@article{MTMT:1669715, title = {Regional distribution of type 2 thyroxine deiodinase messenger ribonucleic acid in rat hypothalamus and pituitary and its regulation by thyroid hormone}, url = {https://m2.mtmt.hu/api/publication/1669715}, author = {Tu, HM and Kim, SW and Salvatore, D and Bartha, Tibor and Legradi, G and Larsen, PR and Lechan, RM}, doi = {10.1210/en.138.8.3359}, journal-iso = {ENDOCRINOLOGY}, journal = {ENDOCRINOLOGY}, volume = {138}, unique-id = {1669715}, issn = {0013-7227}, abstract = {To identify the specific locations of type 2 deiodinase (D2) messenger RNA (mRNA) in the hypothalamus and pituitary gland and determine its regulation by thyroid hormone, we performed in situ hybridization histochemistry, Northern analysis, and quantitative RT-PCR in euthyroid, hypothyroid, and hyperthyroid rats. By in situ hybridization histochemistry, silver grains were concentrated over ependymal cells lining the floor and infralateral walls of the third ventricle extending from the rostral tip of the median eminence (ME) to the infundibular recess, surrounding blood vessels in the arcuate nucleus (ARC), and in the ME adjacent to the portal vessels and overlying the tuberoinfundibular sulci. Silver grains also accumulated over distinct cells in the midportion of the anterior pituitary. In hypothyroid animals, an increase in signal intensity was observed in the caudal hypothalamus, and a marked increase in the number of positive cells occurred in the anterior pituitary. Microdissection of the hypothalamus for Northern and PCR analysis established the authenticity of D2 mRNA in the caudal hypothalamus, and confirmed that the majority of D2 mRNA is concentrated in this region. The distribution of D2 mRNA suggests its expression in specialized ependymal cells, termed tanycytes, originating from the third ventricle. Thus, the tanycyte is the source of the high D2 activity previously found in the ARC-ME region of the hypothalamus. The results indicate that tanycytes may have a previously unrecognized integral role in feedback regulation of TSH secretion by T-4.}, year = {1997}, eissn = {1945-7170}, pages = {3359-3368} } @article{MTMT:1802374, title = {Thyroid hormones increase insulin-like growth factor I content in the medium of rat bone tissue}, url = {https://m2.mtmt.hu/api/publication/1802374}, author = {Lakatos, Péter and Caplice, M D and Khanna, V and Stern, P H}, doi = {10.1002/jbmr.5650081210}, journal-iso = {J BONE MINER RES}, journal = {JOURNAL OF BONE AND MINERAL RESEARCH}, volume = {8}, unique-id = {1802374}, issn = {0884-0431}, abstract = {The mechanism of action of thyroid hormones on bone is still not clear. At low concentrations, they stimulate bone formation; at high concentrations, they elicit bone resorption in vitro and in vivo. In the present study we investigated the effect of T3 and T4 as well as their active and inactive analogs (TRIAC, SKF L-94901, rT3, and DIT) on the IGF-I and TNF-α content in the medium of UMR-106 rat osteoblastic cells and fetal rat limb bones. In the dose-response studies, a biphasic increase in medium IGF-I was observed in both cells and limb bones, with peak stimulatory concentrations of 10-8 M for T3 and 10-7 M for T4 in both systems. At higher concentrations, at which thyroid hormones elicit bone resorption, the stimulatory effect diminished and finally was no longer detectable. The active analogs TRIAC and SKF L-94901 also enhanced IGF-I release in UMR-106 cells. The inactive compounds rT3 and DIT failed to increase IGF-I in these cultures. The protein content of the cell culture wells exposed to high concentrations of thyroid hormones was similar to those containing low concentrations, indicating that the decrease in IGF-I content at high doses was not due to toxic effects. This was also confirmed by trypan blue exclusion. Time course studies with UMR-106 cells revealed a significant increase in medium IGF-I after 2 days of incubation. No significant further increase was observed after this up to 5 days of culture. In contrast, the medium of limb bone cultures showed a linear increase in IGF-I content up to 7 days of culture. No TNF-α production was observed in either UMR-106 cells or fetal limb bones. Also, no increase in medium TNF-α levels was seen in response to thyroid hormones. Based on our results, we conclude that IGF-I may be responsible for some of the anabolic effects of thyroid hormones in bone tissue, but TNF-α, at least in the models we used, does not play a role in the mediation of thyroid hormone action.}, keywords = {PROTEIN; RATS; ARTICLE; tumor necrosis factor alpha; animal; Rats, Sprague-Dawley; Dose-Response Relationship, Drug; nonhuman; animal tissue; animal cell; Tumor Cells, Cultured; Bone metabolism; fetus; Bone and Bones; Insulin-Like Growth Factor I; somatomedin C; liothyronine; Tissue Culture; Culture Media; Tumor Necrosis Factor; Support, U.S. Gov't, P.H.S.; Extremities; Bone Resorption; osteolysis; thyroxine; ossification; bone tissue; protein content; Triiodothyronine; Osteoblasts; osteoblast; Osteosarcoma; thyroid hormones; Thyronines; Triiodothyronine, Reverse; 3,3',5' triiodothyronine; tiratricol; diiodotyrosine; 3,5 dibromo 3' (2,3 dihydro 3 oxo 6 pyridazinylmethyl)thyronine; rat}, year = {1993}, eissn = {1523-4681}, pages = {1475-1481}, orcid-numbers = {Lakatos, Péter/0000-0002-7652-3671} } @article{MTMT:1802379, title = {Evidence for direct non-genomic effects of triiodothyronine on bone rudiments in rats: Stimulation of the inositol phosphate second messenger system}, url = {https://m2.mtmt.hu/api/publication/1802379}, author = {Lakatos, Péter and Stern, P H}, doi = {10.1530/acta.0.1250603}, journal-iso = {ACTA ENDOCRINOL}, journal = {ACTA ENDOCRINOLOGICA}, volume = {125}, unique-id = {1802379}, issn = {0001-5598}, abstract = {Thyroid hormones increase cytosolic free calcium by binding to plasma membrane receptors in several tissues. This calcium increase appears to initiate extranuclear effects in these tissues. Increases in cytosolic calcium are often a consequence of stimulation of inositol phosphate second messenger pathway. Several calcemic hormones act via this signal transduction route. Therefore we investigated the effects of the metabolically active T3 and the inactive analogues 3,5-diiodotyrosine and rT3 on the inositol phosphate pathway in fetal rat limb bone cultures prelabeled with [3H]myoinositol. Labelled inositol and inositol phosphates were separated by HPLC. There was a significant increase in the radioactivity in inositol bis- and trisphosphates after 1 min of exposure to 10-7 mol/l T3. Stimulation was also observed at 10-6 mol/l T3, but not at 10-5 mol/l. Time course studies demonstrated a rapid effect of T3 on inositol phosphates within 30 seconds that lasted through 5 min. After 20 min incubation with T3, no increase was observed in inositol mono- and bisphoshates, and a decrease was seen in inositol trisphosphate. Pretreatment with indomethacin prevented these effects of T3. 3,5-diiodothyrosine and rT3 did not affect inositol phosphate metabolism. These results suggest the existence of plasma membrane-associated receptors for T3 in bone, in addition to the nuclear receptors demonstrated previously. The role of these receptors in the effects of thyroid hormones on bone remains to be established.}, keywords = {Female; RATS; ARTICLE; signal transduction; INOSITOL; animal; Chromatography, High Pressure Liquid; priority journal; Dose-Response Relationship, Drug; Time Factors; Rats, Inbred Strains; nonhuman; animal tissue; animal cell; Cells, Cultured; Bone; pregnancy; fetus; Bone and Bones; liothyronine; cell culture; Tritium; Support, U.S. Gov't, P.H.S.; Indomethacin; indometacin; thyroid gland; Triiodothyronine; membrane receptor; phosphoinositide metabolism; inositol trisphosphate; Second Messenger Systems; cell nucleus receptor; 3,3',5' triiodothyronine; bone cell; inositol phosphate; diiodothyronine; Inositol Phosphates; diiodotyrosine; rat}, year = {1991}, pages = {603-608}, orcid-numbers = {Lakatos, Péter/0000-0002-7652-3671} } @article{MTMT:1660953, title = {INFLUENCE OF THYROID STATUS ON THE MEMBRANES OF RAT-LIVER MITOCHONDRIA - UNIQUE LOCALIZATION OF L-GLYCEROL-3-PHOSPHATE DEHYDROGENASE}, url = {https://m2.mtmt.hu/api/publication/1660953}, author = {BELEZNAI, Z and AMLER, E and RAUCHOVA, H and DRAHOTA, Z and Jancsik, Veronika}, doi = {10.1016/0014-5793(89)80138-3}, journal-iso = {FEBS LETT}, journal = {FEBS LETTERS}, volume = {243}, unique-id = {1660953}, issn = {0014-5793}, year = {1989}, eissn = {1873-3468}, pages = {247-250} }