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This Month in Investigative Urology
This Month in Investigative Urology Differential Expression of SDF-1 Isoforms in Bladder Cancer Gosalbez et al (page 1899) from Miami, Florida and Germany evaluated the expression of 3 stromaderived factor-1 (SDF-1) isoforms as potential biomarkers for bladder cancer (BCa).1 mRNA levels of SDF-1a, b and g were measured in bladder tissues and urine specimens of consecutive patients and correlated with clinical outcome. Only SDF-1b mRNA was significantly over expressed in BCa tissues compared to normal bladder tissues. While SDF-1a was expressed in bladder tissues, SDF-1g expression was undetectable. On multivariate analysis SDF-1b was an independent predictor of metastasis and disease specific mortality. In exfoliated urothelial cells only SDF-1b mRNA was differentially expressed, and sensitive and specific for detecting BCa. In patients with a history of BCa elevated SDF-1b indicated increased risk of recurrence within 6 months. The authors conclude that SDF-1 isoforms are differentially expressed in bladder tissues and exfoliated urothelial cells, and SDF-1b mRNA levels in BCa tissues predict poor prognosis. Since the SDF-1b mRNA level in exfoliated cells detects BCa with high sensitivity, it may be a potential predictor of future recurrence.
Paracrine Mechanism Promotes Kidney Stone in Simulated Metabolic Syndrome Hypothesizing that adipocytes and macrophages increase cellular interactions to accelerate stone formation, Zuo et al (page 1906) from Japan and China developed an in vitro system of renal tubular cells, adipocytes and macrophages to simulate metabolic syndrome (MetS) and investigate molecular communication mechanism among these cells and their involvement in kidney stone formation.2 They co-cultured M-1 mouse renal tubular cells with 3T3-L1 adipocytes and/or RAW264.7 macrophages. Inflammatory markers were up-regulated in M-1 cells. Osteopontin increased in M-1 cells co-cultured with RAW264.7 cells whereas monocyte chemoattractant protein-1 and tumor necrosis
0022-5347/14/1916-1639/0 THE JOURNAL OF UROLOGY® © 2014 by AMERICAN UROLOGICAL ASSOCIATION EDUCATION
AND
RESEARCH, INC.
factor-a were over expressed in M-1 cells cocultured with 3T3-L1 cells. Co-culturing M-1 cells simultaneously with 3T3-L1 and RAW264.7 cells resulted in a significant increase of calcium oxalate monohydrate crystal adhesion to M-1 cells. The authors conclude that since inflammatory cytokine changes were induced by co-culturing renal tubular cells with adipocytes and/or macrophages without direct contact, there may be crosstalk between these cells mediated by soluble factors. They suggest that in MetS macrophages and adipocytes elicit chronic low grade inflammation in renal tubular epithelial cells via a paracrine mechanism. Inflammation related injury may then initiate a cascade of events leading to crystallization, crystal retention and stone.
Testosterone Changes Bladder and Kidney Structure in Juvenile Male Rats Dairiki Shortliffe et al (page 1913) from Stanford, California hypothesized that testosterone (T) has bladder and kidney developmental effects.3 They used prepubertal male rats divided into groups, including sham orchiectomy controls and bilateral orchiectomy with and without vehicle. From week 0 T enanthate or vehicle was injected weekly. Whole bladders and kidneys were evaluated for androgen receptor (AR), bladder collagen-to-smooth muscle ratio (C/M), and renal morphometry and immunohistochemistry. T was not detectable (ND) at week 0 and it remained ND at weeks 1, 6 and 16 in operated rats with vehicle. T was physiological in controls and operated rats with T but the latter had higher levels than controls. Operated rats with T had increased bladder and kidney-to-body weight ratios, and decreased C/M compared to controls and operated rats with vehicle. Operated rats with T had a lower renal total glomerular count but increased AR density. The authors conclude that T in juvenile rats is associated with increased bladder and kidney weight, and decreased bladder C/M and renal glomerular count, and these findings are associated with increased AR density. They suggest that sex hormones affect bladder and renal development, and alteration of the timing and
http://dx.doi.org/10.1016/j.juro.2014.03.076 Vol. 191, 1639-1640, June 2014 Printed in U.S.A.
www.jurology.com
j
1639
1640
THIS MONTH IN INVESTIGATIVE UROLOGY
hormonal levels during developmental windows could cause significant changes to ultimate bladder and kidney structure, which requires more extensive examination.
1. Gosalbez M, Hupe MC, Lokeshwar SD et al: Differential expression of SDF-1 isoforms in bladder cancer. J Urol 2014; 191: 1899.
Karl-Erik Andersson
3. Dairiki Shortliffe LM, Ye Y, Behr B et al: Testosterone changes bladder and kidney structure in juvenile male rats. J Urol 2014; 191: 1913.
Section Editor
2. Zuo L, Tozawa K, Okada A et al: A paracrine mechanism involving renal tubular cells, adipocytes and macrophages promotes kidney stone formation in a simulated metabolic syndrome environment. J Urol 2014; 191: 1906.
Paracrine Mechanism Promotes Kidney Stone in Simulated Metabolic Syndrome Hypothesizing that adipocytes and macrophages increase cellular interactions to accelerate stone formation, Zuo et al (page 1906) from Japan and China developed an in vitro system of renal tubular cells, adipocytes and macrophages to simulate metabolic syndrome (MetS) and investigate molecular communication mechanism among these cells and their involvement in kidney stone formation.2 They co-cultured M-1 mouse renal tubular cells with 3T3-L1 adipocytes and/or RAW264.7 macrophages. Inflammatory markers were up-regulated in M-1 cells. Osteopontin increased in M-1 cells co-cultured with RAW264.7 cells whereas monocyte chemoattractant protein-1 and tumor necrosis
0022-5347/14/1916-1639/0 THE JOURNAL OF UROLOGY® © 2014 by AMERICAN UROLOGICAL ASSOCIATION EDUCATION
AND
RESEARCH, INC.
factor-a were over expressed in M-1 cells cocultured with 3T3-L1 cells. Co-culturing M-1 cells simultaneously with 3T3-L1 and RAW264.7 cells resulted in a significant increase of calcium oxalate monohydrate crystal adhesion to M-1 cells. The authors conclude that since inflammatory cytokine changes were induced by co-culturing renal tubular cells with adipocytes and/or macrophages without direct contact, there may be crosstalk between these cells mediated by soluble factors. They suggest that in MetS macrophages and adipocytes elicit chronic low grade inflammation in renal tubular epithelial cells via a paracrine mechanism. Inflammation related injury may then initiate a cascade of events leading to crystallization, crystal retention and stone.
Testosterone Changes Bladder and Kidney Structure in Juvenile Male Rats Dairiki Shortliffe et al (page 1913) from Stanford, California hypothesized that testosterone (T) has bladder and kidney developmental effects.3 They used prepubertal male rats divided into groups, including sham orchiectomy controls and bilateral orchiectomy with and without vehicle. From week 0 T enanthate or vehicle was injected weekly. Whole bladders and kidneys were evaluated for androgen receptor (AR), bladder collagen-to-smooth muscle ratio (C/M), and renal morphometry and immunohistochemistry. T was not detectable (ND) at week 0 and it remained ND at weeks 1, 6 and 16 in operated rats with vehicle. T was physiological in controls and operated rats with T but the latter had higher levels than controls. Operated rats with T had increased bladder and kidney-to-body weight ratios, and decreased C/M compared to controls and operated rats with vehicle. Operated rats with T had a lower renal total glomerular count but increased AR density. The authors conclude that T in juvenile rats is associated with increased bladder and kidney weight, and decreased bladder C/M and renal glomerular count, and these findings are associated with increased AR density. They suggest that sex hormones affect bladder and renal development, and alteration of the timing and
http://dx.doi.org/10.1016/j.juro.2014.03.076 Vol. 191, 1639-1640, June 2014 Printed in U.S.A.
www.jurology.com
j
1639
1640
THIS MONTH IN INVESTIGATIVE UROLOGY
hormonal levels during developmental windows could cause significant changes to ultimate bladder and kidney structure, which requires more extensive examination.
1. Gosalbez M, Hupe MC, Lokeshwar SD et al: Differential expression of SDF-1 isoforms in bladder cancer. J Urol 2014; 191: 1899.
Karl-Erik Andersson
3. Dairiki Shortliffe LM, Ye Y, Behr B et al: Testosterone changes bladder and kidney structure in juvenile male rats. J Urol 2014; 191: 1913.
Section Editor
2. Zuo L, Tozawa K, Okada A et al: A paracrine mechanism involving renal tubular cells, adipocytes and macrophages promotes kidney stone formation in a simulated metabolic syndrome environment. J Urol 2014; 191: 1906.