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. 2022 Apr 16;12:6398. doi: 10.1038/s41598-022-10476-6

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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NNMT deficiency decreases renal N-Me-2PY and N-Me-4PY and increases SAM/SAH ratio in UUO, thereby increasing the methylation capacity of CTGF. Plasma NAD + metabolites (A) and renal NAD + metabolites (B) were measured in NNMT-KO mice and WT littermates after UUO induction. The values shown are means ± SEM (n = 4–8 per group). (C) SAM levels, SAH levels, and SAM/SAH ratios in the kidneys of NNMT-KO mice and WT littermates after UUO induction. The data represent means ± SEM (n = 8 per group). (D) Bisulfite sequencing of CTGF CpG islands. Each circle indicates a CpG site in the sequence, and each line of circles represents a single cloned allele. Open circles, unmethylated CpG sites; closed circles, methylated CpG sites. UUO, unilateral ureter obstruction; NNMT, nicotinamide N-methyltransferase; NAM, nicotinamide; NMN, nicotinamide mononucleotide; NAD + , nicotinamide adenine dinucleotide; MNA, 1-methylnicotinamide; N-Me-2PY, N-methyl-2-pyridone-5-carboxamide; N-Me-4PY, N-methyl-4-pyridone-3-carboxamide; NA, nicotinic acid; NNO, nicotinamide-N-oxide; SAM, S-adenosylmethionine; SAH, S-adenosylhomocysteine; CTGF, connective tissue growth factor. *P < 0.05, **P < 0.01 versus WT mice. †P < 0.05, ††P < 0.01 versus the same genotype control mice (sham-operated kidney).

NNMT deficiency decreases renal N-Me-2PY and N-Me-4PY and increases SAM/SAH ratio in UUO, thereby increasing the methylation capacity of CTGF. Plasma NAD + metabolites (A) and renal NAD + metabolites (B) were measured in NNMT-KO mice and WT littermates after UUO induction. The values shown are means ± SEM (n = 4–8 per group). (C) SAM levels, SAH levels, and SAM/SAH ratios in the kidneys of NNMT-KO mice and WT littermates after UUO induction. The data represent means ± SEM (n = 8 per group). (D) Bisulfite sequencing of CTGF CpG islands. Each circle indicates a CpG site in the sequence, and each line of circles represents a single cloned allele. Open circles, unmethylated CpG sites; closed circles, methylated CpG sites. UUO, unilateral ureter obstruction; NNMT, nicotinamide N-methyltransferase; NAM, nicotinamide; NMN, nicotinamide mononucleotide; NAD + , nicotinamide adenine dinucleotide; MNA, 1-methylnicotinamide; N-Me-2PY, N-methyl-2-pyridone-5-carboxamide; N-Me-4PY, N-methyl-4-pyridone-3-carboxamide; NA, nicotinic acid; NNO, nicotinamide-N-oxide; SAM, S-adenosylmethionine; SAH, S-adenosylhomocysteine; CTGF, connective tissue growth factor. *P < 0.05, **P < 0.01 versus WT mice. †P < 0.05, ††P < 0.01 versus the same genotype control mice (sham-operated kidney).