps during the various phases of myogenesis. (Review)
-
Results indicate that basal cell carcinoma cells constitute an example in which the thyroid hormone signal is finely tuned by the concerted expression of opposite-acting deiodinases. The dual regulation of Dio2 and Dio3 expression plays a critical role in cell cycle progression and cell death by influencing cyclin D1-mediated entry into the G1-S phase.
-
Two mouse models of early developmental disruption of Dio2 in myocyte precursor exhibit no significant skeletal muscle phenotype.
-
Dio3-/- mice display degeneration of retinal cones, the photoreceptors that mediate daylight and color vision. In Dio2-/- mice, cone function was largely normal but deletion of Dio2 in Dio3-/- mice markedly recovered cone numbers and electroretinogram responses, suggesting counterbalancing roles for both enzymes in cone survival.
-
The consistent association between Calr and Dio2 expression suggests that enhanced expression of these two genes facilitate detrimental effects on cartilage integrity.
-
mice with astrocyte-specific Dio2 inactivation (Astro-D2KO) have normal serum T3 but exhibit anxiety-depression-like behavior as found in open field and elevated plus maze studies and when tested for depression using the tail-suspension and the forced-swimming tests
-
Mice subjected to a running regime have significant increased cartilage damage and synovitis scores. Lack of Dio2 protected against cartilage damage in this model and was reflected in a specific gene expression profile.
-
Perinatal deiodinase 2 expression in hepatocytes defines epigenetic susceptibility to liver steatosis and obesity.
-
Data show that type 2 deiodinase (Dio2) inactivation in skeletal myocytes preserves T3 thyroid hormone content and only mildly disrupts thyroid hormone signaling.
-
D2KO mice do have normal articular cartilage and no other features of spontaneous joint damage, but exhibit increased subchondral bone mineral content
-
The motor alterations observed in D2KO mice indicate an important role for D2 in T3 availability to maintain motor function and muscle strength. Our results suggest a possible implication of D2 in motor disorders.
-
These studies reveal that tissue-specific differences in D2 ubiquitination are an inherent property of the TRH/TSH feedback mechanism
-
congenital severe reduction of thyrotroph Dio2 causes a major impairment of the TSH response to hypothyroidism
-
Within the supportive environment of a research vivarium, mice lacking all three deiodinases can be bred and survive.
-
Systemic changes in thyroid hormone economy as a result of acute food deprivation are not dependent on the deiodinases D1 or D2 but are mediated in part by sequestration of type 4 and type 3 in tissues and their enhanced metabolism by deiodinase D3.
-
Data indicate that deiodinase Dio2 was mainly localized in stroma cells before implantation, whereas deiodinase Dio3 was highly expressed in stromal cells after implantation.
-
Data suggest that hepatic deiodinase type 2 (D2) favors the innate immune response by specifically regulating cellular thyroid hormone levels in macrophages.
-
Data suggest that type 2 deiodinase is induced in inflammation of tanycytes (as in inflammation of periventricular area, arcuate nucleus, and median eminence of hypothalamus); this enzyme induction appears to involve NFkappaB signaling.
