ABSTRACT
Neurogenic erectile dysfunction (NED) caused by pelvic floor surgeries/radiation therapies and associated with Parkinsons disease and diabetes remains a challenging healthcare issue. To facilitate NED research we have developed in vitro and in vivo experimental models. The in vitro model comprises the isolation, culture and treatment of rat major pelvic ganglia (MPG), which then produce outgrowing neurites whose length and molecular composition are indicative of the neurotrophic effect of the treatment agent. Through this approach we have confirmed that the brain-derived neurotrophic factor (BDNF) promotes nerve regeneration by activating the JAK/STAT signaling pathway. This has been further established by our in vivo model, which involves the transection or cruch of cavernous nerves and treatment with BDNF.
Subject(s)
Animals , Humans , Male , Disease Models, Animal , Erectile Dysfunction , Ganglia , In Vitro Techniques , Nerve Regeneration , Pelvis , PenisABSTRACT
<p><b>OBJECTIVE</b>To evaluate the relationship between the deformation of penile artery and the primary artery erectile dysfunction, and to improve the treatment and diagnosis of primary artery erectile dysfunction.</p><p><b>METHODS</b>One case of primary artery erectile dysfunction was presented with its primary clinic data.</p><p><b>RESULTS</b>The dorsal artery of the penis was thin and the bilateral penile arteries were lacking by arteriography. The implantation of a penile prosthesis significantly improved the patient's erectile function.</p><p><b>CONCLUSION</b>The primary artery erectile dysfunction is a relatively rare disease. The possibility of primary artery erectile dysfunction should be kept in mind. Penile prosthesis implantation is an effective means for the treatment of primary artery erectile dysfunction.</p>
Subject(s)
Adult , Humans , Male , Arteries , Congenital Abnormalities , Impotence, Vasculogenic , Diagnostic Imaging , General Surgery , Penile Implantation , Penis , Diagnostic Imaging , RadiographyABSTRACT
<p><b>AIM</b>To identify proteins that are differentially expressed in cells derived from normal and diseased tunica albuginea (TA) as related to Peyronie's disease (PD).</p><p><b>METHODS</b>Cells with characteristics of fibroblasts were isolated from two tissue sources. Those from the plaque of patients with PD were designated as PT cells, and those from the normally-appearing TA of the same patients were designated as NT cells. Messenger RNAs of these cells were analyzed by real-time polymerase chain reaction (RT-PCR) for the expression of monocyte chemoattractant protein 1 (MCP-1). Crude protein lysates were analyzed by surface-enhanced laser desorption/ionization mass spectrometry (SELDI-MS) with IMAC30-Cu, CM10, and H50 chips. Each lysate was then separated into six fractions, which were further analyzed by SELDI-MS.</p><p><b>RESULTS</b>RT- PCR analysis showed that PT cells expressed higher levels of MCP-1 than their counterpart NT cells. SELDI-MS analysis showed that the crude protein lysates of all four cell strains produced similar and reproducible protein profiles on IMAC30-Cu and CM10 chips. Additional SELDI-MS analyses with the fractionated lysates detected three proteins of 11.6 kDa, 14.5 kDa, 22.6 kDa that were upregulated in PT cells and two proteins of 6.3 kDa and 46.9 kDa that were downregulated in PT cells.</p><p><b>CONCLUSION</b>MCP-1, which is often involved in tissue fibrosis, was expressed at higher levels in PT than that in NT cells. Five potential biomarkers for PD were identified by SELDI-MS analysis.</p>
Subject(s)
Humans , Male , Base Sequence , Biomarkers , Cells, Cultured , Chemokine CCL2 , Metabolism , DNA Primers , Mass Spectrometry , Methods , Penile Induration , Metabolism , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
Objective To investigate the effects of dominant-negative truncation mutant?NTCF4, lacking the N-terminal form of TCF4 gene,on biological characteristics of renal cancer cell line GRC-I and explore the molecular mechanisms.Methods GRC-I cell was transfected with pCDNA3-?NTCF4 eukary- otie expression plasmid,pCDNA3 empty vector to construct the stable cell line GRC-I/?NTCF4 and GRC-I/ Mock respectively.The morphological changes of stable cells were observed and the cells growth curve was detected through light microscope.The cellular proliferation activities were determined using the MTT assay. The protein expression of Wnt pathway downstream target gene C-Myc and Cox-2 was evaluated by immuno- cytoehemieal method and Western Blot analysis.Results After the dominant-negative?NTCF4 gene was permanently expressed,the GRC-I/?NTCF4 stable cells morphologically showed that appearance changed from circular to long-spindle shape,growth rate decreased with less karyosehisis found,malignant pheno- types reversed to normal renal tubular cells.MTT assay revealed that the proliferation activities of GRC-1/?NTCF4 cells were inhibited by 11.2%-35.5% compared with GRC-I cells (P＜0.05),while the GRC- I/Mock cells have no difference with the control cells.Immunocytochemical analysis and Western Blot showed that the C-Myc and Cox-2 protein expression level of GRC-I/?ANTCF4 cells were significantly sup- pressed in comparison with that of GRC-I/Mock and GRC-I cells.Conclusions The dominant-negative truncation mutant?NTCF4 could partially inhibit the growth of renal cancer cells and down-regulate the pro- tein expression of Wnt pathway target gene C-Myc and Cox-2.These findings provide a experimental founda- tion for applying cell signal therapy to renal cell cancer by blocking the Wnt signaling pathway.