Effect of S-adenosylmethionine on neointimal formation after balloon injury in obese diabetic rats

Lim, Soo; Moon, Min Kyong; Shin, Hayley; Kim, Tae Hyuk; Cho, Bong Jun; Kim, Min; Park, Ho Seon; Choi, Sung Hee; Ko, Seong Hee; Chung, Myung Hee; Lee, In Kyu; Jang, Hak Chul; Kim, Young–Bum; Park, Kyong Soo

doi:10.1093/cvr/cvr009

Cited by 31 publications

(20 citation statements)

References 51 publications

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“…Previous studies have suggested that low plasma levels of SAM or a decreased SAM/SAH ratio are associated with an increased risk of atherosclerosis (Spijkerman et al, 2005;Wagner and Koury, 2007). A recent study also showed that SAM administration prevents neointimal formation after balloon injury (Lim et al, 2011). However, our study is the first to show that SAM administration prevents endothelial dysfunction in HFD-fed animals.…”

Section: Discussioncontrasting

confidence: 44%

“…Eight-week-old male Sprague-Dawley (SD) rats (Orient, Korea) weighing 250 to 300 g were given normal rat chow or a high fat diet (HFD) that provided 60% of calories as fat (D12492, Research Diets, USA) with or without 30 mg/kg/day of SAM (Dalim Biotech, Korea; Lim et al, 2011). All animal experiments were approved by the Institutional Animal Care and Use Committee of the Asan Institute for Life Sciences.…”

Section: Animals and Experimental Protocolmentioning

confidence: 99%

“…Therefore, it has been suggested that the association between HHcy and cardiovascular disease may be explained by low SAM levels or a low SAM/SAH ratio (Spijkerman et al, 2005;Wagner and Koury, 2007). A recent study reported that SAM administration prevents neointimal formation after balloon injury in obese diabetic rats (Lim et al, 2011). Restenosis after vascular injury and atherosclerosis share common pathogenic mechanisms.…”

Section: Introductionmentioning

confidence: 99%

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S-Adenosyl Methionine Prevents Endothelial Dysfunction by Inducing Heme Oxygenase-1 in Vascular Endothelial Cells

Kim

Hong

Kim

et al. 2013

Molecules and Cells

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* S-adenosyl methionine (SAM) is a key intermediate in themetabolism of sulfur amino acids and is a major methyl donor in the cell. Although the low plasma level of SAM has been associated with atherosclerosis, the effect of SAM administration on atherosclerosis is not known. Endothelial dysfunction is an early prerequisite for atherosclerosis. This study was undertaken to investigate the possible preventive effect of SAM on endothelial dysfunction and the molecular mechanism of its action. SAM treatment prevented endothelial dysfunction in high fat diet (HFD)-fed rats. In cultured human aortic endothelial cells, linoleic acid (LA) increased and SAM decreased cell apoptosis and endoplasmic reticulum stress. Both LA and SAM increased heme oxygenase-1 (HO-1) expression in an NF-E2-related factor 2-dependent manner. However, knockdown of HO-1 reversed only the SAM-induced preventive effect of cell apoptosis. The LA-induced HO-1 expression was dependent on PPARα, whereas SAM induced HO-1 in a PPAR-independent manner. These data demonstrate that SAM treatment prevents endothelial dysfunction in HFDfed animals by inducing HO-1 in vascular endothelial cells. In cultured endothelial cells, SAM-induced HO-1 was responsible for the observed prevention of cell apoptosis. We propose that SAM treatment may represent a new therapeutic strategy for atherosclerosis.

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Section: Discussioncontrasting

confidence: 44%

Section: Animals and Experimental Protocolmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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S-Adenosyl Methionine Prevents Endothelial Dysfunction by Inducing Heme Oxygenase-1 in Vascular Endothelial Cells

Kim

Hong

Kim

et al. 2013

Molecules and Cells

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“…In a rat T2D model, 3 weeks of treatment with s-adenosylmethionine, a modulator of homocysteine production, exerted protective effects against atherosclerosis, partly by increasing serum concentration of adiponectin Ref. [8]. In in vivo and in vitro studies, vanadium compounds exhibited antidiabetic effects, which were mediated by upregulating adiponectin expression and multimerization [76].…”

Section: Natural Compounds and Other Materialsmentioning

confidence: 99%

“…Other drugs used to treat CVD, including angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs), also resulted in increased adiponectin levels [6]. In addition, natural compounds used in foods or nutritional supplements (e.g., resveratrol and S-adenosylmethionine) demonstrated anti-inflammatory actions, which were associated with increased adiponectin levels [7,8].…”

Section: Introductionmentioning

confidence: 99%

Modulation of adiponectin as a potential therapeutic strategy

2014

Self Cite

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High‐glucose concentration aggravates TNF‐alpha‐induced cell viability reduction in human CD146‐positive periodontal ligament cells via TNFR‐1 gene demethylation

Luo

Zhu

et al. 2020

Cell Biology International

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Periodontitis is a chronic inflammatory disease that results in the destruction of periodontal soft tissue and the resorption of alveolar bone. Evidence indicates that in diabetic patients, hyperglycemia suppresses periodontal ligament stem cell (PDLSC) functions and leads to difficulties in periodontal repair. The present study aimed to explore the mechanisms by which high‐glucose concentrations aggravate cell viability reduction in human CD146‐positive PDLCs (CD146+PDLCs) under tumor necrosis factor‐alpha (TNF‐alpha) induction. CD146+PDLCs were isolated from periodontal ligament tissues and treated in the absence or presence of 10 ng/ml of TNF‐alpha and 30 mM glucose. Cell viability was detected using Cell Counting Kit‐8 assays and Luminescent Cell Viability Assays. Western blotting and real‐time polymerase chain reaction were performed to determine tumor necrosis factor‐alpha receptor‐1 (TNFR‐1) protein and messenger RNA expression. Bisulfite and MassArray methylation analyses were used to analyze the methylation status of the TNFR‐1 gene. Our results indicated that cell viability was reduced after treatment with a combination of both high‐glucose concentration and TNF‐alpha. Treatment with 30 mM glucose suppressed DNA methyltransferase (DNMT) activities and DNMT1 protein expression, and this was accompanied by the upregulation of TNFR‐1. Additionally, we found that the CpG island located within the TNFR‐1 gene was hypomethylated under 30 mM glucose conditions. S‐adenosylmethionine, an established methyl donor, reversed TNFR‐1 upregulation and restored cell viability against high‐glucose concentration and TNF‐alpha. In conclusion, the present findings suggest that high‐glucose‐induced CpG island hypomethylation within the TNFR‐1 gene plays an essential role in TNFR‐1 upregulation, and this further enhances the cell viability reduction of CD146+PDLCs caused by TNF‐alpha.

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Effect of S-adenosylmethionine on neointimal formation after balloon injury in obese diabetic rats

Cited by 31 publications

References 51 publications

S-Adenosyl Methionine Prevents Endothelial Dysfunction by Inducing Heme Oxygenase-1 in Vascular Endothelial Cells

S-Adenosyl Methionine Prevents Endothelial Dysfunction by Inducing Heme Oxygenase-1 in Vascular Endothelial Cells

Modulation of adiponectin as a potential therapeutic strategy

High‐glucose concentration aggravates TNF‐alpha‐induced cell viability reduction in human CD146‐positive periodontal ligament cells via TNFR‐1 gene demethylation

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