Biol Reprod Keystone Symposia Conference on Frontiers in Reproductive Biology & Regulation of Fertility.
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BIOLOGY OF REPRODUCTION 73, 213–213 (2005)
DOI: 10.1095/biolreprod.105.044149
© 2005 by the Society for the Study of Reproduction, Inc.

Highlights

Involvement of Protein Kinase C and Cyclic Adenosine 3',5'-Monophosphate-Dependent Kinase in Steroidogenic Acute Regulatory Protein Expression and Steroid Biosynthesis in Leydig Cells. Youngah Jo, Steven R. King, Shafiq A. Khan, and Douglas M. Stocco. Biol Reprod 2005; 73:244–255. Published online 6 April 2005; 10.1095/biolreprod.104.037721

On p. 244 of this issue, Stocco and colleagues (Jo et al.) provide novel and interesting findings on roles of PKA and PKC pathway signaling in regulation of expression and function of steroid acute regulatory protein STAR (also abbreviated as StAR, though not necessarily because of its leading role in steroidogenesis). STAR protein is required for steroidogenesis because it mediates an important and rate-limiting step in steroid biosynthesis=mthe transfer of free cholesterol from the outer to the inner mitochondrial membrane. LH has both immediate effects and longer term (transcriptional) effects on Leydig cells. The rapid stimulation of Leydig cells by LH initiates steroidogenesis, but the precise downstream effector pathways, including roles of PKA and PKC signaling, have been difficult to sort out. In this study cultured Leydig cells and synthetic PKA and PKC activators were used to determine the role of each in regulation of STAR and steroid biosynthesis. The authors find that activation of the PKC pathway can induce transcription and translation of STAR protein, but this is not sufficient for the rapid steroidogenic response. The results illuminate the fact that minimal PKA activity explains immediate phosphorylation and activation of STAR to mediate cholesterol transfer and ultimate steroid synthesis.

Effect of Female Age on Mouse Oocyte Developmental Competence Following Mitochondrial Injury. George A. Thouas, Alan O. Trounson, and Gayle M. Jones. Biol Reprod 2005; 73:366–373. Published online 11 May 2005; 10.1095/biolreprod.105.040956

The deleterious effects of aging on oocyte quality are now well known, although the cellular and molecular bases of oocyte decline are not. On page 366 of this issue, Thouas et al. extend their earlier correlations between mitochondrial function in oocytes and the ability of mouse embryos to develop to the blastocyst stage. Here, they compare the effects of photosensitization with mitochondrial fluorophore rhodamine-123 on the developmental potential of metaphase II oocytes from young and old mice. Furthermore, mitochondrial membrane potential, and zygote metabolism and apoptosis were analyzed in embryos of nonirradiated or photosentizised oocytes of the two age groups. The paper provides genuine evidence that zygotes of aged nonirradiated oocytes possess less ATP and have a lower mitochondrial redox potential compared to those from the young group, and that aged oocytes are especially sensitive to mitochondrial damage causing developmental arrest. These observations are of high relevance for reproductive biology and toxicology and for treatment of infertility by assisted reproduction.

Mary Ann Handel, John Eppig, and Ursula Eichenlaub-Ritter


Related articles in Biol Reprod:

Involvement of Protein Kinase C and Cyclic Adenosine 3',5'-Monophosphate-Dependent Kinase in Steroidogenic Acute Regulatory Protein Expression and Steroid Biosynthesis in Leydig Cells
Youngah Jo, Steven R. King, Shafiq A. Khan, and Douglas M. Stocco
Biol Reprod 2005 73: 244-255. [Abstract] [Full Text]  

Effect of Female Age on Mouse Oocyte Developmental Competence Following Mitochondrial Injury
George A. Thouas, Alan O. Trounson, and Gayle M. Jones
Biol Reprod 2005 73: 366-373. [Abstract] [Full Text]  




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