CTCF inhibits endoplasmic reticulum stress and apoptosis in cardiomyocytes by upregulating RYR2 via inhibiting S100A1

Zeng, Zhu; Huang, Nina; Zhang, Yudan; Wang, Ying; Su, Yufei; Zhang, Huifang; An, Yuan

doi:10.1016/j.lfs.2019.117158

Cited by 25 publications

(12 citation statements)

References 37 publications

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“…Western blotting analysis was used to determine the expression levels of ERS related proteins. TG, thapsigargin; ERS, endoplasmic reticulum stress; HG, high glucose; NG, normal glucose; MA, mannitol; HSPA5, heat shock protein A5; IRE1α, insulin response element 1α; XBP1, X-box binding protein 1; CHOP, C/EBP-homologous protein; ATF6, activating transcription factor 6 ** P<0.01, reported that excessive ERS lead to the apoptosis of cardiomyocytes (27)(28)(29). Thus, how to alleviate ERS-induced injury is a hot topic of research.…”

Section: Discussionmentioning

confidence: 99%

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Rutin alleviates cardiomyocyte injury induced by high glucose through inhibiting apoptosis and endoplasmic reticulum stress

Wang

et al. 2021

Exp Ther Med

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Diabetic cardiomyopathy is a common complication of diabetes, in which endoplasmic reticulum stress (ERS) serves an important role. Rutin can treat the myocardial dysfunction of diabetic rats. However, to the best of our knowledge, studies on the effects of Rutin on myocardial injury caused by diabetes from the perspective of ERS have not previously been reported. In the present study, the role of rutin in the regulation of ERS in myocardial injury was assessed. Different high glucose concentrations were used to treat H9C2 myoblast cells to establish a myocardial damage model. A cell counting kit-8 assay was used to determine cell viability. A lactate dehydrogenase kit was used to detect cytotoxicity. Apoptosis levels were determined using a TUNEL assay. Western blotting was used to determine the expression levels of apoptosis-related proteins and ERS-related proteins, including heat shock protein A family member 5, inositol-requiring enzyme-1α, X-box binding protein 1, activating transcription factor 6, C/EBP-homologous protein (CHOP), cleaved caspase-12 and caspase-12. The anti-apoptotic and anti-ERS effects of Rutin on H9C2 cardiac cells induced by high glucose were examined after the administration of the ERS activator thapsigargin (TG). The results indicated that rutin could dose-dependently inhibit the level of apoptosis and ERS induced by high glucose in H9C2 cells. After administration of the ERS activator TG, it was demonstrated that TG could reverse the anti-apoptotic and anti-ERS effects of rutin on H9C2 cells stimulated with high glucose. Collectively, the present results suggested that rutin may alleviate cardiomyocyte model cell injury induced by high glucose through the inhibition of apoptosis and ERS.

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Section: Discussionmentioning

confidence: 99%

“…Moreover, its pathogenesis is complex and has not been fully defined ( 26 ). In recent years, studies have reported that excessive ERS lead to the apoptosis of cardiomyocytes ( 27-29 ). Thus, how to alleviate ERS-induced injury is a hot topic of research.…”

Section: Discussionmentioning

confidence: 99%

Rutin alleviates cardiomyocyte injury induced by high glucose through inhibiting apoptosis and endoplasmic reticulum stress

Wang

et al. 2021

Exp Ther Med

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“…The unfolded protein response is a prominent feature of ER stress (25). ER stress also contributes to apoptosis and hypertrophic growth of cardiomyocytes (26,27). Attenuation of ER stress prevents cardiomyocyte senescence and improves cardiomyocyte contractility cardiac function (28,29).…”

Section: Er Stressmentioning

confidence: 99%

Cardiomyocyte Senescence and Cellular Communications Within Myocardial Microenvironments

2020

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Cardiovascular diseases have become the leading cause of human death. Aging is an independent risk factor for cardiovascular diseases. Cardiac aging is associated with maladaptation of cellular metabolism, dysfunction (or senescence) of cardiomyocytes, a decrease in angiogenesis, and an increase in tissue scarring (fibrosis). These events eventually lead to cardiac remodeling and failure. Senescent cardiomyocytes show the hallmarks of DNA damage, endoplasmic reticulum stress, mitochondria dysfunction, contractile dysfunction, hypertrophic growth, and senescence-associated secreting phenotype (SASP). Metabolism within cardiomyocytes is essential not only to fuel the pump function of the heart but also to maintain the functional homeostasis and participate in the senescence of cardiomyocytes. The senescence of cardiomyocyte is also regulated by the non-myocytes (endothelial cells, fibroblasts, and immune cells) in the local microenvironment. On the other hand, the senescent cardiomyocytes alter their phenotypes and subsequently affect the non-myocytes in the local microenvironment and contribute to cardiac aging and pathological remodeling. In this review, we first summarized the hallmarks of the senescence of cardiomyocytes. Then, we discussed the metabolic switch within senescent cardiomyocytes and provided a discussion of the cellular communications between dysfunctional cardiomyocytes and non-myocytes in the local microenvironment. We also addressed the functions of metabolic regulators within non-myocytes in modulating myocardial microenvironment. Finally, we pointed out some interesting and important questions that are needed to be addressed by further studies.

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“…Through motif analysis, a key TF CTCF, was found in both the LW100 vs LW70 and LW100 vs LW45 comparisons. CTCF, which is a highly conserved zinc-nger DNA-binding protein, has been found to play a role as a transcriptional repressor of the Myc gene and to be involved in the occurrence of various cardiovascular diseases [74,75]. CTCF has a very large number of binding sites in the mammalian genome (40000-80000), which are mainly concentrated in intergenic regions and introns and overlap with enhancer and promoter sequences.…”

Section: Discussionmentioning

confidence: 99%

The landscape of chromatin accessibility in skeletal muscle during embryonic development in pigs

Yue

Hou

Liu

et al. 2021

Preprint

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Background: The development of skeletal muscle during the embryonic stage in pigs is precisely regulated by transcriptional mechanisms, which depends on chromatin accessibility. However, the landscape of chromatin accessibility in skeletal muscle during embryonic development in pigs has not been reported. To gain insight into the landscape of chromatin accessibility and the associated genome-wide transcriptome during embryonic muscle development, we performed ATAC-seq and RNA-seq on skeletal muscle of pig embryos at 45, 70 and 100 days post coitus (dpc).Results: In total, 21638, 35447 and 60181 unique regions (or peaks) were found across 45 dpc (LW45), 70 dpc (LW70) and 100 dpc (LW100) embryos, respectively. More than 91% of peaks were annotated within -1 kb to 100 bp of transcription start sites (TSSs). First, widespread increases in specific accessible chromatin regions (ACRs) from 45 to 100 dpc embryos suggested that the regulatory mechanisms became increasingly complicated during embryonic development. Second, the findings of integrated ATAC-seq and RNA-seq analyses showed that not only the numbers but also the peak intensities of ACRs could control the expression of associated genes. Finally, motif screening of stage-specific ACRs revealed some transcription factors that regulated muscle development-related genes, such as MyoD, Mef2c, and Mef2d. Motif screening of DPI of common peaks detected that a potential transcriptional repressor, namely CTCF, was identified among those genes that exhibited different change trends between the ATAC-seq and RNA-seq data.Conclusions: This work indicates that chromatin accessibility plays an important regulatory role in the embryonic muscle development of pigs and regulates the temporal and spatial expression patterns of key genes in muscle development by influencing the binding of transcription factors. Our results contribute to a better understanding of the regulatory dynamics of genes involved in pig embryonic skeletal muscle development.

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CTCF inhibits endoplasmic reticulum stress and apoptosis in cardiomyocytes by upregulating RYR2 via inhibiting S100A1

Cited by 25 publications

References 37 publications

Rutin alleviates cardiomyocyte injury induced by high glucose through inhibiting apoptosis and endoplasmic reticulum stress

Rutin alleviates cardiomyocyte injury induced by high glucose through inhibiting apoptosis and endoplasmic reticulum stress

Cardiomyocyte Senescence and Cellular Communications Within Myocardial Microenvironments

The landscape of chromatin accessibility in skeletal muscle during embryonic development in pigs

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