The alteration of inflammatory markers and apoptosis on chronic prostatitis induced by estrogen and androgen

Jia, Yuling; Liu, Xu; Yan, Jian-yan; Chong, Liming; Li, Lei; Ma, Aicui; Zhou, Li; Sun, Zheng

doi:10.1007/s11255-014-0845-4

Cited by 32 publications

(18 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A high abundance of inflammatory cells is associated with development of prostate cancer and with poor outcome [ 101 ], and there is an association between age induced decline in testosterone and increased prostatic inflammation [ 102 , 103 , 104 ]. Although an anti-inflammatory effect of androgens has been demonstrated for the whole prostate [ 105 ], the role of fibroblasts, and indeed fibroblast AR signalling, in this process is unclear. Significantly however, fibroblasts are known to interact with inflammatory immune cells [ 106 ], and testosterone action in synovial fibroblasts has been suggested to have an anti-inflammatory role by inhibition of pro-inflammatory cytokine production [ 107 , 108 ].…”

Section: Possible Mechanisms For the Involvement Of Stromal Ar Sigmentioning

confidence: 99%

Stromal Androgen Receptor in Prostate Cancer Development and Progression

Leach

Buchanan

2017

Cancers

View full text Add to dashboard Cite

Prostate cancer development and progression is the result of complex interactions between epithelia cells and fibroblasts/myofibroblasts, in a series of dynamic process amenable to regulation by hormones. Whilst androgen action through the androgen receptor (AR) is a well-established component of prostate cancer biology, it has been becoming increasingly apparent that changes in AR signalling in the surrounding stroma can dramatically influence tumour cell behavior. This is reflected in the consistent finding of a strong association between stromal AR expression and patient outcomes. In this review, we explore the relationship between AR signalling in fibroblasts/myofibroblasts and prostate cancer cells in the primary site, and detail the known functions, actions, and mechanisms of fibroblast AR signaling. We conclude with an evidence-based summary of how androgen action in stroma dramatically influences disease progression.

show abstract

Section: Possible Mechanisms For the Involvement Of Stromal Ar Sigmentioning

confidence: 99%

Stromal Androgen Receptor in Prostate Cancer Development and Progression

Leach

Buchanan

2017

Cancers

View full text Add to dashboard Cite

show abstract

“…Harris et al () demonstrated that estrogen administration stimulates the transcription of pro‐inflammatory factors such as IL‐1β, IL‐6, MIP‐2, and iNOS in the prostate lateral lobe of Wistar rats. Another study showed that estrogen administration for 30 days increased the prostatic levels of inflammatory markers such as TNF‐α, COX‐2 and CCL‐3 in castrated Sprague–Dawley rats (Jia et al, ).…”

Section: Introductionmentioning

confidence: 99%

Steroidal hormone and morphological responses in the prostate anterior lobe in different cancer grades after Celecoxib and Goniothalamin treatments in TRAMP mice

Silva

Kido

Montico

et al. 2018

Cell Biology International

View full text Add to dashboard Cite

Prostate cancer is the second most diagnosed cancer in the world, and alternative methods to prevent and treat different lesion grades need to be evaluated. The objective was to evaluate the morphological, hormonal, and inflammatory responses in the prostate anterior lobe in transgenic adenocarcinoma of the mouse prostate (TRAMP), following Celecoxib and Goniothalamin (GTN) treatments. All animals were treated for 4 weeks, from 8 weeks of age and euthanized either immediately after treatment (12-week-old mice: immediate response) or later (22-week-old mice: late response). The results showed a significant increase of high-grade prostatic intraepithelial neoplasia (HGPIN) and well-differentiated adenocarcinoma (WDA), according to the age in the control groups. Celecoxib treatment decreased the WDA incidence in the late response group. GTN led to a significant healthy tissue increase, and an LGPIN and HGPIN decrease in the immediate response group. In the late response group, GTN led to healthy area increase and there was no occurrence of WDA. AR and ERα immunoexpressions were reduced by both treatments in the immediate response groups. However, only GTN was able to decrease the ERα level in the late response group. Regarding COX-2 immunoreactivity, both treatments reduced the frequency of this enzyme. We can conclude that the prostate anterior lobe is a good model to study prostate cancer, considering its slow progression. Both treatments led to cancer delay in the prostate anterior lobe. However, GTN pointed towards a better treatment spectrum in the signaling pathways in the prostate microenvironment, particularly in ERα.

show abstract

“…Androgen supplementation has been reported to reduce the expression of inflammatory markers in prostatitis and attenuate the incidence and severity of prostatitis [38, 39]. Testosterone may reduce IL-6 and TNF-α production after LPS challenge by preventing Iκβ-alpha degradation and NF-κβ nuclear translocation [36].…”

Section: Discussionmentioning

confidence: 99%

Testosterone suppresses uropathogenic Escherichia coli invasion and colonization within prostate cells and inhibits inflammatory responses through JAK/STAT-1 signaling pathway

Fan

et al. 2017

PLoS ONE

View full text Add to dashboard Cite

Prostatitis is a common condition in adult men of all ages. Uropathogenic Escherichia coli (UPEC) are most frequent pathogen involved in bacterial prostatitis by refluxing the infected urine into prostatic ducts and resulting in an ascending urethral infection. However, the study about the mechanisms of UPEC to invade, replicate and persist in normal prostate epithelial cell is only few. Given the fact that UPEC is pathogen most frequently involved in prostatitis and that testosterone has been demonstrated to attenuate prostate inflammation caused by other etiologies. In this study we investigated whether the testosterone reduces the prostatitis and related mechanism by regulating IFN-γ/STAT1 signaling pathway. In the current study aimed to clarify whether testosterone influences the process of UPEC-induced prostate inflammation and invasion into the prostate epithelial cells. In addition, we set up a normal prostate cell model for UPEC infection to evaluate the ability to invade the urothelial cells as well as the colonization of intercellular bacterial communities in vitro. By using the model, we examine the effects of testosterone to suppress effectively the invasion and survival of UPEC in the prostate cells, and inhibit LPS-induced inflammatory responses through the JAK/STAT1 pathway have also been indicated. Our results demonstrated testosterone not only suppressed the invasion and colonization of UPEC, but also inhibited the expression of pro-inflammatory IL-1β, IL-6 and IL-8 cytokines expression induced by UPEC in a dose-dependent manner. We found the effective dose of testosterone to suppress UPEC infect prostate cells may be appropriate under 40μg/ml. Our data also revealed 20μg/ml testosterone treated PZ-HPV-7 cells significantly suppressed the LPS-induced JAK/STAT1 pathway and inflammatory responses, and reached to maximal effects at 40μg/ml treatment. These results indicate that testosterone plays an anti-inflammatory role in LPS-induced prostate cell inflammation by down-regulating JAK/STAT1 signaling pathway. Interestingly, the JAK inhibitor and testosterone for 24hr pretreatment rather markedly induced the colonization of UPEC in the PZ-HPV-7 cells. Based on the above data, the suppression of UPEC colonization in the prostate cells by testosterone seems to be unrelated with JAK/STAT signaling pathway, whereas the JAK may involve into the UPEC infection. Summing up these data, our findings have demonstrated the suppressive effects of testosterone on the invasion and survival of UPEC and induced inflammation in prostate epithelial cells. These findings indicate the action mechanism of testosterone as an anti-inflammatory mediator in the prostate cells is regulated through JAK/STAT1 signaling pathway, may be beneficial in treating prostate inflammation. Altogether, this study has provided the possibility that using testosterone in the prevention and clinical treatment of prostatitis is a new direction.

show abstract

The alteration of inflammatory markers and apoptosis on chronic prostatitis induced by estrogen and androgen

Abstract: Estrogen-alone-induced inflammatory response could promote the expression of inflammatory markers; however, T supplementation reduces the expression of inflammatory markers and E2-induced apoptosis occurs dependently on T manipulation in prostatitis.

Cited by 32 publications

References 25 publications

Stromal Androgen Receptor in Prostate Cancer Development and Progression

Stromal Androgen Receptor in Prostate Cancer Development and Progression

Steroidal hormone and morphological responses in the prostate anterior lobe in different cancer grades after Celecoxib and Goniothalamin treatments in TRAMP mice

Testosterone suppresses uropathogenic Escherichia coli invasion and colonization within prostate cells and inhibits inflammatory responses through JAK/STAT-1 signaling pathway

Contact Info

Product

Resources

About