title: AT1 receptor and ACE mRNA are increased in chemically induced carcinoma of rat mammary gland.
abstract: Angiotesin II has except of strong vasoconstrict effect also ability to potentiate protein synthesis and cellular growth. The aim of this study was to investigate the gene expression of components of the renin-angiotensin system, angiotensinogen, renin, angiotensin-converting enzyme and AT(1) receptor, in rat mammary gland and in chemically induced carcinoma of this gland. Retinoids are known to inhibit cell proliferation and induce cell differentiation so they are considered as a promising chemopreventive agents. We studied the effect of 13-cis-retinoic acid on the gene expression of mentioned elements of the renin-angiotensin system in tumour tissue. The expressions in control and carcinoma tissue were investigated using RT-PCR and activity of angiotensin-converting enzyme was measured. The amount of angiotensin-converting enzyme and AT(1) receptor mRNA and angiotensin-converting enzyme activity always showed a significant increase in the carcinoma tissue in comparison with the control. Administration of 13-cis-retinoic acid to rats with induced mammary gland carcinoma was without significant effect on either tumour numbers or tumour burden and volume. Similarly, 13-cis-retinoic acid did not change the angiotensin-converting enzyme expression and activity. The AT(1) receptor gene expression displayed a clear tendency to decrease in tumour tissue after retinoic acid treatment. Our results demonstrate the presence of angiotensin-converting enzyme and AT(1) receptor in control and carcinoma tissue of mammary gland. We assume that both proteins might play a role in development of tumour cells and vasculature.
authors.affiliation: Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska 3, 833 06 Bratislava, Slovakia. k_tybitanclova@post.sk
authors.forename: Katarina
authors.initials: K
authors.lastname: Tybitanclova
authors.forename: Dana
authors.initials: D
authors.lastname: Macejova
authors.forename: Jan
authors.initials: J
authors.lastname: Liska
authors.forename: Julius
authors.initials: J
authors.lastname: Brtko
authors.forename: Stefan
authors.initials: S
authors.lastname: Zorad
mesh_terms: D000808:Angiotensinogen / Q000235:genetics / Q000378:metabolism; D000818:Animals; D005260:Female; D015870:Gene Expression / Q000187:drug effects*; D015474:Isotretinoin / Q000494:pharmacology* / Q000627:therapeutic use; D008321:Mammary Glands, Animal / Q000378:metabolism*; D008325:Mammary Neoplasms, Experimental / Q000139:chemically induced / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism*; D008770:Methylnitrosourea; D007703:Peptidyl-Dipeptidase A / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics / Q000378:metabolism*; D012083:Renin / Q000235:genetics / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000235:genetics / Q000502:physiology; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D000808:Angiotensinogen; D008770:Methylnitrosourea; D007703:Peptidyl-Dipeptidase A; D012083:Renin; D015474:Isotretinoin