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Archives of Medical Research
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(2014)
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53 54 LETTER TO THE EDITOR 55 56 57 58 59 Conflict of Interest Dear Editor: 60 61 The authors declare no conflict of interest. We have read the article by Prado-Uribe et al. (1) ‘‘Role of 62 Thyroid Hormones and mir-208 in Myocardial Remodeling 63 in 5/6 Nephrectomized Rats’’ with great interest. The au64 References thors demonstrated that myocardial miR-208 expression 65 1. Prado-Uribe MD, Soto-Abraham MV, Mora-Villalpando CJ, et al. was dramatically decreased but cardiac fibrosis was markRole of thyroid hormones and mir-208 in myocardial remodeling in 66 edly increased in 5/6 nephrectomized rats when compared 5/6 nephrectomized rats. Arch Med Res 2013;44:616e622. 67 2. Satoh M, Minami Y, Takahashi Y, et al. Expression of microRNA-208 to sham rats. In thyroidectomized group, myocardial 68 is associated with adverse clinical outcomes in human dilated cardioTGF-b expression was significantly reduced, whereas 69 myopathy. J Card Fail 2010;16:404e410. miR-208 was notably augmented. Treatment with thyroxine 70 3. Montgomery RL, Hullinger TG, Semus HM, et al. Therapeutic inhibiin 5/6 nephrectomized rats could induce upregulation of tion of miR-208a improves cardiac function and survival during heart 71 miR-208 and downregulation of TGF-b expression. failure. Circulation 2011;124:1537e1547. 72 4. van Rooij E, Sutherland LB, Qi X, et al. Control of stress-dependent Together we may draw a conclusion that upregulation of 73 cardiac growth and gene expression by a microRNA. Science 2007; miR-208 could prevent cardiac fibrosis in 5/6 nephrectom74 316:575e579. ized rats induced by thyroxine supplementation and miR75 5. Shyu KG, Wang BW, Wu GJ, et al. Mechanical stretch via transforming 208 may have an inverse relationship with cardiac fibrosis. growth factor-beta1 activates microRNA208a to regulate endoglin expres76 However, existing evidence has shown that miR-208 has sion in cultured rat cardiac myoblasts. Eur J Heart Fail 2013;15:36e45. 77 6. Wang BW, Wu GJ, Cheng WP, et al. MicroRNA-208a increases a positive correlation with cardiac fibrosis indicated by 78 myocardial fibrosis via endoglin in volume overloading heart. PLoS myocardial collagen volume fraction in human dilated car79 One 2014;9:e84188. diomyopathy (2). Inhibition of miR-208 expression using 80 antagomiR208 could reduce cardiac fibrosis in response YING HUANGa,b,c Q1 81 to a high-salt diet in rats (3). There was no fibrosis in 82 TAO XUa,b miR-208 lacking mice heart compared with wild-type mice 83 JUN LIa,b induced by thoracic aortic banding (4). Further study re84 a School of Pharmacy vealed that prevention of miR-208 could reduce endoglin 85 Anhui Key Laboratory of Bioactivity of Natural Products and collagen I expression, and overexpression of miR-208 86 Anhui Medical University could obviously increase endoglin and collagen I expresHefei, 230032, China 87 b sion in rat cardiac myoblasts induced by mechanical Key Laboratory of Anti-inflammatory and Immune Medicine 88 Anhui Medical University, Ministry of Education stretch, which may result in cardiac fibrosis (5). Moreover, 89 PR China cardiac fibrosis was apparently augmented resulting from c 90 Department of Cardiology overexpression of miR-208 in aorta-caval (AV) shunt rats, 91 The First Affiliated Hospital of Anhui Medical University but distinctly attenuated after using antagomiR208. MiRHefei, 230032, China 92 208 could induce myocardial fibrosis in AV shunt rats 93 Address reprint requests to: Jun Li, Professor (6). These data argued that downregulation of miR-208 94 School of Pharmacy, Anhui Medical University may prevent cardiac fibrosis. 95 Mei Shan Road, Hefei In summary, these conflicting findings may suggest that 96 Anhui Province the role of miR-208 in cardiac fibrosis is not clearly eluci230032, China 97 dated. The reason for these differences cannot be explained Phone: þ86 551 65161001 98 FAX: þ86 551 65161001 only by different animal models. Whether miR-208 can 99 E-mail: [email protected], [email protected] prevent or promote cardiac fibrosis is still to be determined. 100 Further evidence is needed to identify the function of miRReceived for publication February 12, 2014; accepted March 28, 2014 101 208 in cardiac fibrosis. (ARCMED-D-14-00090). 102 103 104
Role of miR-208 in Cardiac Fibrosis: Prevention or Promotion?
0188-4409/$ - see front matter. Copyright Ó 2014 IMSS. Published by Elsevier Inc. http://dx.doi.org/10.1016/j.arcmed.2014.03.010 ARCMED1909_proof ■ 18-4-2014 9-40-14
1 2
Archives of Medical Research
-
(2014)
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53 54 LETTER TO THE EDITOR 55 56 57 58 59 Conflict of Interest Dear Editor: 60 61 The authors declare no conflict of interest. We have read the article by Prado-Uribe et al. (1) ‘‘Role of 62 Thyroid Hormones and mir-208 in Myocardial Remodeling 63 in 5/6 Nephrectomized Rats’’ with great interest. The au64 References thors demonstrated that myocardial miR-208 expression 65 1. Prado-Uribe MD, Soto-Abraham MV, Mora-Villalpando CJ, et al. was dramatically decreased but cardiac fibrosis was markRole of thyroid hormones and mir-208 in myocardial remodeling in 66 edly increased in 5/6 nephrectomized rats when compared 5/6 nephrectomized rats. Arch Med Res 2013;44:616e622. 67 2. Satoh M, Minami Y, Takahashi Y, et al. Expression of microRNA-208 to sham rats. In thyroidectomized group, myocardial 68 is associated with adverse clinical outcomes in human dilated cardioTGF-b expression was significantly reduced, whereas 69 myopathy. J Card Fail 2010;16:404e410. miR-208 was notably augmented. Treatment with thyroxine 70 3. Montgomery RL, Hullinger TG, Semus HM, et al. Therapeutic inhibiin 5/6 nephrectomized rats could induce upregulation of tion of miR-208a improves cardiac function and survival during heart 71 miR-208 and downregulation of TGF-b expression. failure. Circulation 2011;124:1537e1547. 72 4. van Rooij E, Sutherland LB, Qi X, et al. Control of stress-dependent Together we may draw a conclusion that upregulation of 73 cardiac growth and gene expression by a microRNA. Science 2007; miR-208 could prevent cardiac fibrosis in 5/6 nephrectom74 316:575e579. ized rats induced by thyroxine supplementation and miR75 5. Shyu KG, Wang BW, Wu GJ, et al. Mechanical stretch via transforming 208 may have an inverse relationship with cardiac fibrosis. growth factor-beta1 activates microRNA208a to regulate endoglin expres76 However, existing evidence has shown that miR-208 has sion in cultured rat cardiac myoblasts. Eur J Heart Fail 2013;15:36e45. 77 6. Wang BW, Wu GJ, Cheng WP, et al. MicroRNA-208a increases a positive correlation with cardiac fibrosis indicated by 78 myocardial fibrosis via endoglin in volume overloading heart. PLoS myocardial collagen volume fraction in human dilated car79 One 2014;9:e84188. diomyopathy (2). Inhibition of miR-208 expression using 80 antagomiR208 could reduce cardiac fibrosis in response YING HUANGa,b,c Q1 81 to a high-salt diet in rats (3). There was no fibrosis in 82 TAO XUa,b miR-208 lacking mice heart compared with wild-type mice 83 JUN LIa,b induced by thoracic aortic banding (4). Further study re84 a School of Pharmacy vealed that prevention of miR-208 could reduce endoglin 85 Anhui Key Laboratory of Bioactivity of Natural Products and collagen I expression, and overexpression of miR-208 86 Anhui Medical University could obviously increase endoglin and collagen I expresHefei, 230032, China 87 b sion in rat cardiac myoblasts induced by mechanical Key Laboratory of Anti-inflammatory and Immune Medicine 88 Anhui Medical University, Ministry of Education stretch, which may result in cardiac fibrosis (5). Moreover, 89 PR China cardiac fibrosis was apparently augmented resulting from c 90 Department of Cardiology overexpression of miR-208 in aorta-caval (AV) shunt rats, 91 The First Affiliated Hospital of Anhui Medical University but distinctly attenuated after using antagomiR208. MiRHefei, 230032, China 92 208 could induce myocardial fibrosis in AV shunt rats 93 Address reprint requests to: Jun Li, Professor (6). These data argued that downregulation of miR-208 94 School of Pharmacy, Anhui Medical University may prevent cardiac fibrosis. 95 Mei Shan Road, Hefei In summary, these conflicting findings may suggest that 96 Anhui Province the role of miR-208 in cardiac fibrosis is not clearly eluci230032, China 97 dated. The reason for these differences cannot be explained Phone: þ86 551 65161001 98 FAX: þ86 551 65161001 only by different animal models. Whether miR-208 can 99 E-mail: [email protected], [email protected] prevent or promote cardiac fibrosis is still to be determined. 100 Further evidence is needed to identify the function of miRReceived for publication February 12, 2014; accepted March 28, 2014 101 208 in cardiac fibrosis. (ARCMED-D-14-00090). 102 103 104
Role of miR-208 in Cardiac Fibrosis: Prevention or Promotion?
0188-4409/$ - see front matter. Copyright Ó 2014 IMSS. Published by Elsevier Inc. http://dx.doi.org/10.1016/j.arcmed.2014.03.010 ARCMED1909_proof ■ 18-4-2014 9-40-14
