Effects of castration and testosterone administration on angiotensin II receptor mRNA expression and apoptosis-related proteins in rat urinary bladder.
We investigated the effects of castration and androgen administration on angiotensin II receptor mRNA expression and apoptosis related proteins in the rat bladders. Sprague-Dawley rats were divided into three groups: the control group (sham operation; n = 8), the castration group (castrated, 8 weeks old, n = 8) and the castration plus testosterone group (1% testosterone gel administrated percutaneously into the dorsum daily for 8 weeks starting at 4 weeks after castration, n = 8). Bladder total RNA was extracted, and real-time PCR was performed to quantitatively measure the mRNA expression of angiotensin converting enzyme (ACE), angiotensin II (A II) receptor type 1 (AT1 receptor) and A II receptor type II (AT2 receptor). Western blotting was performed to determine the expression of apoptosis-related proteins. Expression of AT2 receptor mRNA and caspase-3 protein significantly increased in the rat bladder after castration, and these increases were reduced to control levels by testosterone administration. These results suggest that expression of AT2 receptor and caspase-3 in the bladder is androgen-dependent. Expression of Bcl-2 and Bax protein in the rat bladder was not altered by castration. Expression of mitogen-activated protein (MAP) kinase phosphatase-1 protein in the rat urinary bladder was significantly increased by castration, but this increase was smaller with testosterone administration. These results suggest that expression of AT2 receptor mRNA and apoptosis-related proteins in the rat urinary bladder are affected by the change of androgen environment. The present study was the first to clarify the relationship between AT2 receptor and androgen in the urinary bladder.
Nakazawa
Ryuto
R
Department of Urology, St. Marianna University, Kawasaki, Japan.
Tanaka
Masami
M
Takahashi
Takeshi
T
Kobayashi
Shinichi
S
Iwamoto
Teruaki
T
D000728:Androgens / Q000494:pharmacology*; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D015153:Blotting, Western; D053148:Caspase 3 / Q000378:metabolism; D018797:Cell Cycle Proteins / Q000378:metabolism; D054638:Dual Specificity Phosphatase 1; D017874:Immediate-Early Proteins / Q000378:metabolism; D008297:Male; D009919:Orchiectomy; D010749:Phosphoprotein Phosphatases / Q000378:metabolism; D054645:Protein Phosphatase 1; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D044139:Receptor, Angiotensin, Type 2 / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013739:Testosterone / Q000494:pharmacology*; D001743:Urinary Bladder / Q000187:drug effects / Q000378:metabolism*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
D000728:Androgens; D018797:Cell Cycle Proteins; D017874:Immediate-Early Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D044139:Receptor, Angiotensin, Type 2; D051028:bcl-2-Associated X Protein; D013739:Testosterone; D010749:Phosphoprotein Phosphatases; D054645:Protein Phosphatase 1; D054638:Dual Specificity Phosphatase 1; C517021:Dusp1 protein, rat; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases; D053148:Caspase 3