Linked Life Data

21228212

Source:http://linkedlifedata.com/resource/pubmed/id/21228212

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2011-4-21
pubmed:abstractText
Previous studies in MA-10 tumor Leydig cells demonstrated that disruption of the mitochondrial electron-transport chain (ETC), membrane potential (??(m)), or ATP synthesis independently inhibited steroidogenesis. In contrast, studies of primary Leydig cells indicated that the ETC, ??(m), and ATP synthesis cooperatively affected steroidogenesis. These results suggest significant differences between the two systems and call into question the extent to which results from tumor Leydig cells relate to primary cells. Thus, to further understand the similarities and differences between the two systems as well as the impact of ATP disruption on steroidogenesis, we performed comparative studies of MA-10 and primary Leydig cells under similar conditions of mitochondrial disruption. We show that mitochondrial ATP synthesis is critical for steroidogenesis in both primary and tumor Leydig cells. However, in striking contrast to primary cells, perturbation of ??(m) in MA-10 cells did not substantially decrease cellular ATP content, a perplexing finding because ??(m) powers the mitochondrial ATP synthase. Further studies revealed that a significant proportion of cellular ATP in MA-10 cells derives from glycolysis. In contrast, primary cells appear to be almost completely dependent on mitochondrial respiration for their energy provision. Inhibitor studies also suggested that the MA-10 ETC is impaired. This work underscores the importance of mitochondrial ATP for hormone-stimulated steroid production in both MA-10 and primary Leydig cells while indicating that caution must be exercised in extrapolating data from tumor cells to primary tissue.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1529-7268
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
976-85
pubmed:meshHeading
pubmed-meshheading:21228212-Adenosine Triphosphate, pubmed-meshheading:21228212-Animals, pubmed-meshheading:21228212-Cell Line, Tumor, pubmed-meshheading:21228212-Cells, Cultured, pubmed-meshheading:21228212-Electron Transport Chain Complex Proteins, pubmed-meshheading:21228212-Enzyme Inhibitors, pubmed-meshheading:21228212-Glycolysis, pubmed-meshheading:21228212-Kinetics, pubmed-meshheading:21228212-Laser Scanning Cytometry, pubmed-meshheading:21228212-Leydig Cell Tumor, pubmed-meshheading:21228212-Leydig Cells, pubmed-meshheading:21228212-Male, pubmed-meshheading:21228212-Membrane Potential, Mitochondrial, pubmed-meshheading:21228212-Mice, pubmed-meshheading:21228212-Mitochondria, pubmed-meshheading:21228212-Progesterone, pubmed-meshheading:21228212-Rats, pubmed-meshheading:21228212-Steroids, pubmed-meshheading:21228212-Testicular Neoplasms, pubmed-meshheading:21228212-Testosterone, pubmed-meshheading:21228212-Uncoupling Agents
pubmed:year
2011
pubmed:articleTitle
ATP synthesis, mitochondrial function, and steroid biosynthesis in rodent primary and tumor Leydig cells.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, Division of Reproductive Biology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. andrew.midzak@mail.mcgill.ca
pubmed:publicationType
Journal Article, Comparative Study, Research Support, N.I.H., Extramural