Ecto‐diadenosine polyphosphates hydrolase activity on human prostasomes

Minelli, Alba; Allegrucci, Cinzia; Liguori, Lavinia; Ronquist, Gunnar

doi:10.1002/pros.10062

Cited by 16 publications

(10 citation statements)

References 45 publications

(52 reference statements)

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“…by shedding from the plasma membrane; however, alternative sources such as the epididymis cannot be excluded (Dubois et al 2009). Other enzymes that have been reported on prostasomes include 5 0 nucleotidase (Fabiani & Ronquist 1993, alkaline phosphatase, alkaline phosphodiesterase I (Fabiani & Ronquist 1995), neutral endopeptidase (Renneberg et al 2001), TMPRSS2 (Chen et al 2010, ecto-diadenosine polyphosphates hydrolase (Minelli et al 2002), protein kinases A and C (PKA/ PKC), casein kinase II and membrane-bound ATPase (Babiker et al 2006).…”

Section: The Molecular Composition Of Prostasomesmentioning

confidence: 99%

Prostasomes: extracellular vesicles from the prostate

Aalberts¹,

Stout²,

Stoorvogel³

2014

Reproduction

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The term 'prostasomes' is generally used to classify the extracellular vesicles (EVs) released into prostatic fluid by prostate epithelial cells. However, other epithelia within the male reproductive tract also release EVs that mix with 'true' prostasomes during semen emission or ejaculation. Prostasomes have been proposed to regulate the timing of sperm cell capacitation and induction of the acrosome reaction, as well as to stimulate sperm motility where all three are prerequisite processes for spermatozoa to attain fertilising capacity. Other proposed functions of prostasomes include interfering with the destruction of spermatozoa by immune cells within the female reproductive tract. On the other hand, it is unclear whether the distinct presumed functions are performed collectively by a single type of prostasome or by separate distinct sub-populations of EVs. Moreover, the exact molecular mechanisms through which prostasomes exert their functions have not been fully resolved. Besides their physiological functions, prostasomes produced by prostate tumour cells have been suggested to support prostate cancer spread development, and prostasomes in peripheral blood plasma may prove to be valuable biomarkers for prostate cancer.

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Section: The Molecular Composition Of Prostasomesmentioning

confidence: 99%

Prostasomes: extracellular vesicles from the prostate

Aalberts¹,

Stout²,

Stoorvogel³

2014

Reproduction

169

150

View full text Add to dashboard Cite

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“…23,29 Furthermore, hydrolytic enzymes (especially ecto-diadenosine polyphosphate hydrolase that is primarily associated with prostasomes), after fusion in the female genital tract, can be transferred to spermatozoa. 30 The presence of this hydrolase on sperm acrosomal membranes was shown to be critical for the acrosome reaction to occur, 31 emphasizing the role of prostasomes in this context.…”

Section: Prostasomesmentioning

confidence: 99%

Prothrombotic Effects of Prostasomes Isolated from Prostatic Cancer Cell Lines and Seminal Plasma

Babiker¹,

Ekdahl²,

Nilsson³

et al. 2007

Semin Thromb Hemost

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Thromboembolism is well recognized as a major complication of cancer. Many tumor cells overexpress tissue factor (TF), which activates blood coagulation in cancer patients. Inflammatory cells expressing TF are also contributors to this activation. In prostate cancer, we believe that prostasomes may also be involved in the initiation of blood coagulation. Prostasomes are submicron secretory granules derived from the prostate gland. They are surrounded by membrane and their extracellular appearance and membrane architecture are complex. Seminal prostasomes are believed to be necessary for successful fertilization and act as protectors of the spermatozoa in the lower and upper female genital tract. Cells from prostate cancer and its metastases are able to produce and export prostasomes to the extracellular environment. These prostasomes may differ quantitatively rather than qualitatively from their normal counterparts with regard to protein composition and function. A majority of human prostate cancers have been found to overexpress TF, and we have demonstrated by various methods that prostasomes derived from prostate cancer cells express considerably higher levels of TF compared with prostasomes of nonmalignant cell origin. The mechanism related to thromboembolic disease generated by prostasomes in prostatic cancer patients may be the early release of prostasomes from prostate cancer cells into the blood circulation, where they will evoke their blood-clotting effects.

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“…Adenosine deaminase (ADA) [EC 3.5.4.4.] activity was determined by HPLC according to Minelli et al [2002]. Nucleoside phosphorylase (PNP) [EC 2.4.2.1.]…”

Section: Measurement Of Ada and Pnp Activitiesmentioning

confidence: 99%

Effects of adenosine on prostate adenocarcinoma PC‐3 and bladder carcinoma J82 cell lines

Nucciarelli

Mearini

Minelli

2003

Drug Development Research

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Prostate adenocarcinoma PC-3 and bladder carcinoma J82 cell lines were used to investigate the role of adenosine in the modulation of cell growth. Our results show that adenosine inhibited cell proliferation in both cell lines and markedly induced apoptosis only in J82 cells. PC-3 and J82 cells showed typical sigmoid growth curves. Only the J82 growth curve was modified by the addition of adenosine deaminase, indicating that this cell line is sensitive to the presence of endogenous extracellular adenosine. Exogenous extracellular adenosine induced a dose-dependent decrease of cell growth in both cell lines. 2 0 -Deoxyadenosine and dipyridamole were used to investigate whether the growth inhibitory effect of adenosine was related to cellular uptake or to receptor-mediated action. Our results show that 2 0 -deoxyadenosine was a less effective inhibitor for J82 than PC-3 cells. Dipyridamole reduced the inhibitory effect of adenosine in both cell lines. The determination of viability associated with Hoechst staining showed that adenosine clearly induced apoptosis in J82 cell lines but was less effective in PC-3 cell lines. In conclusion, we have shown that the growth of prostate adenocarcinoma PC-3 and bladder carcinoma J82 cell lines is inhibited by adenosine and that adenosine is capable of inducing apoptosis, although to a different extent in both cell lines. Drug Dev.

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Ecto‐diadenosine polyphosphates hydrolase activity on human prostasomes

Abstract: The existence of an enzyme capable of degrading diadenosine compounds and can be transferred to human spermatozoa suggests new physiological implications for the role of prostasomes in fertilization.

Cited by 16 publications

References 45 publications

Prostasomes: extracellular vesicles from the prostate

Prostasomes: extracellular vesicles from the prostate

Prothrombotic Effects of Prostasomes Isolated from Prostatic Cancer Cell Lines and Seminal Plasma

Effects of adenosine on prostate adenocarcinoma PC‐3 and bladder carcinoma J82 cell lines

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