Fasciola hepatica-Induced Immune Suppression of Spleen Mononuclear Cell Proliferation: Role of Nitric Oxide

1998 ◽  
Vol 87 (2) ◽  
pp. 145-154 ◽  
Author(s):  
Laura Cervi ◽  
Gabriela Rossi ◽  
Hugo Cejas ◽  
Diana Teresa Masih
Keyword(s):  
Nitric Oxide ◽  
Cell Proliferation ◽  
Mononuclear Cell ◽  
Immune Suppression ◽  
Fasciola Hepatica

scholarly journals APOPTOSIS AND CELL PROLIFERATION IN CHRONIC TONSILLITIS AND OROPHARYNGEAL CARCINOMA: ROLE OF NITRIC OXIDE AND CYTOKINES

2004 ◽  
Vol 148 (2) ◽  
pp. 225-227 ◽  
Author(s):  
Tomas Kucera ◽  
Hana Pacova ◽  
David Vesely ◽  
Jaromir Astl ◽  
Jindrich Martinek
Keyword(s):  
Nitric Oxide ◽  
Cell Proliferation ◽  
Chronic Tonsillitis ◽  
Oropharyngeal Carcinoma

Regulation of stellate cell proliferation by lipopolysaccharide: Role of endogenous nitric oxide

1998 ◽  
Vol 13 (S1) ◽  
pp. S6-S13 ◽  
Author(s):  
NORIFUMI KAWADA ◽  
SHUICHI SEKI ◽  
TETSUO KUROKI ◽  
MASAYASU INOUE
Keyword(s):  
Nitric Oxide ◽  
Cell Proliferation ◽  
Stellate Cell ◽  
Endogenous Nitric Oxide

Role of nitric oxide-based immunotherapy in augmenting prostate cancer progression by targeting androgen receptor heterogeneity.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e17537-e17537
Author(s):  
Himanshu Arora ◽  
Anastasia Vedenko ◽  
Derek J. Van Booven ◽  
Manish Narasimman
Keyword(s):  
Prostate Cancer ◽  
Nitric Oxide ◽  
Cell Proliferation ◽  
Androgen Receptor ◽  
Significant Proportion ◽  
Dependent Manner ◽  
Independent State ◽  
M1 Macrophage ◽  
Androgen Independent

e17537 Background: A significant proportion of men with Prostate Cancer (PCa) develop castration resistant prostate cancer (CRPC) and do not respond to hormonal agents that decrease androgens. In trying to understand the causes of androgen resistance that develop in CRPC, it is considered most relevant to study the role of Androgen receptor (AR) in the development and progression of PCa from androgen dependent to androgen independent state. Recent studies have highlighted the significance of tumor microenvironment (TME) in regulation of PCa progression in addition to AR. A key molecule in the regulation of TME interactions is nitric oxide (NO). We have shown in our recent study, the critical association of NO with the TME in CRPC. However, the effects of NO to modulate the progression of PCa to CRPC with respect to AR still remains largely unexplored. Methods: 22RV1, LNCaP, LNCaPAPIPC(cells expressing no AR), and LNCaPshAR/pATK (cells expressing low AR), cells were used for the study. Cell proliferation was first assessed by MTT assay. The castrated SCID mice were grafted with 22RV1 cells and were treated with GSNO at the dosage of 10mg/kg/day IP. After treatment, animals were humanely sacrificing. Tumor RNA and proteins were analysed for markers that are important for PCa progression using qPCR, western blot and cytokine antibody array. Animal experiments were carried out in compliance with the IACUC of University of Miami. GraphPad Prism (GraphPad Software) was used for statistical analysis. Results: In addition to reducing the tumor burden, the expression of anti-inflammatory (M2) macrophages (CD206 and Arginase1) is decreased and that of the pro-inflammatory (M1) macrophage (iNOS) is increased in mice which received increased NO levels. Furthermore, to study the effects of NO on progression of PCa from androgen dependent to androgen independent stage, we characterized the LNCAP cell models with differential extent of AR knockdown (LNCaP, LNCaPshAR/pATK and LNCaPAPIPC) for the effects of increased NO levels. Results showed that NO had significant impact on cell proliferation on androgen dependent PCa cells however the effects were negligible in cells expressing low or no AR, suggesting that effects of NO on PCa cell proliferation are AR dependent. Conclusions: Our results suggest that during PCa progression, NO suppresses TAMs to target the TME in an AR dependent manner. Further studies are undergoing to establish the impacts of NO in PCa progression.

Sign in / Sign up

Export Citation Format

Share Document