Tannic acid as a plant-derived polyphenol exerts vasoprotection via enhancing KLF2 expression in endothelial cells

Yang, Xu; Liu, Peng; Xu, Suowen; Koroleva, Marina; Zhang, Shuya; Si, Shuyi; Jin, Zheng Gen

doi:10.1038/s41598-017-06803-x

Cited by 48 publications

(35 citation statements)

References 31 publications

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“…These studies indicate the widespread anti-inflammatory properties of statins through the modulation of KLF2. In addition to statins, phenol compounds such as tannic acid and resveratrol, are capable of inducing endothelial KLF2 and preventing inflammation ( 148 , 149 ). Acting via sirtuin 1 and MEK5/MEF2-dependent mechanisms, resveratrol induces the expression of KLF2-dependent atheroprotective genes ( 149 ).…”

Section: Pharmacological Modulation Of Klfsmentioning

confidence: 99%

Krüppel-Like Factors in Vascular Inflammation: Mechanistic Insights and Therapeutic Potential

Sweet

Fan

Hsieh

et al. 2018

Front. Cardiovasc. Med.

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The role of inflammation in vascular disease is well recognized, involving dysregulation of both circulating immune cells as well as the cells of the vessel wall itself. Unrestrained vascular inflammation leads to pathological remodeling that eventually contributes to atherothrombotic disease and its associated sequelae (e.g., myocardial/cerebral infarction, embolism, and critical limb ischemia). Signaling events during vascular inflammation orchestrate widespread transcriptional programs that affect the functions of vascular and circulating inflammatory cells. The Krüppel-like factors (KLFs) are a family of transcription factors central in regulating vascular biology in states of homeostasis and disease. Given their abundance and diversity of function in cells associated with vascular inflammation, understanding the transcriptional networks regulated by KLFs will further our understanding of the pathogenesis underlying several pervasive health concerns (e.g., atherosclerosis, stroke, etc.) and consequently inform the treatment of cardiovascular disease. Within this review, we will discuss the role of KLFs in coordinating protective and deleterious responses during vascular inflammation, while addressing the potential targeting of these critical transcription factors in future therapies.

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Section: Pharmacological Modulation Of Klfsmentioning

confidence: 99%

Krüppel-Like Factors in Vascular Inflammation: Mechanistic Insights and Therapeutic Potential

Sweet

Fan

Hsieh

et al. 2018

Front. Cardiovasc. Med.

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show abstract

“…KLF2 may inhibit the expression of proinflammatory factors through recruiting both chromatin modulators p300 and cyclic adenosine monophosphate response element binding protein (CBP)‐associated factor (PCAF), which is a NF‐κB coactivators . Xu et al has also been shown to support the theory that KLF2 possesses anti‐inflammatory and antiatherosclerotic effects. Furthermore, Nrf2 has been proven to be an important transcription factor in the protection against oxidative stress, specifically in the context of the central nervous system .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐25 aggravates Aβ1‐42‐induced hippocampal neuron injury in Alzheimer's disease by downregulating KLF2 via the Nrf2 signaling pathway in a mouse model

Duan

2019

J of Cellular Biochemistry

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Recently, numerous microRNAs (miRNAs) have been considered as key players in the regulation of neuronal processes. The purpose of the present study is to explore the effect of miR‐25 on hippocampal neuron injury in Alzheimer's disease (AD) induced by amyloid β (Aβ) peptide fragment 1 to 42 (Aβ1‐42) via Kruppel‐like factor 2 (KLF2) through the nuclear factor‐E2‐related factor 2 (Nrf2) signaling pathway. A mouse model of AD was established through Aβ1‐42 induction. The underlying regulatory mechanisms of miR‐25 were analyzed through treatment of miR‐25 mimics, miR‐25 inhibitors, or small interfering RNA (siRNA) against KLF2 in hippocampal tissues and cells isolated from AD mice. The targeting relationship between miR‐25 and KLF2 was predicted using a target prediction program and verified by luciferase activity determination. MTT assay was used to evaluate the proliferative ability and flow cytometry to detect cell cycle distribution and apoptosis. KLF2 was confirmed as a target gene of miR‐25. When the mice were induced by Aβ1‐42, proliferation was suppressed while apoptosis was promoted in hippocampal neurons as evidenced by lower levels of KLF2, Nrf2, haem oxygenase, glutathione S transferase α1, glutathione, thioredoxin, and B‐cell lymphoma‐2 along with higher bax level. However, such alternations could be reversed by treatment of miR‐25 inhibitors. These findings indicate that miR‐25 may inhibit hippocampal neuron proliferation while promoting apoptosis, thereby aggravating hippocampal neuron injury through downregulation of KLF2 via the Nrf2 signaling pathway.

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“…A follow-up study by the same research group confirmed the upregulation of both KLF2- and Nrf2-induced transcriptomes by shear stress [ 103 ]. Highlighting the importance of KLF2 in maintaining endothelial homeostasis, its molecular inducers such as statins [ 104 ], resveratrol [ 105 ], suberanilohydroxamic acid [ 106 ] and tannic acid [ 107 ] were recently suggested as a potential therapy for atherosclerosis treatment and prophylaxis.…”

Section: Application Of Whole-transcriptome Sequencing To Endothelmentioning

confidence: 99%

Whole-Transcriptome Sequencing: A Powerful Tool for Vascular Tissue Engineering and Endothelial Mechanobiology

et al. 2018

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Among applicable high-throughput techniques in cardiovascular biology, whole-transcriptome sequencing is of particular use. By utilizing RNA that is isolated from virtually all cells and tissues, the entire transcriptome can be evaluated. In comparison with other high-throughput approaches, RNA sequencing is characterized by a relatively low-cost and large data output, which permits a comprehensive analysis of spatiotemporal variation in the gene expression profile. Both shear stress and cyclic strain exert hemodynamic force upon the arterial endothelium and are considered to be crucial determinants of endothelial physiology. Laminar blood flow results in a high shear stress that promotes atheroresistant endothelial phenotype, while a turbulent, oscillatory flow yields a pathologically low shear stress that disturbs endothelial homeostasis, making respective arterial segments prone to atherosclerosis. Severe atherosclerosis significantly impairs blood supply to the organs and frequently requires bypass surgery or an arterial replacement surgery that requires tissue-engineered vascular grafts. To provide insight into patterns of gene expression in endothelial cells in native or bioartificial arteries under different biomechanical conditions, this article discusses applications of whole-transcriptome sequencing in endothelial mechanobiology and vascular tissue engineering.

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Tannic acid as a plant-derived polyphenol exerts vasoprotection via enhancing KLF2 expression in endothelial cells

Cited by 48 publications

References 31 publications

Krüppel-Like Factors in Vascular Inflammation: Mechanistic Insights and Therapeutic Potential

Krüppel-Like Factors in Vascular Inflammation: Mechanistic Insights and Therapeutic Potential

MicroRNA‐25 aggravates Aβ1‐42‐induced hippocampal neuron injury in Alzheimer's disease by downregulating KLF2 via the Nrf2 signaling pathway in a mouse model

Whole-Transcriptome Sequencing: A Powerful Tool for Vascular Tissue Engineering and Endothelial Mechanobiology

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