Disease relevance of AR

• In the prostate, AR was presented in both the epithelial and stromal cells and the AR mRNA level was higher in hyperplasia than in normal prostate tissues (P<0.05) [1].
• Our objective was to determine whether the selective beta blocker, metoprolol, or the nonselective intrinsic sympathomimetic activity (ISA)-blocker pindolol, reduce infarct size as a function of an area at risk (AR) in a permanent infarction model in dogs and which blocker is preferable in regards to myocardial function [2].
• Myocardial infarct size (IS) was evaluated using the tetrazolium staining technique and expressed as a percent of area at risk (AR) [3].
• The grade of differentiation of hepatoid carcinomas did not affect AR expression [4].
• CCK mediation of satiety via the A-receptor subtype suggest a role for CCK in the management of obesity [5].

High impact information on AR

• AN/AR was smaller in preconditioned versus control dogs that received no treatment (6 +/- 2% versus 19 +/- 3%, P < .01), H-7 (2 +/- 2% versus 14 +/- 5%, P < .02), or polymyxin B (10 +/- 3% versus 29 +/- 5%, P < .01) during the preconditioning or control period [6].
• In PH beagles, ET-1 infusion increased SAP, which was attenuated by FR139317 (an endothelin type [ET] A receptor antagonist), and produced a dose-dependent decrease in PAP, which was attenuated by RES-701-1 (an ETB receptor antagonist) [7].
• Stimulation of the renin-angiotensin system by endothelin subtype A receptor blockade in conscious dogs [8].
• Deferoxamine administered at the time of reperfusion, however, had no significant effect on infarct size (AN/AR = 54.3 +/- 8.7%, p = NS vs. controls) [9].
• Compound 6 produces potent anorectic activity via the CCK-A receptor system [5].

Chemical compound and disease context of AR

• During herniorrhaphy of dogs with perineal hernia, levator ani (non-castrated, n = 12; castrated, n = 7) and/or coccygeus (noncastrated, n = 5; castrated, n = 4) muscle biopsy specimens were obtained for estrogen and androgen receptor analyses [10].
• Androgen receptor content of nafoxidine treated experimentally induced canine prostatic hyperplasia [11].
• An estrogen stimulated increase in prostatic androgen receptor content has been postulated as the mechanism by which canine prostatic hyperplasia can be induced in the castrate dog treated with androstanediol and estradiol but not by androstanediol alone [11].

Biological context of AR

• To further characterize AR function in a model species of relevance to bone and pharmaceutical research, we cloned a partial canine AR from a canine kidney cDNA library and then cloned the remaining 5' segment by PCR from canine ventral prostate cDNA [12].
• In addition, the inactivation of AR binding activity by radiation was attributed to a loss of binding sites, with no significant change in the Kd [13].
• The present findings suggest that there is a basal expression of AR in the canine uterus throughout the estrus cycle that may not be influenced by sex steroid hormones [14].
• During pregnancy and in the postpartum period nuclear staining for AR was nearly absent [14].
• There was no evident effect of the stage of ovarian cycle on uterine AR mRNA levels [15].

Anatomical context of AR

• Immunohistochemistry using an antibody directed to the C-terminal 19 amino acids of the human AR showed strong staining of the secretory epithelial cells in canine ventral prostate [12].
• Northern analysis of poly-A+ RNA from ventral prostate revealed three very low abundance transcripts of approximately 9 kb and RT-PCR analysis showed relatively high expression of AR in canine ventral prostate, testis, and kidney, with lower levels detectable in spleen, skeletal muscle, heart, and liver [12].
• Increased number of neurons expressing androgen receptor in the basolateral amygdala of pathologically aggressive dogs [16].
• To find out whether androgens can have a direct impact on the canine uterus, androgen receptors (AR) were identified immunohistochemically in uterine tissue [14].
• Nuclear staining for AR was observed in cells of the surface epithelium, glandular ducts, basal glands and stroma of the endometrium, and in myometrial smooth muscle cells [14].

Associations of AR with chemical compounds

• Androgen may direct the proliferation, differentiation and regression of stromal cells by regulating the expression of TGFbgr, bFGF, AR and smooth muscle cell specific proteins [1].
• Binding of DHT also resulted in the stimulation of an androgen responsive-luciferase reporter following cotransfection with the canine AR into 293 cells [12].
• This indicates that genomic androgen actions, which are mediated through the AR are of minor importance in the testosterone modulation of canine aggression within the BNG [16].
• To maximize the binding activity, molybdate and dithiothreitol were included during AR extraction [13].
• The area of necrosis (AN) was identified histologically with triphenyl tetrazolium chloride and calculated as percent of AR [17].

Other interactions of AR

• There was also clear expression of the steroidogenic enzymes 5alpha-reductase, aromatase, and the AR [18].
• In contrast with earlier findings on estrogen receptor-alpha and progesterone receptors, no significant changes in androgen receptor expression were observed during the estrus cycle [14].

Analytical, diagnostic and therapeutic context of AR

• Within the early phase of castration (<d7), the expression of AR was increased rapidly [1].
• To our knowledge, this is the first report relative to AR immunohistochemistry in canine mammary cancer and to estrogens or androgens in serum of dogs with benign or malignant mammary tumors [19].
• Molecular cloning and functional characterization of the canine androgen receptor [12].
• The IS/AR ratio for the control group was 29.8 +/- 4.4% (n = 17), which was substantially greater (p less than 0.001) than that of the preconditioned groups: P1, 3.9 +/- 1.3% (n = 14); P6, 0.4 +/- 0.3% (n = 5); and P12, 2.9 +/- 2.8% (n = 5) [20].
• Collateral blood flow was assessed with radioactive microspheres; area at risk (AR) was delineated by injection of blue dye; and the area of necrosis (AN) was measured by tetrazolium staining [6].

References