Experimental hypothyroidism reduced significiantly MAP-2 immunoreactivity in both the CA3 and CA1 regions and caused degeneration, including edema and vascular dilation, in the hippocampus.
However, splenic hypotrophy is more marked in hypothyroid mice than in TRα1/TRβ-knockout mice and the splenic population of T-lymphocytes is not significantly impaired in these mice in contrast with the reduction found in hypothyroidism.
We found that loss of Vps34 in thyrocytes causes (i) disorganization of thyroid parenchyma, with abnormal thyrocyte and follicular shape and reduced PAS<sup>+</sup> colloidal spaces; (ii) severe noncompensated hypothyroidism with extremely low T4 levels (0.75 ± 0.62 μg/dL) and huge thyrotropin plasma levels (19,300 ± 10,500 mU/L); (iii) impaired <sup>125</sup>I organification at comparable uptake and frequent occurrence of follicles with luminal Tg but nondetectable T4-bearing Tg; (iv) intense signal in thyrocytes for the lysosomal membrane marker, LAMP-1, as well as Tg and the autophagy marker, p62, indicating defective lysosomal proteolysis; and (v) presence of macrophages in the colloidal space.
We found that loss of Vps34 in thyrocytes causes (i) disorganization of thyroid parenchyma, with abnormal thyrocyte and follicular shape and reduced PAS<sup>+</sup> colloidal spaces; (ii) severe noncompensated hypothyroidism with extremely low T4 levels (0.75 ± 0.62 μg/dL) and huge thyrotropin plasma levels (19,300 ± 10,500 mU/L); (iii) impaired <sup>125</sup>I organification at comparable uptake and frequent occurrence of follicles with luminal Tg but nondetectable T4-bearing Tg; (iv) intense signal in thyrocytes for the lysosomal membrane marker, LAMP-1, as well as Tg and the autophagy marker, p62, indicating defective lysosomal proteolysis; and (v) presence of macrophages in the colloidal space.
Therefore, the study suggests that hypothyroidism could affect male reproductive function by disturbing expression of AR, changing the activity of Ca<sup>2+</sup>-ATPase, inducing oxidative stress and then leading to activation of p38MAPK and JNK signaling in the testicular mitochondria.
Similarly, expression of TRα-1, TRβ-1, TSHR, ERK1/2 and RAR proteins and mRNA in the uterus of non-treated hypothyroid rats also decreased (P < 0.05 when compared to euthyroid and thyroxine-treated hypothyroid rats).
Interestingly, in the hypothyroid state, CMNS caused concomitant activation of two signaling pathways that are usually reciprocally regulated - AMPK and mTOR signaling - which manifested as increased β-oxidation, MHC-I expression, and protein synthesis.
Compared with EU and EU+B groups, a reduction in fT4, and ERK1/2 levels and elevation in TSH in brain tissue, Moreover, a significant elevation in 8-OH deoxyguanosine and caspase-3 levels, confirmed with increase percentage DNA-damage in the brain and thyroid tissues in hypothyroid control rats.
Interestingly, in the hypothyroid state, CMNS caused concomitant activation of two signaling pathways that are usually reciprocally regulated - AMPK and mTOR signaling - which manifested as increased β-oxidation, MHC-I expression, and protein synthesis.
<b>Results:</b> Galectin-3 concentrations were significantly higher in patients with hypothyroidism compared to the control group (2.89 (1.17-10.79); 1.95 (1.15-6.11) ng/mL, <i>p</i> = .001, respectively).
Interestingly, in the hypothyroid state, CMNS caused concomitant activation of two signaling pathways that are usually reciprocally regulated - AMPK and mTOR signaling - which manifested as increased β-oxidation, MHC-I expression, and protein synthesis.
However, when compared to hypothyroid rats T2 significantly increases, without bringing to the euthyroid value, the content of both mature (nSREBP-1), and precursor (pSREBP-1) forms of the SREBP-1 protein as well as their ratio.
Our first patient had aquaporin-4 antibody-positive NMOSD with concurrent hypothyroidism, SLE, and muscle specific kinase antibody-positive MG. Our second patient had seronegative NMOSD with concurrent acetylcholine receptor antibody-positive MG.
<b>Significance</b>: Our finding in the present study indicated that PPARγ agonist pioglitazone prevented the brain tissues from oxidative damage and learning and memory impairments in juvenile hypothyroid rats.