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. 2018 Dec 18;43(2):749–760. doi: 10.3892/ijmm.2018.4034

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Copyright: © Zhu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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DDAH2 activates the DDAH/ADMA/NOS/NO pathway in diabetic rats with myocardial fibrosis. (A) Serum ADMA content in diabetic rats following 20 weeks of treatment with lentivirus expressing DDAH2 or shDDAH2, and/or L-NNA. (B) DDAH activity in myocardial tissues of diabetic rats following 20 weeks of treatment with lentivirus expressing DDAH2 or shDDAH2, and/or L-NNA. (C) NOS activity in myocardial tissues of diabetic rats following 20 weeks of treatment with lentivirus expressing DDAH2 or shDDAH2, and/or L-NNA. (D) NO content in myocardial tissues of diabetic rats following 20 weeks of treatment with lentivirus expressing DDAH2 or shDDAH2, and/or L-NNA. (E) mRNA and (F) protein levels of PRMT1, DDAH2 and DDAH1 in myocardial tissues of rats following 20 weeks of treatment with lentivirus expressing DDAH2 or shDDAH2, and/or L-NNA. Data are presented as the mean ± standard deviation and were analyzed by one-way analysis of variance. ^*P<0.05, vs. model group All data are representative of three independent experiments. DDAH, dimethylarginine dimethylaminohydrolase; ADMA, asymmetric N^G, N^Gdimethyl-L-arginine; PRMT1, protein arginine N-methyltransferase 1; NC, negative control; shRNA, short hairpin RNA; ADMA, asymmetric dimethylarginine; NOS, nitric oxide synthase; NO, nitric oxide; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.

DDAH2 activates the DDAH/ADMA/NOS/NO pathway in diabetic rats with myocardial fibrosis. (A) Serum ADMA content in diabetic rats following 20 weeks of treatment with lentivirus expressing DDAH2 or shDDAH2, and/or L-NNA. (B) DDAH activity in myocardial tissues of diabetic rats following 20 weeks of treatment with lentivirus expressing DDAH2 or shDDAH2, and/or L-NNA. (C) NOS activity in myocardial tissues of diabetic rats following 20 weeks of treatment with lentivirus expressing DDAH2 or shDDAH2, and/or L-NNA. (D) NO content in myocardial tissues of diabetic rats following 20 weeks of treatment with lentivirus expressing DDAH2 or shDDAH2, and/or L-NNA. (E) mRNA and (F) protein levels of PRMT1, DDAH2 and DDAH1 in myocardial tissues of rats following 20 weeks of treatment with lentivirus expressing DDAH2 or shDDAH2, and/or L-NNA. Data are presented as the mean ± standard deviation and were analyzed by one-way analysis of variance. ^*P<0.05, vs. model group All data are representative of three independent experiments. DDAH, dimethylarginine dimethylaminohydrolase; ADMA, asymmetric N^G, N^Gdimethyl-L-arginine; PRMT1, protein arginine N-methyltransferase 1; NC, negative control; shRNA, short hairpin RNA; ADMA, asymmetric dimethylarginine; NOS, nitric oxide synthase; NO, nitric oxide; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.