Epigenetic changes in renal genes dysregulated in mouse and rat models of type 1 diabetes

Komers, Radko; Mar, Daniel; Denisenko, Oleg; Xu, Bei; Oyama, T; Bomsztyk, Karol

doi:10.1038/labinvest.2013.47

Cited by 43 publications

(36 citation statements)

References 52 publications

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“…A previous report showed that upregulation of CCL2, linked to hypermethylation of H3K4 and hypomethylation of H3K27, is associated with kidney damage in diabetes (108). In addition, we recently demonstrated that CCL2 expression is upregulated in macrophages after peripheral nerve injury in a model of neuropathic pain, and is linked to a shift toward euchromatin, based on H3K4me 3 and H3K9Ac modifications (109) (Figure 1).…”

Section: Histone Methylation and Ccl2mentioning

confidence: 64%

Epigenetic regulation of CC-chemokine ligand 2 in nonresolving inflammation

Kiguchi

Saika

Kobayashi

et al. 2014

Biomolecular Concepts

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Inflammation mediated by the crosstalk between leukocytes and resident tissue cells is crucial for the maintenance of homeostasis. Because chemokine ligands and receptors, which recruit a variety of leukocytes, are widely distributed among tissues, it is important to understand the mechanisms regulating inflammatory disease. Chemokines such as CC-chemokine ligand 2 (CCL2) amplify and maintain inflammation through chemokine-cytokine networks after the recruitment of circulating leukocytes. Chemokine-dependent nonresolving inflammation occurs in the peripheral and central nervous systems, and underlies several intractable diseases, including cancer and neuropathic pain. The chronic upregulation of chemokines is often mediated by epigenetic mechanisms consisting of DNA methylation, histone modification, and nucleosome positioning. In particular, histone acetylation and methylation have been shown to play important roles in the upregulation of chemokine expression. In addition to CCL2, several other chemokines strongly contribute to neuropathic pain through epigenetic induction. Consequently, targeting epigenetic changes may have therapeutic potential for nonresolving inflammatory diseases such as neuropathic pain. Further research into the epigenetics of inflammatory diseases should promote the development of novel and effective treatment strategies for intractable inflammatory diseases.

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Section: Histone Methylation and Ccl2mentioning

confidence: 64%

Epigenetic regulation of CC-chemokine ligand 2 in nonresolving inflammation

Kiguchi

Saika

Kobayashi

et al. 2014

Biomolecular Concepts

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“…In an in vivo study [67], increases in RNA polymerase II recruitment and H3K4me2, but decreases in H3K27me3 levels, were associated with the expression of diabetic nephropathy-related genes in mouse and rat models of diabetic nephropathy, with some differences between the two species. In other studies, high glucose increased the expression of the redox-regulating protein p66Shc by inhibiting promoter DNAme and increasing H3K9ac in podocytes in vitro and in experimental diabetic nephropathy [68].…”

Section: Introductionmentioning

confidence: 99%

Epigenetic mechanisms in diabetic complications and metabolic memory

2014

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The incidence of diabetes and its associated micro- and macrovascular complications is greatly increasing worldwide. The most prevalent vascular complications of both type 1 and type 2 diabetes include nephropathy, retinopathy, neuropathy and cardiovascular diseases. Evidence suggests that both genetic and environmental factors are involved in these pathologies. Clinical trials have underscored the beneficial effects of intensive glycaemic control for preventing the progression of complications. Accumulating evidence suggests a key role for epigenetic mechanisms such as DNA methylation, histone post-translational modifications in chromatin, and non-coding RNAs in the complex interplay between genes and the environment. Factors associated with the pathology of diabetic complications, including hyperglycaemia, growth factors, oxidant stress and inflammatory factors can lead to dysregulation of these epigenetic mechanisms to alter the expression of pathological genes in target cells such as endothelial, vascular smooth muscle, retinal and cardiac cells, without changes in the underlying DNA sequence. Furthermore, long-term persistence of these alterations to the epigenome may be a key mechanism underlying the phenomenon of ‘metabolic memory’ and sustained vascular dysfunction despite attainment of glycaemic control. Current therapies for most diabetic complications have not been fully efficacious, and hence a study of epigenetic mechanisms that may be involved is clearly warranted as they can not only shed novel new insights into the pathology of diabetic complications, but also lead to the identification of much needed new drug targets. In this review, we highlight the emerging role of epigenetics and epigenomics in the vascular complications of diabetes and metabolic memory.

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“…Aldosterone plays a significant role in the development of CKD and evidence suggests that FKBP51 protein and mRNA expression are induced by aldosterone in the kidney and intestinal tissues [108][109][110] . On the other hand, CypA has a role in renal acidosis 111 , diabetic nephropathy 112 and renal cell carcinoma 113 . Furthermore, Pin1 inhibition affects CKD associated with secondary parathyroidism 114 .…”

Section: The Role Of Ppiases In Ckdmentioning

confidence: 99%

The Role of Peptidyl Prolyl Isomerases in Aging and Vascular Diseases

McClements¹,

Annett²,

Yakkundi³

et al. 2015

CMP

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Peptidyl prolyl isomerases (PPIases) are proteins belonging to the immunophilin family and are characterised by their cis-trans isomerization activity at the X-Pro peptide bond, in addition to their tetratricopeptide repeat (TPR) domain, important for interaction with the molecular chaperone, Hsp90. Due to this unique structure these proteins are able to facilitate proteinprotein interactions which can impact significantly on a range of cellular processes such as cell signalling, differentiation, cell cycle progression, metabolic activity and apoptosis.Malfunction and/or dysregulation of most members of this class of proteins promotes cellular damage and tissue/organ failure, predisposing to ageing and age-related diseases. Many individual genes within the PPIase family are associated with several age-related diseases including cardiovascular diseases (CVDs), atherosclerosis, type II diabetes (T2D), chronic kidney disease (CDK), neurodegeneration, cancer and age-related macular degeneration (AMD), in addition to the ageing process itself. This review will focus on the different roles of PPIases, and their therapeutic/biomarker potential in these age-related vascular diseases.

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Epigenetic changes in renal genes dysregulated in mouse and rat models of type 1 diabetes

Cited by 43 publications

References 52 publications

Epigenetic regulation of CC-chemokine ligand 2 in nonresolving inflammation

Epigenetic regulation of CC-chemokine ligand 2 in nonresolving inflammation

Epigenetic mechanisms in diabetic complications and metabolic memory

The Role of Peptidyl Prolyl Isomerases in Aging and Vascular Diseases

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