[Expressions of SIgA and alpha 1-AR in benign prostatic hyperplasia combined with chronic prostatitis and their implications].

OBJECTIVE: To explore the expressions of SIgA and alpha l-AR in benign prostatic hyperplasia (BPH) complicated by chronic prostatitis (CP) and their implications. METHODS: According to the preoperative findings of expressed prostatic secretion (EPS), transrectal prostate ultrasonography, prostate-specific antigen (PSA), international prostate symptom score (IPSS), clinical symptoms, chronic pelvic pain syndrome (CPPS) and postoperative histopathology, 62 cases of BPH pathologically confirmed after transurethral plasma kinetic resection of the prostate (PKRP) were divided into a BPH group (n = 32) and a BPH + CP group (n = 30). The expressions of SIgA and alpha 1-AR in the prostate tissue were determined by immunohistochemistry and PT-PCR. RESULTS: Of the 62 cases, 30 were found to be BPH + CP, and the other 32 to be BPH. The expressions of SIgA and alpha1-AR were significantly higher in the BPH + CP than in the BPH group (0.380 8 +/- 0.144 3 vs 0.295 4 +/- 0.008 4 and 0.440 5 +/- 0.104 1 vs 0.383 2 +/- 0.013 6, P < 0.05). CONCLUSION: The upregulated expressions of SIgA and alpha1-AR expression in BPH complicated by CP suggest a certain association between CP and BPH, and that inflammation may be a pathogenic factor of BPH and correlate with its pathological development.

Transcriptome Analysis in High Temperature Inhibiting Spermatogonial Stem Cell Differentiation In Vitro.

As one of the factors of male infertility, high temperature induces apoptosis of differentiated spermatogenic cells, sperm DNA oxidative damage, and changes in morphology and function of Sertoli cells. Spermatogonial stem cells (SSCs) are a type of germline stem cells that maintain spermatogenesis through self-renewal and differentiation. At present, however, the effect of high temperature on SSC differentiation remains unknown. In this study, an in vitro SSC differentiation model was used to investigate the effect of heat stress treatment on SSC differentiation, and RNA sequencing (RNA-seq) was used to enrich the key genes and pathways in high temperature inhibiting SSC differentiation. Results show that 2 days of 37 °C or 43 °C (30 min per day) heat stress treatment significantly inhibited SSC differentiation. The differentiation-related genes c-kit, stra8, Rec8, Sycp3, and Ovol1 were down-regulated after 2 and 4 days of heat stress at 37 °C. The transcriptome of SSCs was significantly differentially expressed on days 2 and 4 after heat stress treatment at 37 °C. In total, 1660 and 7252 differentially expressed genes (DEGs) were identified by RNA-seq in SSCs treated with heat stress at 37 °C for 2 and 4 days, respectively. KEGG pathway analysis showed that p53, ribosome, and carbon metabolism signaling pathways promoting stem cell differentiation were significantly enriched after heat stress treatment at 37 °C. In conclusion, 37 °C significantly inhibited SSC differentiation, and p53, ribosome, and carbon metabolism signaling pathways were involved in this differentiation inhibition process. The results of this study provide a reference for further investigation into the mechanism by which high temperature inhibits SSC differentiation.

High temperature suppressed SSC self-renewal through S phase cell cycle arrest but not apoptosis.

BACKGROUND: High temperature has a very adverse effect on mammalian spermatogenesis and eventually leads to sub- or infertility through either apoptosis or DNA damage. However, the direct effects of heat stress on the development of spermatogonial stem cells (SSCs) are still unknown because SSCs are rare in the testes. METHODS: In the present study, we first used in vitro-cultured SSCs to study the effect of heat shock treatment on SSC development. Then, we used RNA-Seq analysis to identify new genes or signalling pathways implicated in the heat stress response. RESULTS: We found that 45 min of 43 °C heat shock treatment significantly inhibited the proliferation of SSCs 2 h after treatment but did not lead to apoptosis. In total, 17,822 genes were identified by RNA-Seq after SSC heat shock treatment. Among these genes, we found that 200 of them had significantly changed expression, with 173 upregulated and 27 downregulated genes. The number of differentially expressed genes in environmental information processing pathways was 37, which was the largest number. We screened the candidate JAK-STAT signalling pathway on the basis of inhibition of cell cycle progression and found that the JAK-STAT pathway was inhibited after heat shock treatment. The flow cytometry results further confirmed that heat stress caused S phase cycle arrest of SSCs. CONCLUSION: Our results showed that heat shock treatment at 43 °C for 45 min significantly inhibited SSC self-renewal through S phase cell cycle arrest but not apoptosis.