The MA-10 Cell Line as a Model of insl3 Regulation and Leydig Cell Function

<p>Leydig cells produce testosterone in response to luteinizing hormone (LH) via the cyclic adenosine monophosphate (cAMP)/protein kinase A pathway. Additionally, these cells are responsible for producing insulin-like peptide 3 (INSL3), a peptide hormone that is essential for testicular descent. The <em>insl3</em> promoter in Leydig cells can be activated by cAMP through the transcription factor Nur77, which has also been shown to regulate the promoters of the steroidogenic enzymes, <em>cyp17</em> and <em>3</em><em>b-hsd</em>. While the mechanism of LH action on testosterone production is well characterized, the effect of LH on <em>insl3</em> abundance has yet to be shown directly. The MA-10 Leydig cells treated with hCG exhibited a transient and robust increase in <em>nur77</em> mRNA, while <em>insl3</em> mRNA abundance remained unchanged. Further, cAMP failed to affect <em>insl3</em> mRNA, though <em>nur77</em> mRNA abundance was significantly increased. Inhibition of LH-receptor-linked signal transduction pathways in the presence of hCG implicated multiple signaling networks in the regulation of both <em>insl3</em> and <em>nur77.</em> Treatment with hCG or cAMP did not affect the abundance of <em>3</em><em>b-hsd</em> mRNA. Interestingly, though the MA-10 cell line has been reported to lack CYP17 activity and mRNA and so produce progesterone instead of testosterone, <em>cyp17</em> mRNA was present and inducible by hCG and cAMP. The addition of hCG, testosterone, nor the combination of hCG and testosterone affected <em>insl3</em> mRNA abundance. Though hCG consistently increased <em>nur77</em> mRNA abundance, the addition of testosterone did not enhance the effects of hCG. Collectively, these results indicate that <em>insl3</em> is regulated by factors other than LH/CG and cAMP in the MA-10 cell line.</p>

Name thesis:degree_name

MS in Agriculture - Animal Science

Discipline thesis:degree_discipline

Animal Science

Year dc:date.available

2011

Author dc:creator

• Strong, Mary E

Contributors dc:contributor

• Daniel G. Peterson

• Leydig Cell
• INSL3
• cryptorchidism
• testicular descent
• cell signaling
• Other Animal Sciences

Identifier

10.15368/theses.2011.148

OAI identifier oai:identifier

oai:digitalcommons.calpoly.edu:theses-1630