Elevated histone H3 acetylation is associated with genes involved in T lymphocyte activation and glutamate decarboxylase antibody production in patients with type 1 diabetes

Wang, Yanfei; Hou, Can; Wisler, Jon; Singh, Kiran; Wu, Chao; Xie, Zhiguo; Lu, Qianjin; Zhou, Zhiguang

doi:10.1111/jdi.12867

Cited by 18 publications

(4 citation statements)

References 49 publications

(60 reference statements)

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“…Protein acetylation is a major mechanism for regulating various protein functions and properties, including DNA replication and transcriptional activity 66, protein stability, FA metabolism 67, subcellular localization 68, and apoptosis 69. CD36 contains four acetylation sites, Lys52, Lys166, Lys231, and Lys403, but little is known regarding their biological functions 67.…”

Section: Regulation and Localization Of Cd36mentioning

confidence: 99%

CD36 tango in cancer: signaling pathways and functions

2019

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CD36, a scavenger receptor expressed in multiple cell types, mediates lipid uptake, immunological recognition, inflammation, molecular adhesion, and apoptosis. CD36 is a transmembrane glycoprotein that contains several posttranslational modification sites and binds to diverse ligands, including apoptotic cells, thrombospondin-1 (TSP-1), and fatty acids (FAs). Beyond fueling tumor metastasis and therapy resistance by enhancing lipid uptake and FA oxidation, CD36 attenuates angiogenesis by binding to TSP-1 and thereby inducing apoptosis or blocking the vascular endothelial growth factor receptor 2 pathway in tumor microvascular endothelial cells. Moreover, CD36-driven lipid metabolic reprogramming and functions in tumor-associated immune cells lead to tumor immune tolerance and cancer development. Notable advances have been made in demonstrating the regulatory networks that govern distinct physiological properties of CD36, and this has identified targeting CD36 as a potential strategy for cancer treatment. Here, we provide an overview on the structure, regulation, ligands, functions, and clinical trials of CD36 in cancer.

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Section: Regulation and Localization Of Cd36mentioning

confidence: 99%

CD36 tango in cancer: signaling pathways and functions

2019

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“…The five prototypical examples to be discussed in this article include 1) DNA methylation, 2) Histone modifications, 3) Chromatin Remodeling 4) microRNAs and 5) long non-coding RNAs (67,68) [Figure 2, reviewed in Singh et al, 2020 (24)]. These different situations point to a unique aspect of genomic regulation in that external factors, outside the domain of DNA sequences, can regulate complex disease processes (69)(70)(71)(72). T2DM has a very complex inheritance pattern with an intricate intersection between genetics and environmental factors.…”

Section: Epigenetics and Diabetic Vasculopathymentioning

confidence: 99%

Epigenetic basis of diabetic vasculopathy

et al. 2022

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Type 2 diabetes mellitus (T2DM) causes peripheral vascular disease because of which several blood-borne factors, including vital nutrients fail to reach the affected tissue. Tissue epigenome is sensitive to chronic hyperglycemia and is known to cause pathogenesis of micro- and macrovascular complications. These vascular complications of T2DM may perpetuate the onset of organ dysfunction. The burden of diabetes is primarily because of a wide range of complications of which nonhealing diabetic ulcers represent a major component. Thus, it is imperative that current research help recognize more effective methods for the diagnosis and management of early vascular injuries. This review addresses the significance of epigenetic processes such as DNA methylation and histone modifications in the evolution of macrovascular and microvascular complications of T2DM.

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“…DNA methylation is catalyzed by DNA methyltransferase (DNMT) in mammals [25,26]. On the other hand, higher acetylation levels of histones are associated with the activation of transcription [27]. Histone acetylation is catalyzed by histone acetyltransferase (HAT), whereas histone deacetylation is catalyzed by histone deacetylase (HDAC) [28,29].…”

Section: Introductionmentioning

confidence: 99%

The Synergism of PGN, LTA and LPS in Inducing Transcriptome Changes, Inflammatory Responses and a Decrease in Lactation as Well as the Associated Epigenetic Mechanisms in Bovine Mammary Epithelial Cells

Sun

Dong

et al. 2020

Toxins

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Mastitis is usually caused by a variety of pathogenic bacteria that include both Gram-positive and Gram-negative bacteria. Lipopolysaccharide (LPS) is the pathogen-associated molecular pattern (PAMP) of Gram-negative bacteria, and peptidoglycan (PGN) and lipoteichoic acid (LTA) are those of Gram-positive bacteria. The effects of LPS, PGN and/or LTA on inflammatory response and lactation in bovine mammary epithelial cells (BMECs) are well studied, but the epigenetic mechanisms of their effects received less attention. Furthermore, since the three PAMPs are often simultaneously present in the udder of cows with mastitis, it has implications in practice to study their additive effects. The results show that co-stimulation of bovine mammary epithelial cells with PGN, LTA, and LPS induced a higher number of differentially expressed genes (DEGs) and greater expressions of inflammatory factors including interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor-α (TNF-α), chemokine (C-X-C motif) ligand (CXCL)1, and CXCL6. In addition, co-stimulation further increased DNA hypomethylation compared with sole LPS stimulation. Co-stimulation greatly decreased casein expression but did not further decrease histone acetylation levels and affect the activity of histone acetyltransferase (HAT) and histone deacetylase (HDAC), compared with sole LPS stimulation. Collectively, this study demonstrated that PGN, LTA, and LPS had an additive effect on inducing transcriptome changes and inflammatory responses in BMECs, probably through inducing a greater decrease in DNA methylation. Co-stimulation with PGN, LTA, and LPS decreased casein expression to a greater degree, but it might not be linked to histone acetylation and HAT and HDAC activity.

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Elevated histone H3 acetylation is associated with genes involved in T lymphocyte activation and glutamate decarboxylase antibody production in patients with type 1 diabetes

Abstract: The present study generates a genome-wide histone acetylation profile specific to CD4 T lymphocytes in type 1 diabetes patients who are glutamic acid decarboxylase antibody-positive, which is instrumental in improving our understanding of the epigenetic involvement in autoimmune diabetes.

Cited by 18 publications

References 49 publications

CD36 tango in cancer: signaling pathways and functions

CD36 tango in cancer: signaling pathways and functions

Epigenetic basis of diabetic vasculopathy

The Synergism of PGN, LTA and LPS in Inducing Transcriptome Changes, Inflammatory Responses and a Decrease in Lactation as Well as the Associated Epigenetic Mechanisms in Bovine Mammary Epithelial Cells

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