Monocarboxylic acid transporter 1 (MCT1) maintains axonal function by transferring lactic acid from oligodendrocytes to axons. Subarachnoid hemorrhage (SAH) induces white matter injury, but the involvement of MCT1 is unclear. In this study, the SAH model of adult male Sprague-Dawley rats was used to explore the role of MCT1 in white matter injury after SAH. At 48 h after SAH, oligodendrocyte MCT1 was significantly reduced, and the exogenous overexpression of MCT1 significantly improved white matter integrity and long-term cognitive function. Motor training after SAH significantly increased the number of ITPR2
Animals ; Male ; MicroRNAs/genetics* ; Monocarboxylic Acid Transporters/genetics* ; Rats ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage ; Symporters/genetics* ; White Matter/injuries*

BACKGROUNDIodine deficiency is a major factor affecting thyroid auto-regulation, the quantity of iodine may greatly influence the synthesis of thyroid hormones (THs). It has long been believed that TH enters the cell through passive diffusion. Recent studies have suggested that several transporters could facilitate transportation of TH. The monocarboxylate transporter 8 (MCT8) was identified as a very active and specific TH transporter. The purpose of this study was to investigate whether iodine insufficient affected the expression of MCT8 in the thyroid gland.

METHODSSixty BALB/c mice were randomly divided into two groups: control group was fed with standard feed (iodine concentration of 300 µg/kg); while low-iodine (LI) group received iodine-insufficient feed (iodine concentration of 20-40 µg/kg). After 3 months, 10 mice of each group were sacrificed. The remaining 20 mice of each group were kept till 6 months. From the LI group, we randomly selected 15 mice and injected triiodothyronine (T3, 100 µg/kg body weight per day) intraperitoneally for 24, 48 or 72 hours (5 mice for each time-point). Then, all the mice were sacrificed. Mouse serum thyroxine (T4), T3, and thyroid-stimulating hormone (TSH) levels were determined by chemiluminescence immunoassay (CIA). The protein content or messenger RNA (mRNA) level of thyroid MCT8 was measured by Western blotting analysis or real time RT-PCR respectively. MCT8 subcellular location in thyroid tissues was probed with immunohistochemistry (IHC) assay.

RESULTSWe found that mouse serum T3 and T4 levels decreased and TSH level increased by the end of the third month. Consistent with these findings, there was significant goiter and hypothyroidism in the LI group. Meanwhile, the MCT8 mRNA increased to 1.36-fold of the level in the control group at the 3(rd) month. At 6(th) month, the serum T4 level in LI mice remained at a lower level, and MCT8 mRNA expression continued rising to nearly 1.60-fold compared with the control group. The protein content was also about 3 times higher than that in the control group. IHC results also revealed MCT8 was of higher expression and localized in the cytoplasm of thyroid follicular cells. After providing exogenous T3 to iodine deficient mice, the serum T3 and T4 gradually increased, whereas MCT8 mRNA and protein both started to decrease and returned to the same level as the control group.

CONCLUSIONThere is a compensatory increase in thyroid MCT8 expression to enhance its capability to transport TH from thyroid to the blood circulation in iodine deficient mice.

Animals ; Iodine ; deficiency ; Mice ; Mice, Inbred BALB C ; Monocarboxylic Acid Transporters ; genetics ; metabolism ; Thyroid Gland ; metabolism ; Thyrotropin ; blood ; Thyroxine ; blood ; Triiodothyronine ; blood

To validate the expressions of G protein-coupled receptor 81 (GPR81), monocarboxylate transporter (MCT) 1 and MCT4 in cervical squamous carcinoma and to explore their role in the onset of cervical squamous carcinoma.
 Methods: Immunohistochemical method was used to detect the expressions of GPR81, MCT1 and MCT4 in 16 normal cervical tissue and 44 cervical squamous carcinoma tissue. The associations of these proteins expression with cervical squamous carcinoma or clinicopathological factors were analyzed.
 Results: The expressions of GPR81, MCT1 and MCT4 in cervical squamous carcinoma tissue were higher than those in normal cervical tissue (P<0.01). In cervical squamous carcinoma group, the expressions of GPR81, MCT1 and MCT4 in clinical stage I-II group were lower than those in clinical stage III-IV group, with significant difference (P<0.05). The expressions of GPR81, MCT1 and MCT4 in middle-differentiated tumor group were lower than those in low-differentiated tumor group, but there was no significant difference between the two groups (P>0.05). No difference of the expressions of GPR81, MCT1 and MCT4 were found between cases with or without lymphatic metastasis (P>0.05). No correlation was found among GPR81, MCT1 and MCT4 in cervical squamous carcinoma (P>0.05).
 Conclusion: GPR81, MCT1 and MCT4 may be associated with the onset of cervical squamous carcinoma, and GPR81 may be associated with the progression of cervical squamous carcinoma.
Carcinoma, Squamous Cell ; genetics ; physiopathology ; Disease Progression ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Monocarboxylic Acid Transporters ; genetics ; Muscle Proteins ; genetics ; Receptors, G-Protein-Coupled ; genetics ; Symporters ; genetics ; Uterine Cervical Neoplasms ; genetics ; physiopathology

OBJECTIVETo investigate brazilein's role in energy metabolism of cerebral ischemia-reperfusion in mice.

METHODFourty mice were randomly divided into the sham group, ischemia group, brazilein 5 mg x kg(-1) group and brazilein 10 mg x kg(-1) group, each with ten cases. Cerebral ischemia model was the built. Mice were injected with brazilein three days before the operation, then they were killed. Cerebrum homogenate was prepared for the detecting of ATP, ADP, AMP and lactic acid by HPLC, expressions of MCT1 and MCT2 in mRNA level by RT-PCR.

RESULTThe lactic acid in cerebrum increased sharply 20 minutes after cerebral ischemia and decreased 1 hour after reperfusion, then returned to the normal level 24 hours after reperfusion. The charge of energy decreased significantly at the beginning of the ischemia-reperfusion, and the charge restored 1 hour after reperfusion though it was still much lower than the normal level at the time point of 24 hours. Moreover, MCT1 and MCT2 upregulated accompanied with the increase of lactate, MCT2 mRNA enhanced in brazilein 5 mg x kg(-1) group (P < 0.05) while both the two factors increased in brazilein 10 mg x kg(-1) group (P < 0.01).

CONCLUSIONBrazilein might protect neurons by changing the charge of energy.

Animals ; Benzopyrans ; administration & dosage ; Brain Ischemia ; drug therapy ; genetics ; metabolism ; Disease Models, Animal ; Energy Metabolism ; drug effects ; Gene Expression ; drug effects ; Humans ; Indenes ; administration & dosage ; Male ; Mice ; Mice, Inbred ICR ; Monocarboxylic Acid Transporters ; genetics ; metabolism ; Random Allocation ; Reperfusion Injury ; drug therapy ; genetics ; metabolism ; Symporters ; genetics ; metabolism