- Email: [email protected]
Response and Rebuttal to Letter to the Editor regarding “Taurine Supplementation Improves Erectile Function in Rats with Streptozotocin-Induced Type 1 Diabetes via Amelioration of Penile Fibrosis and Endothelial Dysfunction”
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Letters to the Editor renal inflammation in murine unilateral ureteral obstruction. J Urol 2014;191:1508-1516.
Peyronie’s fibrotic plaque and in its rat model. Nitric Oxide 2002;7:262-276.
4. Vernet D, Ferrini MG, Valente EG, et al. Effect of nitric oxide on the differentiation of fibroblasts into myofibroblasts in the
5. Serini G, Gabbiani G. Mechanisms of myofibroblast activity and phenotypic modulation. Exp Cell Res 1999;250:272-283.
Response and Rebuttal to Letter to the Editor regarding “Taurine Supplementation Improves Erectile Function in Rats with Streptozotocin-Induced Type 1 Diabetes via Amelioration of Penile Fibrosis and Endothelial Dysfunction” To the Editor:
Although a-smooth muscle actin (a-SMA) is recognized as a marker of myofibroblasts, its expression is not limited to these cells. In the study of erectile dysfunction (ED), many studies have used the percentage of a-SMA area to assess smooth muscle content.1e4 In some other models of fibrosis (eg, plaque of Peyronie’s disease and unilateral ureteral obstruction), there are no smooth muscle cells in the injury site, so a-SMA could indicate the number of myofibroblasts. However, in rat penile tissue, a-SMAepositive cellular constituents include smooth muscle cells and myofibroblasts.1 Thus, it might not be appropriate to evaluate myofibroblasts by a-SMA expression. Loss of cavernous smooth muscle cell (CSMC) mass has been reported in diabetic rats with ED.5 In addition, Wei et al6 reported that the expression of a-SMA decreased in the CSMCs of diabetic rats with ED. The overall effect is the downregulation of a-SMA. In line with previous studies,7 our work indicated that a-SMA was decreased in the penis of diabetic rats with ED. We evaluated smooth muscle content using different markers (a-SMA and smooth muscle myosin heavy chains), and the results consistently showed that smooth muscle cells were decreased in this condition (in the supplemental data). The altered expression of a-SMA is determined by the loss of CSMCs and the generation of myofibroblasts, where the former could play a larger role. Taken together, we believe that a-SMA is not a specific marker for CSMCs or myofibroblasts, and that it is acceptable to use it to evaluate smooth muscle content in penile tissues. Yajun Ruan, MD1,2, Mingchao Li, MD, PhD1,2, Tao Wang, MD, PhD1,2, Jun Yang, MD, PhD1,2, Ke Rao, MD, PhD1,2, Shaogang Wang, MD, PhD1,2, Weiming Yang, MD, PhD1,2, Jihong Liu, MD, PhD1,2, and Zhangqun Ye, MD, PhD1,2 Department of Urology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan, China
J Sex Med 2016;13:1570e1572
Institute of Urology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan, China Corresponding Author: Tao Wang, MD, PhD, Department of Urology, Huazhong University of Science and Technology, 1095 Jiefang Road, Wuhan, Hubei 430030, China. Tel: þ86-027-83663673; Fax: þ86-027-8366-3673; E-mail: [email protected] Conflicts of Interest: The authors report no conflicts of interest. Funding: None. http://dx.doi.org/10.1016/j.jsxm.2016.07.019
STATEMENT OF AUTHORSHIP Category 1 (a) Conception and Design Yajun Ruan; Mingchao Li; Tao Wang; Jihong Liu (b) Acquisition of Data Jun Yang; Ke Rao (c) Analysis and Interpretation of Data Yajun Ruan; Mingchao Li; Shaogang Wang; Weiming Yang Category 2 (a) Drafting the Article Yajun Ruan; Tao Wang (b) Revising It for Intellectual Content Tao Wang; Jihong Liu; Zhangqun Ye Category 3 (a) Final Approval of the Completed Article Yajun Ruan; Mingchao Li; Tao Wang; Jun Yang; Ke Rao; Shaogang Wang; Weiming Yang; Jihong Liu; Zhangqun Ye
REFERENCES 1. Gonzalez-Cadavid NF. Mechanisms of penile fibrosis. J Sex Med 2009;6(Suppl. 3):353-362. 2. El-Sakka AI, Yassin AA. Amelioration of penile fibrosis: myth or reality. J Androl 2010;31:324-335.
1572 3. Castiglione F, Hedlund P, Van der Aa F, et al. Intratunical injection of human adipose tissue-derived stem cells prevents fibrosis and is associated with improved erectile function in a rat model of Peyronie’s disease. Eur Urol 2013;63:551-560. 4. Lin G, Li H, Zhang X, et al. Novel therapeutic approach for neurogenic erectile dysfunction: effect of neurotrophic tyrosine kinase receptor type 1 monoclonal antibody. Eur Urol 2015;67:716-726. 5. Burchardt T, Burchardt M, Karden J, et al. Reduction of endothelial and smooth muscle density in the corpora
Letters to the Editor cavernosa of the streptozotocin induced diabetic rat. J Urol 2000;164:1807-1811. 6. Wei AY, He SH, Zhao JF, et al. Characterization of corpus cavernosum smooth muscle cell phenotype in diabetic rats with erectile dysfunction. Int J Impot Res 2012;24:196-201. 7. Zhou F, Li GY, Gao ZZ, et al. The tgf-beta1/smad/ctgf pathway and corpus cavernosum fibrous-muscular alterations in rats with streptozotocin-induced diabetes. J Androl 2012;33:651-659.
J Sex Med 2016;13:1570e1572
Letters to the Editor renal inflammation in murine unilateral ureteral obstruction. J Urol 2014;191:1508-1516.
Peyronie’s fibrotic plaque and in its rat model. Nitric Oxide 2002;7:262-276.
4. Vernet D, Ferrini MG, Valente EG, et al. Effect of nitric oxide on the differentiation of fibroblasts into myofibroblasts in the
5. Serini G, Gabbiani G. Mechanisms of myofibroblast activity and phenotypic modulation. Exp Cell Res 1999;250:272-283.
Response and Rebuttal to Letter to the Editor regarding “Taurine Supplementation Improves Erectile Function in Rats with Streptozotocin-Induced Type 1 Diabetes via Amelioration of Penile Fibrosis and Endothelial Dysfunction” To the Editor:
Although a-smooth muscle actin (a-SMA) is recognized as a marker of myofibroblasts, its expression is not limited to these cells. In the study of erectile dysfunction (ED), many studies have used the percentage of a-SMA area to assess smooth muscle content.1e4 In some other models of fibrosis (eg, plaque of Peyronie’s disease and unilateral ureteral obstruction), there are no smooth muscle cells in the injury site, so a-SMA could indicate the number of myofibroblasts. However, in rat penile tissue, a-SMAepositive cellular constituents include smooth muscle cells and myofibroblasts.1 Thus, it might not be appropriate to evaluate myofibroblasts by a-SMA expression. Loss of cavernous smooth muscle cell (CSMC) mass has been reported in diabetic rats with ED.5 In addition, Wei et al6 reported that the expression of a-SMA decreased in the CSMCs of diabetic rats with ED. The overall effect is the downregulation of a-SMA. In line with previous studies,7 our work indicated that a-SMA was decreased in the penis of diabetic rats with ED. We evaluated smooth muscle content using different markers (a-SMA and smooth muscle myosin heavy chains), and the results consistently showed that smooth muscle cells were decreased in this condition (in the supplemental data). The altered expression of a-SMA is determined by the loss of CSMCs and the generation of myofibroblasts, where the former could play a larger role. Taken together, we believe that a-SMA is not a specific marker for CSMCs or myofibroblasts, and that it is acceptable to use it to evaluate smooth muscle content in penile tissues. Yajun Ruan, MD1,2, Mingchao Li, MD, PhD1,2, Tao Wang, MD, PhD1,2, Jun Yang, MD, PhD1,2, Ke Rao, MD, PhD1,2, Shaogang Wang, MD, PhD1,2, Weiming Yang, MD, PhD1,2, Jihong Liu, MD, PhD1,2, and Zhangqun Ye, MD, PhD1,2 Department of Urology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan, China
J Sex Med 2016;13:1570e1572
Institute of Urology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan, China Corresponding Author: Tao Wang, MD, PhD, Department of Urology, Huazhong University of Science and Technology, 1095 Jiefang Road, Wuhan, Hubei 430030, China. Tel: þ86-027-83663673; Fax: þ86-027-8366-3673; E-mail: [email protected] Conflicts of Interest: The authors report no conflicts of interest. Funding: None. http://dx.doi.org/10.1016/j.jsxm.2016.07.019
STATEMENT OF AUTHORSHIP Category 1 (a) Conception and Design Yajun Ruan; Mingchao Li; Tao Wang; Jihong Liu (b) Acquisition of Data Jun Yang; Ke Rao (c) Analysis and Interpretation of Data Yajun Ruan; Mingchao Li; Shaogang Wang; Weiming Yang Category 2 (a) Drafting the Article Yajun Ruan; Tao Wang (b) Revising It for Intellectual Content Tao Wang; Jihong Liu; Zhangqun Ye Category 3 (a) Final Approval of the Completed Article Yajun Ruan; Mingchao Li; Tao Wang; Jun Yang; Ke Rao; Shaogang Wang; Weiming Yang; Jihong Liu; Zhangqun Ye
REFERENCES 1. Gonzalez-Cadavid NF. Mechanisms of penile fibrosis. J Sex Med 2009;6(Suppl. 3):353-362. 2. El-Sakka AI, Yassin AA. Amelioration of penile fibrosis: myth or reality. J Androl 2010;31:324-335.
1572 3. Castiglione F, Hedlund P, Van der Aa F, et al. Intratunical injection of human adipose tissue-derived stem cells prevents fibrosis and is associated with improved erectile function in a rat model of Peyronie’s disease. Eur Urol 2013;63:551-560. 4. Lin G, Li H, Zhang X, et al. Novel therapeutic approach for neurogenic erectile dysfunction: effect of neurotrophic tyrosine kinase receptor type 1 monoclonal antibody. Eur Urol 2015;67:716-726. 5. Burchardt T, Burchardt M, Karden J, et al. Reduction of endothelial and smooth muscle density in the corpora
Letters to the Editor cavernosa of the streptozotocin induced diabetic rat. J Urol 2000;164:1807-1811. 6. Wei AY, He SH, Zhao JF, et al. Characterization of corpus cavernosum smooth muscle cell phenotype in diabetic rats with erectile dysfunction. Int J Impot Res 2012;24:196-201. 7. Zhou F, Li GY, Gao ZZ, et al. The tgf-beta1/smad/ctgf pathway and corpus cavernosum fibrous-muscular alterations in rats with streptozotocin-induced diabetes. J Androl 2012;33:651-659.
J Sex Med 2016;13:1570e1572