scholarly journals Human Prostate Epithelial Cells Activate the AIM2 Inflammasome upon Cellular Senescence: Role of POP3 Protein in Aging-Related Prostatic Inflammation

Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 366
Author(s):  
Ravichandran Panchanathan ◽  
Vaikundamoorthy Ramalingam ◽  
Hongzhu Liu ◽  
Divaker Choubey
Keyword(s):  
Epithelial Cells ◽  
Cell Line ◽  
Type I ◽  
Mrna Levels ◽  
Normal Prostate ◽  
Prostate Hyperplasia ◽  
Prostate Epithelial Cells ◽  
Prostatic Inflammation ◽  
Benign Prostate

Increased levels of type I (T1) interferon (IFN)-inducible POP3 protein in myeloid cells inhibit activation of the AIM2 inflammasome and production of IL-1β and IL-18 proinflammatory cytokines. The AIM2 mRNA levels were significantly higher in benign prostate hyperplasia (BPH) than the normal prostate. Further, human normal prostate epithelial cells (PrECs), upon becoming senescent, activated an inflammasome. Because in aging related BPH senescent PrECs accumulate, we investigated the role of POP3 and AIM2 proteins in pre-senescent and senescent PrECs. Here we report that the basal levels of the POP3 mRNA and protein were lower in senescent (versus young or old) PrECs that exhibited activation of the T1 IFN response. Further, treatment of PrECs and a BPH cell line (BPH-1) that expresses the androgen receptor (AR) with the male sex hormone dihydrotestosterone (DHT) increased the basal levels of POP3 mRNA and protein, but not AIM2, and inhibited activation of the AIM2 inflammasome. Of interest, a stable knockdown of POP3 protein expression in the BPH-1 cell line increased cytosolic DNA-induced activation of AIM2 inflammasome. These observations suggest a potential role of POP3 protein in aging-related prostatic inflammation.

Escherichia coli , a common constituent of benign prostate hyperplasia‐associated microbiota induces inflammation and DNA damage in prostate epithelial cells

The Prostate ◽  
2020 ◽  
Vol 80 (15) ◽  
pp. 1341-1352 ◽  
Author(s):  
Sumeet Jain ◽  
Ajit Gopal Samal ◽  
Biswajit Das ◽  
Biswaranjan Pradhan ◽  
Nilanjan Sahu ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Dna Damage ◽  
Epithelial Cells ◽  
Benign Prostate Hyperplasia ◽  
Prostate Hyperplasia ◽  
Prostate Epithelial Cells ◽  
Benign Prostate

Comparison of human normal and neoplastic prostate epithelial cells by TEM and quantitative image analysis and morphometry (QIAM)

1994 ◽  
Vol 52 ◽  
pp. 86-87
Author(s):  
J. T. Gau ◽  
M. L. Grove ◽  
S. Strom ◽  
R. Orsini ◽  
K. C. Song ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Membrane Trafficking ◽  
Growth Regulation ◽  
Cellular Growth ◽  
Cell Trafficking ◽  
Normal Prostate ◽  
Prostate Cell ◽  
Prostate Epithelial Cells

Prostate cancer is the most common tumor in men in the U.S.A. The regulation of growth control in normal prostate cells and its contribution to tumor progression is a subject of intense investigation.Recently our group developed culture techniques that allowed us to study normal and neoplastic human prostate epithelial cells from human prostatectomy specimens. Since quantitative evaluation of intracellular compartments will be critical to defining the role of membrane trafficking in the growth regulation, we used TEM and QIAM to characterize normal and neoplastic prostate epithelial cells invivo, as well as in vitro. This work will serve as a baseline to subsequent studies using perturbants of cell trafficking and conditions ;hat promote or block cellular growth, to investigate the role of growth factors and stromal/epithelial nteraction in prostate growth regulation.Normal and neoplastic tissues were sampled for ultrastructural examination from grid mapped radical prostatectomy specimens that were processed for whole mounts. The SV40 immortalized "normal" prostate cell line (P69) was provided by Dr. Strom.

scholarly journals Role of the PI3K/Akt pathway in cadmium induced malignant transformation of normal prostate epithelial cells

2020 ◽  
Vol 409 ◽  
pp. 115308 ◽  
Author(s):  
Priyanka Kulkarni ◽  
Pritha Dasgupta ◽  
Nadeem S. Bhat ◽  
Yutaka Hashimoto ◽  
Sharanjot Saini ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Malignant Transformation ◽  
Akt Pathway ◽  
Normal Prostate ◽  
Prostate Epithelial Cells

scholarly journals Prostate Stem Cells in the Development of Benign Prostate Hyperplasia and Prostate Cancer: Emerging Role and Concepts

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Akhilesh Prajapati ◽  
Sharad Gupta ◽  
Bhavesh Mistry ◽  
Sarita Gupta
Keyword(s):  
Prostate Cancer ◽  
Stem Cells ◽  
Benign Prostate Hyperplasia ◽  
Normal Prostate ◽  
Prostate Hyperplasia ◽  
Regulatory Factors ◽  
Prostate Cells ◽  
Hormonal Imbalance ◽  
Benign Prostate ◽  
Insight Into

Benign Prostate hyperplasia (BPH) and prostate cancer (PCa) are the most common prostatic disorders affecting elderly men. Multiple factors including hormonal imbalance, disruption of cell proliferation, apoptosis, chronic inflammation, and aging are thought to be responsible for the pathophysiology of these diseases. Both BPH and PCa are considered to be arisen from aberrant proliferation of prostate stem cells. Recent studies on BPH and PCa have provided significant evidence for the origin of these diseases from stem cells that share characteristics with normal prostate stem cells. Aberrant changes in prostate stem cell regulatory factors may contribute to the development of BPH or PCa. Understanding these regulatory factors may provide insight into the mechanisms that convert quiescent adult prostate cells into proliferating compartments and lead to BPH or carcinoma. Ultimately, the knowledge of the unique prostate stem or stem-like cells in the pathogenesis and development of hyperplasia will facilitate the development of new therapeutic targets for BPH and PCa. In this review, we address recent progress towards understanding the putative role and complexities of stem cells in the development of BPH and PCa.

scholarly journals Proteolytic cleavage and truncation of NDRG1 in human prostate cancer cells, but not normal prostate epithelial cells

2013 ◽  
Vol 33 (3) ◽  
Author(s):  
Mohammad K. Ghalayini ◽  
Qihan Dong ◽  
Des R. Richardson ◽  
Stephen J. Assinder
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Western Blot ◽  
Cancer Cells ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Metastasis Suppressor ◽  
Normal Prostate ◽  
Truncated Protein ◽  
Prostate Epithelial Cells

NDRG1 (N-myc downstream regulated gene-1) is a metastasis suppressor that is down-regulated in prostate cancer. NDRG1 phosphorylation is associated with inhibition of metastasis and Western blots indicate two bands at ~41 and ~46 kDa. Previous investigations by others suggest the higher band is due to NDRG1 phosphorylation. However, the current study using a dephosphorylation assay and the Phos-tag (phosphate-binding tag) SDS/PAGE assay, demonstrated that the 46 kDa NDRG1 protein band was not due to phosphorylation. Further experiments showed that the NDRG1 protein bands were not affected upon glycosidase treatment, despite marked effects of these enzymes on the glycosylated protein, fetuin. Analysis using RT–PCR (reverse transcriptase–PCR) demonstrated only a single amplicon, and thus, the two bands could not result from an alternatively spliced NDRG1 transcript. Western-blot analysis of prostate cancer cell lysates identified the 41 kDa band to be a truncated form of NDRG1, with MS confirming the full and truncated proteins to be NDRG1. Significantly, this truncated protein was not present in normal human PrECs (prostate epithelial cells). Western-blot analysis using anti-NDRG1 raised to its N-terminal sequence failed to detect the truncated protein, suggesting that it lacked N-terminus amino acids (residues 1–49). Sequence analysis predicted a pseudotrypsin protease cleavage site between Cys49–Gly50. Such cleavage of NDRG1 in cancer cells may result in loss of NDRG1 tumour suppressive activity.

scholarly journals Effects of Estradiol on Prostate Epithelial Cells in the Castrated Rat

2002 ◽  
Vol 50 (11) ◽  
pp. 1517-1523 ◽  
Author(s):  
G. Pelletier
Keyword(s):  
Epithelial Cells ◽  
Cdna Probe ◽  
Concomitant Administration ◽  
Hybridization Signal ◽  
Mrna Levels ◽  
Nuclear Staining ◽  
Cytoplasmic Staining ◽  
Prostate Epithelial Cells ◽  
Strong Hybridization ◽  
Rat Prostate

There is evidence that estrogens can modulate the activity of prostate epithelial cells. To determine whether estradiol can have a direct influence on rat prostate, this study examined the effects of estradiol-17β (E2) administered alone or in combination with dihydrotestosterone (DHT) to castrated rats for 3 weeks on prostate binding protein (PBP) C1 mRNA expression and androgen receptor (AR) localization. PBP C1 mRNA levels were measured by semi-quantitative in situ hybridization using a 35S-labeled cDNA probe. In intact animals, strong hybridization signal could be observed in prostate sections after 12 hr of exposure to Kodak X-Omat films. In castrated rats, no PBP C1 mRNA could be detected even with longer exposure times, an effect that was prevented by administration of DHT. E2 administered alone induced a detectable hybridization signal, and the concomitant administration of E2 and DHT induced an increase in PBP C1 mRNA that significantly exceeded that obtained in animals that received only DHT. In prostate epithelial cells of intact animals, AR immunostaining was restricted to the nucleus. In castrated animals the alveoli were decreased in size and the epithelial cells were atrophied. AR staining was weak and was detected in both cytoplasm and nucleus. DHT administration completely obviated the effect of castration on epithelial cell histology and on AR immunostaining distribution and intensity. Interestingly, E2 administration alone induced moderate hypertrophy of epithelial cells compared to the histological appearance of cells in untreated castrated rats. Moreover, in E2-treated animals the nuclear staining was much stronger than that detected in untreated castrated rats, whereas the cytoplasmic staining was not modified by the treatment. In animals that received both DHT and E2, the staining was similar to that seen in DHT-treated rats. These results suggest that E2 can influence the activity of rat prostate epithelial cells by mechanisms that remain to be fully clarified.

scholarly journals Anti-proliferative activities of finasteride in benign prostate epithelial cells require stromal fibroblasts and c-Jun gene

PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0172233 ◽  
Author(s):  
Kai Wang ◽  
Song Jin ◽  
Dongdong Fan ◽  
Mingshuai Wang ◽  
Nianzeng Xing ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Stromal Fibroblasts ◽  
Prostate Epithelial Cells ◽  
Benign Prostate

scholarly journals Role of Osteoglycin in the Linkage between Muscle and Bone

2012 ◽  
Vol 287 (15) ◽  
pp. 11616-11628 ◽  
Author(s):  
Ken-ichiro Tanaka ◽  
Erika Matsumoto ◽  
Yoshiko Higashimaki ◽  
Takenobu Katagiri ◽  
Toshitsugu Sugimoto ◽  
...  
Keyword(s):  
Transcriptional Activity ◽  
Type I Collagen ◽  
C2c12 Cells ◽  
Type I ◽  
Mrna Levels ◽  
Humoral Factors ◽  
Anabolic Activity ◽  
Morphogenetic Protein ◽  
Muscle Tissues

The interaction between muscle tissues and bone metabolism is incompletely understood. We hypothesized that there might be some humoral factors that are produced in muscle tissues and exhibit bone anabolic activity. We, therefore, performed comparative DNA microarray analysis between mouse myoblastic C2C12 cells transfected with either stable empty vector or ALK2 (R206H), the mutation that constitutively activates the bone morphogenetic protein (BMP) receptor, to search for muscle-derived bone anabolic factors. Twenty-five genes whose expression was decreased to <1/4, were identified; these included osteoglycin (OGN). Stable overexpression of OGN significantly decreased the levels of Runx2 and Osterix mRNA compared with those in cells transfected with vector alone in MC3T3-E1 cells. On the other hand, it significantly enhanced the levels of alkaline phosphatase (ALP), type I collagen (Col1), and osteocalcin (OCN) mRNA as well as β-catenin and mineralization. A reduction in endogenous OGN level showed the opposite effects to those of OGN overexpression in MC3T3-E1 and mouse calvarial osteoblastic cells. Transient OGN overexpression significantly suppressed the levels of Runx2, Osterix, ALP, Col1, and OCN mRNA induced by BMP-2 in C2C12 cells. The conditioned medium from OGN-overexpressed and OGN-suppressed myoblastic cells enhanced and decreased, respectively, the levels of ALP, Col1, and β-catenin in MC3T3-E1 cells. Moreover, OGN increased Smad3/4-responsive transcriptional activity as well as Col1 mRNA levels independently of endogenous TGF-β in these cells. In conclusion, this study suggests that OGN may be a crucial humoral bone anabolic factor that is produced by muscle tissues.

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