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Manna E, Bank S, Maiti S, et al. Neutralization by Acetyl Salicylic Acid of the Testosterone induced Impaired Maspin Synthesis Stimulated by Estriol in Neutrophils through Nitric Oxide Synthesis. Int J Biomed Sci. 2015;11(4):176-84
Manna, E., Bank, S., Maiti, S., Jana, P., & Sinha, A. K. (2015). Neutralization by Acetyl Salicylic Acid of the Testosterone induced Impaired Maspin Synthesis Stimulated by Estriol in Neutrophils through Nitric Oxide Synthesis. International journal of biomedical science : IJBS, 11(4), 176-84.
Manna, Emili, et al. "Neutralization by Acetyl Salicylic Acid of the Testosterone induced Impaired Maspin Synthesis Stimulated by Estriol in Neutrophils through Nitric Oxide Synthesis." International journal of biomedical science : IJBS vol. 11,4 (2015): 176-84.
Manna E, Bank S, Maiti S, Jana P, Sinha AK. Neutralization by Acetyl Salicylic Acid of the Testosterone induced Impaired Maspin Synthesis Stimulated by Estriol in Neutrophils through Nitric Oxide Synthesis. Int J Biomed Sci. 2015 Dec;11(4):176-84. PMID: 26759534; PMCID: PMC4699133.
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Int J Biomed Sci. 2015 Dec;11(4):176-84.

Neutralization by Acetyl Salicylic Acid of the Testosterone induced Impaired Maspin Synthesis Stimulated by Estriol in Neutrophils through Nitric Oxide Synthesis.

International journal of biomedical science : IJBS

Emili Manna, Sarbashri Bank, Smarajit Maiti, Pradipta Jana, Asru K Sinha

Affiliations

  1. Sinha Institute of Medical Science & Technology, Garia, Calcutta-700084, India;; Department of Biochemistry, Cell and Molecular Therapeutic Lab, OIST, Vidyasagar University, Midnapur, India.
  2. Department of Biochemistry, Cell and Molecular Therapeutic Lab, OIST, Vidyasagar University, Midnapur, India.
  3. Sinha Institute of Medical Science & Technology, Garia, Calcutta-700084, India;

PMID: 26759534 PMCID: PMC4699133

Abstract

PURPOSE: Maspin, an anti breast cancer protein in the mammary cell and normal neutrophil has been reported to be synthesised by the stimulation of NO production induced by estriol. The role of testosterone was investigated in the synthesis of maspin in relation to that of estriol.

METHODS: Fifty normal female between the ages of 25-65 years old participated in the study. Maspin synthesis was demonstrated by in vitro translation of maspin mRNA, followed by the quantification of maspin by enzyme linked immune absorbent assay. NO was determined by methomoglobin method.

RESULTS: Incubation of the neutrophils in HBSS both with 30 nM estriol resulted in the synthesis of 1.8 ngm maspin with simultaneous increase of NO synthesis. In contrast incubating neutrophils with 20 nM testosterone in the presence of estriol inhibited maspin synthesis to 0.33 nM with simultaneous inhibition of NO synthesis from 1.89 nM to 0 nM at the same time. Addition of 0.2µM flutamide, a testosterone receptor blocker to the incubation mixture restored the synthesis of maspin by 60.64 %. Incubation of 25µM aspirin that stimulated NO synthesis restored the inhibition of maspin synthesis by testosterone by 79.1%. I-NAME, an inhibitor of nitric oxide synthase, abolished both maspin and NO synthesis. Scatchard plot of estriol binding in the presence of testosterone demonstrated that the male sex hormone inhibited the female sex hormone binding to its receptor by "cross talk" between the receptors. It was found that while 1.02 × 10(3) molecules of estriol bind each neutrophil at equilibrium, in the presence of testosterone (20nM) in the binding mixture decreases the binding of estriol to 0.5 × 10(3) with little change in the dissociation constant compared to controls.

CONCLUTION: Estriol was found to stimulate maspin synthesis through the stimulation of NO, testosterone inhibited maspin synthesis through the inhibition of NO synthesis.

Keywords: Nitric oxide; cross-talk; flutamide; maspin; steroid receptors

References

  1. Proc Natl Acad Sci U S A. 1988 Nov;85(22):8664-7 - PubMed
  2. Cancer Res. 2001 Sep 15;61(18):6945-51 - PubMed
  3. Int J Mol Med. 2008 Sep;22(3):333-8 - PubMed
  4. Eur Urol. 1997;32(4):391-5; discussion 395-6 - PubMed
  5. Methods Enzymol. 1974;31:583-9 - PubMed
  6. Life Sci. 1991;49(16):1129-39 - PubMed
  7. J Clin Microbiol. 2000 Dec;38(12):4326-31 - PubMed
  8. Int J Cancer. 2002 Jul 20;100(3):261-5 - PubMed
  9. Eur J Biochem. 1979 Sep;99(2):247-52 - PubMed
  10. Folia Biol (Praha). 1980;26(2):81-93 - PubMed
  11. J Breast Cancer. 2012 Jun;15(2):181-8 - PubMed
  12. Blood. 1976 Jul;48(1):149-61 - PubMed
  13. J Anal Toxicol. 1982 May-Jun;6(3):148-52 - PubMed
  14. Ann Surg. 1988 Jan;207(1):75-9 - PubMed
  15. BMC Cancer. 2014 Feb 28;14:142 - PubMed
  16. Acta Oncol. 2006;45(2):184-7 - PubMed
  17. J Biol Chem. 1990 Mar 25;265(9):4976-81 - PubMed
  18. Expert Opin Ther Targets. 2006 Jun;10(3):401-8 - PubMed
  19. J Biol Chem. 1999 Oct 15;274(42):29628-32 - PubMed
  20. Diagn Pathol. 2011 Apr 16;6:36 - PubMed
  21. J Cell Physiol. 2006 Dec;209(3):617-24 - PubMed
  22. Endocr Relat Cancer. 1999 Jun;6(2):175-80 - PubMed
  23. J Natl Cancer Inst. 2015 Jul 16;107(9):null - PubMed
  24. J Immunol. 1972 Jul;109(1):129-35 - PubMed
  25. J Clin Oncol. 2007 Jul 1;25(19):2685-90 - PubMed
  26. Am J Hematol. 2007 Nov;82(11):986-95 - PubMed
  27. Breast Cancer Res. 2014 Nov 15;16(6):469 - PubMed

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