Search

Objective: Testosterone is either neutral or has a harmful effect on the male cardiovascular system. But the role of imbalance of testosterone (T) and estrogen (E2) (T/E2 ratio) in male CHD has been less studied. This study was carried out with the purpose of evaluating the relationship between T/E2 ratio and CHD. Methods: Fifty-five male CHD patients (aged 61.25 ± 3.44) and 60 age-matched controls (aged 59.54 ± 1.44) were selected in this research. Results: Compared with control group, levels of both serum T and E2 decreased, but only E2 had statistical significance (P=0.001). The normal testosterone (T)/estradiol (E2) ratio is 1.7 ± 0.12, but the ratio of T/E2 (3.28 ± 0.58) changed significantly in men with CHD group (P<0.05). With the imbalance of T/E2 ratio in CHD group, we further used a linear and multiple regression methods to analyze the correlation between sex hormones and CHD risk factors. The results showed serum T was positively associated with TG (r=0.439, P<0.01) and D-dimer (r=0.258, P<0.05), but negatively associated with HDL-C (r=-0.267, P<0.05) and Hs-CRP (r=-0.214, P<0.05). However, E2 was highly positive associated with TG (r=0.783, P<0.01) and HDL-C (r=0.515, P<0.01), but was negative related with LDL-C (r=-0.219, P<0.05), TC/LDL (r=-0.236, P<0.05) and D-dimer. Multiple linear regression method also showed the same results between E2 and HDL-C (P=0.020), LDL-C (P=0.000), which showed E2's protective role in cases. However, T/E2's effect is more significative than E2's, and the values between T/E2 and index are HDL-C (r=-0.624, P<0.01), LDL-C (r=0.348, P<0.01), TC/HDL (r=0.237, P<0.05), Hs-CRP (r=0.248, P<0.05) and D-dimer (r=0.249, P<0.05). Multiple linear regression method also showed the positive relationship between T/E2 and HDL-C (P=0.000), D-dimer (P=0.000), and negative relationships between T/E2 and TC (P=0.000), TG (P=0.000) or HDL/LDL (P=0.000). Conclusion: The balance of T/E2 ratio, rather than the absolute levels of androgens, is crucial in modulating the effect of androgens on CHD in males. [ABSTRACT FROM AUTHOR]

Protein phosphatase 2A (PP2A) is indispensable in development, and deficits of PP2A and deterioration of neuronal axons have been observed in several neurodegenerative disorders, but the direct link between PP2A and the neuronal axon development is still missing. Here, we show that PP2A is essential for axon development in transfected rat brain and the dissociated hippocampal neurons. Upregulation of PP2A catalytic subunit (PP2Ac) not only promotes formation and elongation of the functional axons but also rescues axon retardation induced by PP2A inhibition. PP2A can dephosphorylate collapsin response mediator protein-2 (CRMP2) that implements the axon polarization, whereas constitutive expression of phosphomimic-CRMP2 abrogates the effect of PP2A upregulation. We also demonstrate that PP2Ac is enriched in the distal axon of the hippocampal neurons. Our results reveal a mechanistic link between PP2A and axonogenesis/axonopathy, suggesting that upregulation of PP2A may be a promising therapeutic for some neurodegenerative disorders.