DataSheet_1_cAMP-specific phosphodiesterase 8A and 8B isoforms are differentially expressed in human testis and Leydig cell tumor.pdf

Cyclic adenosine monophosphate/Protein kinase A (cAMP/PKA) signaling pathway is the master regulator of endocrine tissue function. The level, compartmentalization and amplitude of cAMP response are finely regulated by phosphodiesterases (PDEs). PDE8 is responsible of cAMP hydrolysis and its expression has been characterized in all steroidogenic cell types in rodents including adrenal and Leydig cells in rodents however scarce data are currently available in humans. Here we demonstrate that human Leydig cells express both PDE8A and PDE8B isoforms. Interestingly, we found that the expression of PDE8B but not of PDE8A is increased in transformed Leydig cells (Leydig cell tumors-LCTs) compared to non-tumoral cells. Immunofluorescence analyses further reveals that PDE8A is also highly expressed in specific spermatogenic stages. While the protein is not detected in spermatogonia it accumulates nearby the forming acrosome, in the trans-Golgi apparatus of spermatocytes and spermatids and it follows the fate of this organelle in the later stages translocating to the caudal part of the cell. Taken together our findings suggest that 1) a specific pool(s) of cAMP is/are regulated by PDE8A during spermiogenesis pointing out a possible new role of this PDE8 isoform in key events governing the differentiation and maturation of human sperm and 2) PDE8B can be involved in Leydig cell transformation.</p

Evaluation of effects of age, sex, BMI, WC, HC, WHR and UFDI on AHI with multivariate regression analysis in patients with metabolic syndrome (adjusted R² = 52483790; p<00002).

<p>Evaluation of effects of age, sex, BMI, WC, HC, WHR and UFDI on AHI with multivariate regression analysis in patients with metabolic syndrome (adjusted R² = 52483790; p<00002).</p

Baseline Characteristics of the Study Population, according to the severity of sleep disordered breathing.

<p>Values represent mean±standard deviation unless otherwise indicated.</p><p>#Number of patients with MetS. Percentage values in parentheses.</p>a<p>p<0.05 vs. no OSA.</p>b<p>p<0.01 vs no OSA.</p>c<p>p<0.001 vs no OSA.</p

Percentage of patients with metabolic syndrome (MetS) according to sleep disordered breathing.

<p>Percentage of patients with metabolic syndrome (MetS) according to sleep disordered breathing.</p

Linear regression analysis between epicardial fat thickness (EFT) and upper body fat deposition index (UFDI).

<p>r = 0.51223; p<0.001</p

Characteristics of patients with metabolic syndrome according to the severity of sleep disordered breathing.

<p>Values represent mean±standard deviation unless otherwise indicated.</p>a<p>p<0.05 vs no OSA.</p>b<p>p<0.01 vs no OSA.</p>c<p>p<0.001 vs. no OSA.</p

Body composition (upper) echocardiographic findings and cIMT measurements (lower) according to the severity of sleep disordered breathing.

<p>Values represent mean±standard deviation unless otherwise indicated.</p>a<p>p<0.05 vs no OSA.</p>b<p>p<0.01 vs no OSA.</p>c<p>p<0.001 vs. no OSA.</p