Differences in cholesterol incorporation into mitochondria from hepatoma AS-30D and human term placenta.
Cholesterol transport for steroidogenesis in the human placental mitochondria is an enigma as, contrary to other steroidogenic tissues, the human placenta does not express steroidogenic acute regulatory protein (StAR), a protein known to be required for efficient utilization of cholesterol by adrenal and gonadal mitochondria. These observations suggest the possibility that cholesterol transport in human placental mitochondria involves a similar system to that present in other non-steroidogenic tissues. We studied cholesterol incorporation into mitochondria isolated from AS-30D hepatoma cells and the human placenta. Mitochondria from both sources incorporated cholesterol in vitro. There were no differences in cholesterol incorporation into hepatoma mitochondria treated with or without trypsin. In contrast, the human placental mitochondria treated with trypsin did not incorporate exogenous cholesterol. The presence of ATP increased the uptake of cholesterol by human placental mitochondria. This increase was inhibited by vanadate. These results suggest that cholesterol incorporation into human placental mitochondria is mediated by protein(s).
D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D001692:Biological Transport; D002784:Cholesterol / Q000378:metabolism*; D005260:Female; D006801:Humans; D008114:Liver Neoplasms, Experimental / Q000648:ultrastructure*; D008928:Mitochondria / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000378:metabolism*; D010920:Placenta / Q000648:ultrastructure*; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar; D014357:Trypsin / Q000494:pharmacology; D014638:Vanadates / Q000494:pharmacology