Synthesis and Secretion of Angiotensin II by the Prostate Gland in Vitro

O'Mahony, Orla A.; Barker, Stewart; Puddefoot, J. R.; Vinson, Gavin P.

doi:10.1210/en.2004-0565

Cited by 28 publications

(29 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…More surprisingly, there is considerable evidence that the male reproductive organs contain reninangiotensin system components, such as angiotensinogen, renin, angiotensin I -converting enzyme, and AT 1 and AT 2 receptors. O'Mahony et al suggested that the prostate gland may be the source of angiotensin II found in seminal fluid and that angiotensin II production may be regulated by androgen (39,40). Based on this accumulated evidence and our results, the prostate itself seems to be a target for angiotensin, and the prostatic renin-angiotensin system may affect the development of prostate cancer.…”

Section: Discussionsupporting

confidence: 73%

Antiproliferative activity of angiotensin II receptor blocker through cross-talk between stromal and epithelial prostate cancer cells

Uemura

Ishiguro

Nagashima

et al. 2005

Molecular Cancer Therapeutics

View full text Add to dashboard Cite

We showed previously that angiotensin II activated the proliferation of prostate cancer cells and that angiotensin II receptor blockers (ARB) could inhibit it. Here, we investigated whether angiotensin II exerts mitogenic effects on the cross-talk between stromal and cancer cells and whether an ARB can inhibit tumor growth through actions on stromal cells. Cell proliferation and interleukin-6 secretion of prostate stromal PrSC cells stimulated with angiotensin II, tumor necrosis factor-A, or epidermal growth factor were examined in the absence and presence of ARB. We examined the effect of ARB on mitogenactivated protein kinase (MAPK) phosphorylation of PrSC and PC-3 cells treated with conditioned medium of PrSC cells and determined the effect of ARB on tumor growth induced by paracrine factors from PrSC cells. Angiotensin II activated the cell proliferation and interleukin-6 secretion of PrSC cells, and ARB inhibited it. Angiotensin II, tumor necrosis factor-A, or epidermal growth factor induced MAPK phosphorylation in PrSC cells, and this phosphorylation was inhibited by ARB. Conditioned medium of PrSC cells with angiotensin II activated MAPK phosphorylation in PC-3 cells, and ARB-treated conditioned medium of PrSC cells inhibited it. The tumor growth and angiogenesis of a mixture of PC-3 with PrSC were inhibited by ARB administration, whereas those of PC-3 xenografts were not inhibited. ARB exerted an antiproliferative effect on prostate cancer through paracrine factors from stromal cells. Because prostate stromal cells are thought to be involved in the initiation and development of prostate cancer, the present data suggest the possibility that ARBs are a novel therapeutic class of agents for prostate cancer.

show abstract

Section: Discussionsupporting

confidence: 73%

Antiproliferative activity of angiotensin II receptor blocker through cross-talk between stromal and epithelial prostate cancer cells

Uemura

Ishiguro

Nagashima

et al. 2005

Molecular Cancer Therapeutics

View full text Add to dashboard Cite

show abstract

“…Intriguingly, a 3-fold to 5-fold higher concentration of angiotensin II was confirmed in seminal fluid in comparison with that in blood (32), which strongly supports the existence of RAS in the prostate gland. Likewise, it was reported that there was a high concentration of angiotensin II in pancreatic cancer tissue compared with that in normal tissue (33), and RAS components, including angiotensinogen, angiotensin II receptor type 1, and renin, have been identified in the islets of Langerhans (34).…”

Section: Discussionsupporting

confidence: 58%

Angiotensin II Induces Oxidative Stress in Prostate Cancer

Uemura

Ishiguro

et al. 2008

Molecular Cancer Research

View full text Add to dashboard Cite

Angiotensin II has been shown to be a cytokine especially acting as a growth factor. A local renin-angiotensin system has been identified in the prostate gland, and the physiologic function of angiotensin II seems to be similar in prostate cancer, as we previously reported. In the present study, we explored the biological role of angiotensin II in oxidative stress of prostate cancer cells. Activated Akt was determined, and the expression of oxidative stress-related proteins (p47phox, manganese superoxide dismutase 2, glutathione peroxidase) was examined by Western blotting in LNCaP cells, which were stimulated with angiotensin II and/or an angiotensin II receptor type 1 blocker, candesartan. To examine DNA damage induced by angiotensin II, 8-hydroxy-2 ¶-deoxyguanosine was determined, and Western blots were analyzed to detect checkpoint proteins including p53, Chk2, and cdc2. Immunocytochemical studies of inducible nitric oxide synthase and superoxide anion radical (O 2 À ) were done in LNCaP cells stimulated with angiotensin II. The phosphorylation of Akt was induced by angiotensin II treatment and inhibited by candesartan, as well as by LY294002, an inhibitor of phosphoinositide 3-kinase. Oxidative stress-related proteins were up-regulated by angiotensin II and inhibited by pretreatment with candesartan or catalase. The level of 8-hydroxy-2 ¶-deoxyguanosine was increased by angiotensin II and conversely decreased by candesartan. Immunocytochemical studies showed that angiotensin II enhanced an inflammatory marker, inducible nitric oxide synthase, and the production of O 2 À radical. The hypothesis that angiotensin II has the potential to induce oxidative stress, which may be implicated in carcinogenesis of the prostate gland through long-term exposure to chronic inflammation is proposed. (Mol Cancer Res 2008;6(2):250 -8)

show abstract

“…It has been suggested that ACE2 may oppose the effects of ACE on the organ and tissue levels through the generation of Ang-(1-7) by the local RAS [15]. The local RAS systems have been detected in various species and in diverse organs, such as the brain, the testes, the prostate, the pancreas, the adrenal gland, and the mammary glands [16][17][18][19][20][21][22]. The local RAS systems enable the generation of Ang II, and may therefore exert biological activity on an organ level.…”

Section: Introductionmentioning

confidence: 99%

ACE and ACE2 expression in normal and malignant skin lesions

Grzegrzółka

Swiatko

Puła

et al. 2013

Folia Histochem Cytobiol.

View full text Add to dashboard Cite

Abstract:The renin-angiotensin system (RAS) is known mainly as a regulator of cardiovascular homeostasis. However, it has also been shown to mediate processes such as proliferation, apoptosis, angiogenesis, and carcinogenesis. Nonmelanoma skin cancers (NMSC) -including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) -are among the most common cancers. The aim of the present study was to determine the immunohistochemical expression of angiotensin-converting enzyme (ACE), angiotensin-converting enzyme 2 (ACE2), and Ki-67 antigen in archival samples of normal skin, actinic keratosis, and malignant skin lesions. Cytoplasmic-nuclear ACE immunoreactivity was observed in 99% of examined cases of both normal skin and cancers. Significantly higher ACE immunoreactivity occurred in normal skin, as compared with BCC and SCC (p < 0.01, p < 0.0001, respectively). Additionally, ACE immunoreactivity was also significantly higher in BCC, compared with SCC (p < 0.05). ACE2 immunoreactivity was noted in basal epidermal layers and in sebaceous gland cells in normal skin, though not in NMSC. These novel observations suggest that ACE and skin RAS may be involved in the pathogenesis of malignant skin lesions.

show abstract

Synthesis and Secretion of Angiotensin II by the Prostate Gland in Vitro

Cited by 28 publications

References 50 publications

Antiproliferative activity of angiotensin II receptor blocker through cross-talk between stromal and epithelial prostate cancer cells

Antiproliferative activity of angiotensin II receptor blocker through cross-talk between stromal and epithelial prostate cancer cells

Angiotensin II Induces Oxidative Stress in Prostate Cancer

ACE and ACE2 expression in normal and malignant skin lesions

Contact Info

Product

Resources

About