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  • DeFranco, Donald B.  (11)
  • Wang, Zhou  (11)
  • 1
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    Upregulation of androgen‐responsive genes and transforming growth factor‐β1 cascade genes in a rat model of non‐bacterial prostatic inflammation
    Wiley ; 2014
    In:  The Prostate Vol. 74, No. 4 ( 2014-04), p. 337-345
    Details
    In: The Prostate, Wiley, Vol. 74, No. 4 ( 2014-04), p. 337-345
    Abstract: Prostatic inflammation is associated with the development of prostatic hyperplasia. We investigated the effects of prostatic inflammation on expression levels of androgen‐responsive genes and growth factors in the prostate. METHODS Prostatic inflammation was induced by formalin injection into bilateral ventral lobes of the prostate of male SD rats. After 28 days, the prostate was harvested for analyses of proinflammatory cytokines, androgen‐responsive genes in the epithelium, and TGF‐β1 cascade genes in the stroma. Some rats were given a COX‐2 inhibitor (celecoxib; 10 mg/kg/day) by oral gavage for 28 days. RESULTS The formalin‐injected prostate exhibited widespread low‐grade inflammation ( 〈 50 leukocytes/10,000 μm 2 ) along with focal high‐grade inflammation ( 〉 100 leukocytes/10,000 μm 2 ) in limited areas. Compared to control, formalin‐injected prostate exhibited a 2.5‐fold to sixfold increased protein expression of IL‐1α, IL‐1β, and IL‐6. In the low‐grade inflammatory regions, threefold to ninefold and twofold to threefold upregulations of mRNA levels of androgen receptors/androgen‐responsive genes and TGF‐β1 cascade genes were respectively, observed in the epithelium and stroma obtained by laser‐capture microdissection. Positive staining for androgen receptors in the epithelial nuclei, and TGF‐β1, IL‐6, and COX‐2 in the stroma was increased in the low‐grade inflammation area. COX‐2 inhibitor treatment suppressed these upregulations of cytokines, androgen‐responsive, and TGF‐β1 cascade genes. CONCLUSIONS Prostatic inflammation induced increased expression of androgen‐responsive genes in the epithelium and TGF‐β1 cascade genes in the stroma, which were suppressed by COX‐2 inhibitors, suggesting that activation of these genes in the low‐grade inflammatory region might be involved in the development of symptomatic BPH. Prostate 74:337–345, 2014 . © 2013 Wiley Periodicals, Inc.
    Type of Medium: Online Resource
    ISSN: 0270-4137 , 1097-0045
    URL: Issue
    URL: Article
    DOI: 10.1002/pros.v74.4
    DOI: 10.1002/pros.22668
    Language: English
    Publisher: Wiley
    Publication Date: 2014
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  • 2
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    Effects of Estrogen Receptor β Stimulation in a Rat Model of Non‐Bacterial Prostatic Inflammation
    Wiley ; 2017
    In:  The Prostate Vol. 77, No. 7 ( 2017-05), p. 803-811
    Details
    In: The Prostate, Wiley, Vol. 77, No. 7 ( 2017-05), p. 803-811
    Abstract: There is increasing evidence showing that chronic non‐bacterial prostatic inflammation is involved in the pathogenesis of benign prostatic hyperplasia (BPH) and male lower urinary tract symptoms (LUTS). It has also been reported that estrogen receptor β (ERβ) could have an immunoprotective role in prostatic tissue. Therefore, we investigated the effect of ERβ‐activation on not only prostatic inflammation, but also bladder overactive conditions in a rat model with nonbacterial prostatic inflammation. METHODS Male Sprague‐Dawley rats (8 weeks, n = 15) were divided into three groups: sham‐saline group (n = 5), formalin‐vehicle group (n = 5), and formalin‐treatment group (n = 5). The sham‐saline group had sham operation and 50 μl normal saline injected into each ventral lobe of the prostate. The formalin‐vehicle group had 50 μl 5% formalin injection into bilateral ventral lobes of the prostate. The formalin‐treatment group was treated with 3α‐Adiol (a selective ERβ agonist precursor) at a dose of 3 mg/kg daily from 2 days before induction of prostatic inflammation, whereas formalin‐vehicle rats received vehicle (olive oil). In each group, conscious cystometry was performed on day 28 after intraprostatic formalin injection or sham treatment. After cystometry, the bladder and prostate were harvested for evaluation of mRNA expression and histological analysis. RESULTS In cystometric investigation, the mean number of non‐voiding contractions was significantly greater and voiding intervals were significantly shorter in formalin‐vehicle rats than those in sham‐saline rats ( P   〈  0.05). In RT‐qPCR analysis, mRNA expression of NGF, P2X2, and TRPA1 receptors was significantly increased in the bladder mucosa, and mRNA expression of TNF‐α, iNOS and COX2 in the ventral lobes of prostate was significantly increased in formalin‐vehicle rats compared with sham‐saline rats ( P   〈  0.05). In addition, relative mRNA expression ratio of ERβ to ERα (ERβ/ERα) in the ventral lobes of prostate was significantly decreased in formalin‐vehicle rats compared with sham‐saline rats ( P   〈  0.05). These changes were ameliorated by 3α‐Adiol administration in formalin‐treatment rats. CONCLUSIONS These results indicate that ERβ activation by 3α‐Adiol administration, which normalized the ERβ/ERα expression ratio in the prostate, can improve not only prostatic inflammation, but also bladder overactivity. Therefore, ERβ agonists might be useful for treating irritative bladder symptoms in patients with symptomatic BPH associated with prostatic inflammation. Prostate 77:803–811, 2017 . © 2017 Wiley Periodicals, Inc.
    Type of Medium: Online Resource
    ISSN: 0270-4137 , 1097-0045
    URL: Issue
    URL: Article
    DOI: 10.1002/pros.v77.7
    DOI: 10.1002/pros.23320
    Language: English
    Publisher: Wiley
    Publication Date: 2017
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  • 3
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    Long‐lasting bladder overactivity and bladder afferent hyperexcitability in rats with chemically‐induced prostatic inflammation
    Wiley ; 2019
    In:  The Prostate Vol. 79, No. 8 ( 2019-06), p. 872-879
    Details
    In: The Prostate, Wiley, Vol. 79, No. 8 ( 2019-06), p. 872-879
    Abstract: Benign prostatic hyperplasia (BPH) is one of the major causes of lower urinary tract symptoms (LUTS), including storage LUTS such as urinary frequency and urgency. Recently, a growing number of clinical studies indicate that prostatic inflammation could be an important pathophysiological mechanism inducing storage LUTS in patients with BPH. Here we aimed to investigate whether nonbacterial prostatic inflammation in a rat model induced by intraprostatic formalin injection can lead to long‐lasting bladder overactivity and changes in bladder afferent neuron excitability. Methods Male Sprague‐Dawley rats were divided into four groups (n = 12 each): normal control group, 1‐week prostatic inflammation group, 4‐week inflammation group, and 8‐week inflammation group. Prostatic inflammation was induced by formalin (10%; 50 µL per lobe) injection into bilateral ventral lobes of the prostate. Voiding behavior was evaluated in metabolic cages for each group. Ventral lobes of the prostate and the bladder were then removed for hematoxylin and eosin (HE) staining to evaluate inflammation levels. Continuous cystometrograms (CMG) were recorded to measure intercontraction intervals (ICI) and voided volume per micturition. Whole‐cell patch clamp recordings were performed on dissociated bladder afferent neurons labeled by fluorogold injected into the bladder wall, to examine the electrophysiological properties. Results Results of metabolic cage measurements showed that formalin‐treated rats exhibited significantly ( P   〈  0.05) increases in micturition episodes/12 hours and decrease in voided volume per micturition at every time point post injection. Continuous CMG illustrated the significant ( P   〈  0.05) higher number of nonvoiding contractions per void and shorter ICI in formalin‐treated rats compared with control rats. HE staining showed significant prostatic inflammation, which declined gradually, in prostate tissues of formalin‐induced rats. In patch clamp recordings, capsaicin‐sensitive bladder afferent neurons from rats with prostatic inflammation had significantly ( P   〈  0.05) lower thresholds for spike activation and a “multiple” firing pattern compared with control rats at every time point post injection. Conclusions Formalin‐induced prostatic inflammation can lead to long‐lasting bladder overactivity in association with bladder afferent neuron hyperexcitability. This long‐lasting model could be a useful tool for the study of inflammation‐related aspects of male LUTS pathophysiology.
    Type of Medium: Online Resource
    ISSN: 0270-4137 , 1097-0045
    URL: Issue
    URL: Article
    DOI: 10.1002/pros.v79.8
    DOI: 10.1002/pros.23794
    Language: English
    Publisher: Wiley
    Publication Date: 2019
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  • 4
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    E‐cadherin is downregulated in benign prostatic hyperplasia and required for tight junction formation and permeability barrier in the prostatic epithelial cell monolayer
    Wiley ; 2019
    In:  The Prostate Vol. 79, No. 11 ( 2019-08), p. 1226-1237
    Details
    In: The Prostate, Wiley, Vol. 79, No. 11 ( 2019-08), p. 1226-1237
    Abstract: We previously reported the presence of prostate‐specific antigen (PSA) in the stromal compartment of benign prostatic hyperplasia (BPH). Since PSA is expressed exclusively by prostatic luminal epithelial cells, PSA in the BPH stroma suggests increased tissue permeability and the compromise of epithelial barrier integrity. E‐cadherin, an important adherens junction component and tight junction regulator, is known to exhibit downregulation in BPH. These observations suggest that the prostate epithelial barrier is disrupted in BPH and E‐cadherin downregulation may increase epithelial barrier permeability. Methods The ultra‐structure of cellular junctions in BPH specimens was observed using transmission electron microscopy (TEM) and E‐cadherin immunostaining analysis was performed on BPH and normal adjacent specimens from BPH patients. In vitro cell line studies using benign prostatic epithelial cell lines were performed to determine the impact of small interfering RNA knockdown of E‐cadherin on transepithelial electrical resistance and diffusion of fluorescein isothiocyanate (FITC)‐dextran in transwell assays. Results The number of kiss points in tight junctions was reduced in BPH epithelial cells as compared with the normal adjacent prostate. Immunostaining confirmed E‐cadherin downregulation and revealed a discontinuous E‐cadherin staining pattern in BPH specimens. E‐cadherin knockdown increased monolayer permeability and disrupted tight junction formation without affecting cell density. Conclusions Our results indicate that tight junctions are compromised in BPH and loss of E‐cadherin is potentially an important underlying mechanism, suggesting targeting E‐cadherin loss could be a potential approach to prevent or treat BPH.
    Type of Medium: Online Resource
    ISSN: 0270-4137 , 1097-0045
    URL: Issue
    URL: Article
    DOI: 10.1002/pros.v79.11
    DOI: 10.1002/pros.23806
    Language: English
    Publisher: Wiley
    Publication Date: 2019
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  • 5
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    Differential impact of paired patient‐derived BPH and normal adjacent stromal cells on benign prostatic epithelial cell growth in 3D culture
    Wiley ; 2020
    In:  The Prostate Vol. 80, No. 14 ( 2020-10), p. 1177-1187
    Details
    In: The Prostate, Wiley, Vol. 80, No. 14 ( 2020-10), p. 1177-1187
    Abstract: Benign prostatic hyperplasia (BPH) is an age‐related disease characterized by nonmalignant abnormal growth of the prostate, which is also frequently associated with lower urinary tract symptoms. The prostate with BPH exhibits enhanced growth not only in the epithelium but also in the stroma, and stromal‐epithelial interactions are thought to play an important role in BPH pathogenesis. However, our understanding of the mechanisms of stromal‐epithelial interactions in the development and progression of BPH is very limited. Methods Matched pairs of glandular BPH and normal adjacent prostate specimens were obtained from BPH patients undergoing simple prostatectomy for symptomatic BPH. Tissues were divided further into fresh specimens for culture of primary prostatic stromal cells, and specimens were embedded in paraffin for immunohistochemical analyses. Proliferation assays, immunohistochemistry, and immunoblotting were used to characterize the primary prostate stromal cells and tissue sections. Coculture of the primary stromal cells with benign human prostate epithelial cell lines BHPrE1 or BPH‐1 was performed in three‐dimensional (3D) Matrigel to determine the impact of primary stromal cells derived from BPH on epithelial proliferation. The effect of stromal‐conditioned medium (CM) on BHPrE1 and BPH‐1 cell growth was tested in 3D Matrigel as well. Results BPH stromal cells expressed less smooth muscle actin and calponin and increased vimentin, exhibiting a more fibroblast and myofibroblast phenotype compared with normal adjacent stromal cells both in culture and in corresponding paraffin sections. Epithelial spheroids formed in 3D cocultures with primary BPH stromal cells were larger than those formed in coculture with primary normal stromal cells. Furthermore, CM from BPH stromal cells stimulated epithelial cell growth while CM from normal primary stromal cells did not in 3D culture. Conclusions These findings suggest that the stromal cells in BPH tissues are different from normal adjacent stromal cells and could promote epithelial cell proliferation, potentially contributing to the development and progression of BPH.
    Type of Medium: Online Resource
    ISSN: 0270-4137 , 1097-0045
    URL: Issue
    URL: Article
    DOI: 10.1002/pros.v80.14
    DOI: 10.1002/pros.24044
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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  • 6
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    Bladder overactivity and afferent hyperexcitability induced by prostate‐to‐bladder cross‐sensitization in rats with prostatic inflammation
    Wiley ; 2019
    In:  The Journal of Physiology Vol. 597, No. 7 ( 2019-04), p. 2063-2078
    Details
    In: The Journal of Physiology, Wiley, Vol. 597, No. 7 ( 2019-04), p. 2063-2078
    Abstract: There is clinical evidence showing that prostatic inflammation contributes to overactive bladder symptoms in male patients; however, little is known about the underlying mechanisms In this study, we investigated the mechanism that prostatic inflammation causes detrusor overactivity by using a rat model of chemically induced prostatic inflammation. We observed a significant number of dorsal root ganglion neurons with dichotomized afferents innervating both prostate and bladder. We also found that prostatic inflammation induces bladder overactivity and urothelial NGF overexpression in the bladder, both dependent on activation of the pelvic nerve, as well as changes in ion channel expression and hyperexcitability of bladder afferent neurons. These results indicate that the prostate‐to‐bladder cross‐sensitization through primary afferent pathways in the pelvic nerve, which contain dichotomized afferents, could be an important mechanism contributing to bladder overactivity and afferent hyperexcitability induced by prostatic inflammation.
    Type of Medium: Online Resource
    ISSN: 0022-3751 , 1469-7793
    URL: Issue
    URL: Article
    DOI: 10.1113/tjp.2019.597.issue-7
    DOI: 10.1113/JP277452
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 1475290-6
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  • 7
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    The role of prostaglandin and E series prostaglandin receptor type 4 receptors in the development of bladder overactivity in a rat model of chemically induced prostatic inflammation
    Wiley ; 2019
    In:  BJU International Vol. 124, No. 5 ( 2019-11), p. 883-891
    Details
    In: BJU International, Wiley, Vol. 124, No. 5 ( 2019-11), p. 883-891
    Abstract: To evaluate, using a rat model of non‐bacterial prostatic inflammation, the prostaglandin production and expression profiles of E‐series prostaglandin (EP) receptor subtypes, which are reportedly implicated in the development of overactive bladder, in the bladder mucosa, and to investigate the effect of EP receptor type 4 (EP4) blockade on bladder overactivity after prostatic inflammation. Methods Male Sprague‐Dawley rats were used. Prostatic inflammation was induced by formalin injection (5%; 50 μL per lobe) into the bilateral ventral lobes of the prostate. At 10 days after induction of prostatic inflammation or vehicle injection, bladder tissues from the deeply anaesthetized rats were harvested and separated into mucosal and detrusor layers. Then, prostaglandin E2 (PGE2) concentrations and protein levels of PGE2 receptors (EP1–4) in the bladder mucosa and detrusor were measured by ELISA and Western blotting, respectively. In separate groups of control and formalin‐treated rats, awake cystometry was performed to evaluate the changes in bladder activity after prostatic inflammation. In addition, the effect of intravesical administration of a selective EP4 antagonist (ONO‐AE3‐208; 30 μ m ) on bladder activity was evaluated in control rats and rats with prostatic inflammation. Results PGE2 concentration and protein levels of EP4, but not other EP receptor subtypes, in the bladder mucosa and detrusor layers were significantly increased in formalin‐injected rats vs vehicle‐injected control rats. In cystometry, rats with prostatic inflammation exhibited a significant decrease in intercontraction intervals (ICIs) compared with control rats. Intravesical application of ONO‐AE3‐208 (30 μ m ), but not vehicle application, significantly increased ICIs in rats with prostatic inflammation, whereas ONO‐AE3‐208 at this concentration did not significantly affect any cystometric values in control rats. Conclusions Because intravesical administration of an EP4 antagonist effectively improved bladder overactivity after prostatic inflammation, EP4 activation, along with increased PGE2 production in the bladder mucosa, seems to be an important contributing factor to bladder overactivity induced by prostatic inflammation. Thus, blockade of EP4 in the bladder could be a therapeutic approach to male lower urinary tract symptoms attributable to benign prostatic hyperplasia with prostatic inflammation.
    Type of Medium: Online Resource
    ISSN: 1464-4096 , 1464-410X
    URL: Issue
    URL: Article
    DOI: 10.1111/bju.v124.5
    DOI: 10.1111/bju.14845
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2019983-1
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  • 8
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    Influence of E. coli -induced prostatic inflammation on expression of androgen-responsive genes and transforming growth factor beta 1 cascade genes in rats : Androgen and TGFβ1 Cascade Genes In Prostatitis
    Wiley ; 2015
    In:  The Prostate Vol. 75, No. 4 ( 2015-03), p. 381-389
    Details
    In: The Prostate, Wiley, Vol. 75, No. 4 ( 2015-03), p. 381-389
    Type of Medium: Online Resource
    ISSN: 0270-4137
    URL: Issue
    URL: Article
    DOI: 10.1002/pros.v75.4
    DOI: 10.1002/pros.22924
    Language: English
    Publisher: Wiley
    Publication Date: 2015
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  • 9
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    Effects of dutasteride in a rat model of chemically induced prostatic inflammation—Potential role of estrogen receptor β
    Wiley ; 2020
    In:  The Prostate Vol. 80, No. 16 ( 2020-12), p. 1413-1420
    Details
    In: The Prostate, Wiley, Vol. 80, No. 16 ( 2020-12), p. 1413-1420
    Abstract: Dutasteride administration reportedly improves lower urinary tract symptoms in patient with chronic, histologically‐identified prostatic inflammation, potentially through estrogen receptor β (ERβ), activation of which has anti‐inflammatory effects in the prostate tissue. Therefore, we investigated the effect of dutasteride on intraprostatic inflammatory responses and bladder activity using a rat model of chemically induced prostatic inflammation. Methods Male Sprague–Dawley rats at 10 weeks old were used. Prostatic inflammation was induced by 5% formalin injection into ventral lobes of the prostate and saline was injected in the control group (control, n  = 5). Rats with prostatic inflammation were divided into dutasteride therapy (dutasteride, n  = 5) and placebo groups (placebo, n  = 5). Dutasteride was administrated at a dose of 0.5 mg/kg daily from 2 days before induction of prostatic inflammation whereas placebo rats received vehicle only. Twenty‐eight days later, cystometry was performed in a conscious condition to measure non‐voiding contractions (NVCs), intercontraction intervals (ICI) and postvoid residual volume (RV). After cystometry, the prostate was excised for analysis of messenger RNA (mRNA) expression levels of ERα, ERβ, interleukin‐1β (IL‐1β), and IL‐18 by quantitative polymerase chain reaction. Results The mean number of NVCs was significantly greater in placebo group than that of control group without prostatic inflammation ( p   〈  .05), and ICI were significantly decreased in placebo group compared with control group ( p   〈  .05). On the contrary, there was no significant change in NVCs or ICI between control and dutasteride groups. RV was not significantly different among three groups. Gene expression levels of ERα, IL‐1β, and IL‐18 was significantly increased in placebo rats compared with control rats ( p   〈  .05), but not significantly different between control and dutasteride rats. On the other hand, the mRNA expression level of ERβ was significantly decreased in placebo rats ( p   〈  .05), but not in dutasteride rats, compared with control rats. Conclusion Dutasteride treatment improved not only prostatic inflammation evident as increased gene expression levels in IL‐1β and IL‐18, but also bladder overactivity shown by increased NVCs during bladder filling. These therapeutic effects were associated with the restored expression of anti‐inflammatory ERβ. Therefore, dutasteride might be effective via ERβ modulation for the treatment of prostatic inflammation in addition to its previously known, anti‐androgenic effects on benign prostatic hyperplasia.
    Type of Medium: Online Resource
    ISSN: 0270-4137 , 1097-0045
    URL: Issue
    URL: Article
    DOI: 10.1002/pros.v80.16
    DOI: 10.1002/pros.24071
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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  • 10
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    Tight junction protein claudin‐1 is downregulated by TGF‐β1 via MEK signaling in benign prostatic epithelial cells
    Wiley ; 2020
    In:  The Prostate Vol. 80, No. 14 ( 2020-10), p. 1203-1215
    Details
    In: The Prostate, Wiley, Vol. 80, No. 14 ( 2020-10), p. 1203-1215
    Abstract: Benign prostatic hyperplasia (BPH) is arguably the most common disease in aging men. Although the etiology is not well understood, chronic prostatic inflammation is thought to play an important role in BPH initiation and progression. Our recent studies suggest that the prostatic epithelial barrier is compromised in glandular BPH tissues. The proinflammatory cytokine transforming growth factor beta 1 (TGF‐β1) impacts tight junction formation, enhances epithelial barrier permeability, and suppresses claudin‐1 messenger RNA expression in prostatic epithelial cells. However, the role of claudin‐1 in the prostatic epithelial barrier and its regulation by TGF‐β1 in prostatic epithelial cells are not clear. Methods The expression of claudin‐1 was analyzed in 22 clinical BPH specimens by immunohistochemistry. Human benign prostate epithelial cell lines BPH‐1 and BHPrE1 were treated with TGF‐β1 and transfected with small interfering RNAs specific to claudin‐1. Epithelial monolayer permeability changes in the treated cells were measured using trans‐epithelial electrical resistance (TEER). The expression of claudin‐1, E‐cadherin, N‐cadherin, snail, slug, and activation of mitogen‐activated proteins kinases (MAPKs) and AKT was assessed following TGF‐β1 treatment using Western blot analysis. Results Claudin‐1 expression was decreased in glandular BPH tissue compared with adjacent normal prostatic tissue in patient specimens. TGF‐β1 treatment or claudin‐1 knockdown in prostatic epithelial cell lines increased monolayer permeability. TGF‐β1 decreased levels of claudin‐1 and increased levels of snail and slug as well as increased phosphorylation of the MAPK extracellular signal‐regulated kinase‐1/2 (ERK‐1/2) in both BPH‐1 and BHPrE1 cells. Overexpression of snail or slug had no effect on claudin‐1 expression. In contrast, PD98059 and U0126, inhibitors of the upstream activator of ERK‐1/2 (ie, MEK‐1/2) restored claudin‐1 expression level as well as the epithelial barrier. Conclusion Our findings suggest that downregulation of claudin‐1 by TGF‐β1 acting through the noncanonical MEK‐1/2/ERK‐1/2 pathway triggers increased prostatic epithelial monolayer permeability in vitro. These findings also suggest that elevated TGF‐β1 may contribute to claudin‐1 downregulation and compromised epithelial barrier in clinical BPH specimens.
    Type of Medium: Online Resource
    ISSN: 0270-4137 , 1097-0045
    URL: Issue
    URL: Article
    DOI: 10.1002/pros.v80.14
    DOI: 10.1002/pros.24046
    Language: English
    Publisher: Wiley
    Publication Date: 2020
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