Homocysteine-induced extracellular superoxide dismutase and its epigenetic mechanisms in monocytes

Abstract

have realised that we made a number of serious errors.These errors relate to (1) inaccurate writing and textual discrepancies, particularly in the Materials and methods, (2) mislabelling of figures and inappropriate presentation of data and (3) re-use of western blot bands in Fig. 6B, some of which we previously published in a recent paper in DNA and Cell Biology (Yideng et al., 2007) to represent different samples.At the request of The Journal of Experimental Biology, an investigation into how these errors arose was carried out by a multi-disciplinary academic committee at Ningxia Medical College. Their findings were as follows: (1) the textual inaccuracies resulted from our carelessness and limited English language skills; (2) all images within the paper were obtained from our experimental results; and (3) the reuse of images resulted from unscientific file-naming conventions and negligence on the part of the corresponding author. During the period of completing this article, we kept copies of the images on both our office and home computers and also on portable hard disks. Due to our carelessness in file-naming, we mistook previous images that should have been deleted from our computers as images relating to the current article, resulting in the re-use of our previously published images and mislabelling of figures and inappropriate presentation of data.As a consequence, we wish to retract the paper (Yideng et al., 2008). In line with the recommendations of the committee, we also intend to repeat all experiments to verify the results.We have learnt many valuable lessons from this experience and sincerely apologise to the editors and readers for our carelessness.

Individuality and epigenetics in obesity

“…Most of them produce hypermethylation in the promoter (CASP8, IGFBP3, RARA) and are related to enhanced susceptibility to several kinds of tumours (64,76,82), although some of them are involved in different metabolic diseases such as hypertension (HSD11B2) (81), atherosclerosis (PPARG) (62), diabetes (PPARGC1) and endotoxin tolerance (71). Remarkably, some genes of this list may play a role in obesity development and related processes, especially in adipogenesis (59)(60)(61)(62)(63)(64)(65)(66)(67)69,70,81), inflammation (66,67,(71)(72)(73)(74)(75)(76) or insulin signalling (71,(78)(79)(80)(81)(82).…”

Association of Aberrations in One Carbon Metabolism with Intimal Medial Thickening in Patients with Type 2 Diabetes Mellitus

“…The most crucial end-product of this pathway i.e., SAM, a universal methyl donor, modulates oxidative stress by potentiating SOD and GST activity and restoring GSH [11]. Decreased SAM with subsequent increase in SAH blocks the methyltransferases resulting in decreased cellular methylation, which in turn is associated with altered gene expression i.e., up regulation of MCP-1 [13], PDGF [14] and down regulation of SOD [41]. Further, long term depletion of folate/methyl from the diet was shown to decrease reduced/oxidized GSH ratio, alter activity of Mn-SOD, catalase and glutathione peroxidase and induce irreparable oxidative DNA damage [18].…”

“…Decreased levels of folate are known to be associated with defective synthesis of purines and uracil misincorporation in DNA [10]. Decreased SAM with increased S-adenosylhomocysteine (SAH) blocks methyltransferases, further leading to decreased cellular methylation [11] and is associated with altered gene expression i.e., up regulation of monocyte chemo attractant protein-1 (MCP-I) [12], platelet derived growth factor (PDGF) [13], down regulation of SOD [14]. All the above events are likely to trigger the cascade of events leading to atherosclerosis and arterial thrombosis.…”

Epigenetic Effects of Nutrients and the Promise for Refined Cardiovascular Disease Prevention

“…Taken together, the available data suggest that hyperhomocysteinaemia per se is not an underlying cause of DNA hypomethylation in atherosclerosis, although it is possible that Hcy operates as an active modifier of DNA methylation in synergy with other yet unidentified factors. This goes without saying that, as we mentioned above, the relevance of hyperhomocysteinemia in atherosclerosis has been questioned [19].…”

“…First, at a biochemical level, excess Hcy causes the accumulation of its own precursor Sadenosyl-homocysteine (SAH), an inhibitor of DNA methyltransferase enzymes [18]. Second, hyperhomocysteinaemia has been implicated in atherogenesis, although the results of clinical studies have not been entirely consistent [19]. Therefore, it has been hypothesized that the main consequence of hyperhomocysteinaemia is DNA hypomethylation via a reduction of SAM bioavailability.…”