@article{MTMT:1802369,
	title = {Endothelin receptors, second messengers, and actions in bone},
	url = {https://m2.mtmt.hu/api/publication/1802369},
	author = {Stern, P H and Tatrai, A and Semler, D E and Suk, Kyeong Lee and Lakatos, Péter and Strieleman, P J and Tarjan, G and Sanders, J L},
	journal-iso = {J NUTR},
	journal = {JOURNAL OF NUTRITION},
	volume = {125},
	unique-id = {1802369},
	issn = {0022-3166},
	abstract = {Endothelins are a class of peptides that are produced by and elicit responses in many tissues. A growing literature documents the presence and effects of endothelins in bone. Both endothelin(A) and endothelin(B) receptors have been demonstrated in osteoblastic cells by ligand binding. Major signal transduction pathways for endothelin in bone cells appear to be stimulation of phospholipid turnover, by activation of A, C and D phospholipases, stimulation of calcium flux from intracellular and extracellular stores and activation of tyrosine kinases. Endothelins also modulate calcium signaling elicited by other agents in osteoblastic cells. The parathyroid hormone-stimulated calcium transient in GMR-106 cells is enhanced by endothelins, acting through an endothelin(B) receptor, whereas the parathyroid hormone-stimulated increase in cyclic AMP is inhibited by endothelins. Phenotypic responses to endothelin-1 include changes in alkaline phosphatase activity, stimulation of osteocalcin and osteopontin message, stimulation of collagen and noncollagenous protein synthesis, inhibition of osteoclast motility and stimulation of prostaglandin-dependent resorption. Endothelin-1 also enhances the interleukin-1-induced increase in interleukin- 6. Endothelins can also potentially affect calcium metabolism through their actions to inhibit the secretion of parathyroid hormone.},
	keywords = {TISSUE DISTRIBUTION; calcium; MOUSE; signal transduction; human; animal; conference paper; Bone; ENDOTHELINS; ENDOTHELIN; Bone and Bones; Support, U.S. Gov't, P.H.S.; endothelin receptor; drug receptor binding; bone tissue; second messenger; osteoblast; calcium metabolism; Second Messenger Systems; Receptors, Endothelin; rat},
	year = {1995},
	eissn = {1541-6100},
	pages = {2028S-2032S},
	orcid-numbers = {Lakatos, Péter/0000-0002-7652-3671}
}

@article{MTMT:1802378,
	title = {Effects of endothelin-1 on signal transduction in UMR-106 osteoblastic cells},
	url = {https://m2.mtmt.hu/api/publication/1802378},
	author = {Tatrai, A and Lakatos, Péter and Thompson, S and Stern, P H},
	doi = {10.1002/jbmr.5650071012},
	journal-iso = {J BONE MINER RES},
	journal = {JOURNAL OF BONE AND MINERAL RESEARCH},
	volume = {7},
	unique-id = {1802378},
	issn = {0884-0431},
	abstract = {Endothelin-1 is now recognized to affect the functions of a number of tissues and to activate calcium/phospholipid second messenger pathways in target cells. In the present study, we characterized its effects on signal transduction in UMR-106 cells. To study calcium transients elicited by endothelin-1, cells were loaded either with fluo-3 (for the measurement of cytosolic free calcium) or chlortetracycline (for the measurement of intracellularly stored calcium) as fluorescent probes. Intracellular production of inositol phosphates and cyclic AMP was also measured. Endothelin-1 elicited dose-dependent cytosolic calcium transients with an ED50 of 20 nM. This effect was also seen in EGTA-containing or calcium-free medium; however, the signals were reduced in magnitude. The dihydropyridine calcium channel antagonist nifedipine did not affect the response. Repeated administration of endothelin-1 resulted in homologous desensitization of the response. A 4 minute pretreatment with phorbol ester reduced the initial response to endothelin-1 in both calcium-containing and calcium-free media. A 24 h pretreatment with indomethacin had no effect on response. Using chlortetracycline as an indicator, a significant reduction in intracellularly stored calcium by endothelin-1 was observed. This was prevented by 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate, a blocker of calcium release from internal stores. Endothelin-1 also stimulated the dose-dependent production of inositol phosphates by UMR-106 cells. Indomethacin was also without effect on this process. The increase in inositol trisphosphates was seen within the same time frame as the increase in cytosolic calcium. Endothelin-1 did not influence cyclic AMP production over 5 minutes in these cells. In conclusion, endothelin-1 has a significant effect on UMR-106 osteoblastic cells to activate the calcium and inositol phosphate second messenger systems. Our findings raise the intriguing question of the physiologic role of endothelin-I in bone metabolism.},
	keywords = {calcium; ARTICLE; MOUSE; signal transduction; controlled study; Dose-Response Relationship, Drug; nonhuman; animal cell; Cells, Cultured; ENDOTHELINS; Cytosol; indometacin; calcium cell level; nifedipine; cyclic AMP; Osteoblasts; osteoblast; endothelin 1; Inositol Phosphates},
	year = {1992},
	eissn = {1523-4681},
	pages = {1201-1209},
	orcid-numbers = {Lakatos, Péter/0000-0002-7652-3671}
}

@article{MTMT:1802376,
	title = {Endothelin-1 actions on resorption, collagen and noncollagen protein synthesis, and phosphatidylinositol turnover in bone organ cultures},
	url = {https://m2.mtmt.hu/api/publication/1802376},
	author = {Tatrai, A and Foster, S and Lakatos, Péter and Shankar, G and Stern, P H},
	doi = {10.1210/endo.131.2.1639010},
	journal-iso = {ENDOCRINOLOGY},
	journal = {ENDOCRINOLOGY},
	volume = {131},
	unique-id = {1802376},
	issn = {0013-7227},
	abstract = {The effects of endothelin-1 (ET) on several tissues are mediated by prostaglandins. In this study, we investigated the actions of ET on bone and determined whether they are mediated through prostaglandin-dependent pathways. Bone resorption, collagen, and non-collagen protein synthesis and inositol phosphate (IP) production were studied in neonatal mouse calvaria and fetal rat limb bone cultures. The effects of ET in the calvaria model were examined in the presence or absence of the cyclooxygenase inhibitor indomethacin (INDO). Bone resorption was stimulated by ET in the neonatal mouse calvaria, and this effect was inhibited by INDO. 45Ca release in the fetal rat limb bones was not affected by ET. ET stimulated collagen and noncollagen protein synthesis significantly in the calvaria model in the presence but not in the absence of INDO, suggesting that the anabolic effects of ET were masked by endogenous prostaglandin production. ET increased phosphatidylinositol turnover in both bone organ cultures. Although the addition of INDO reduced IP production slightly in the mouse calvaria, it was still significantly stimulated by ET. Our results demonstrate that ET has marked effects on bone tissue in vitro. Effects on resorption appear to be prostaglandin dependent, whereas the anabolic effects were not prostaglandin mediated. The stimulatory effects of ET on protein synthesis could be mediated through the IP signaling pathway. Since ET stimulates both bone resorption and anabolism, this peptide may have a role in the coupling of bone remodeling.},
	keywords = {PROTEINS; calcium; MICE; RATS; ARTICLE; animal; priority journal; Rats, Inbred Strains; nonhuman; animal tissue; Animals, Newborn; ENDOTHELINS; PROSTAGLANDIN; COLLAGEN; fetus; Bone and Bones; Support, U.S. Gov't, P.H.S.; Indomethacin; protein synthesis; bone remodeling; Bone Resorption; osteolysis; calcium transport; phosphate metabolism; endothelin 1; organ culture; long bone; Phosphatidylinositols; PROSTAGLANDIN SYNTHESIS; collagen synthesis; phosphatidylinositol; Calcium Radioisotopes; calvaria; rat},
	year = {1992},
	eissn = {1945-7170},
	pages = {603-607},
	orcid-numbers = {Lakatos, Péter/0000-0002-7652-3671}
}