EOLA1 Inhibits Lipopolysaccharide-Induced Vascular Cell Adhesion Molecule-1 Expression by Association with MT2A in ECV304 Cells

Leng, Weiling; Lei, Xiaotian; Meng, Hao; Ouyang, Xinshou; Liang, Ziwen

doi:10.1155/2015/301562

Cited by 7 publications

(9 citation statements)

References 16 publications

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“…Meanwhile, we found that when the baseline level of systemic inflammation (HsCRP, PCT, IL-6, WBC, and NE%) and the important factors affecting ulcer healing (ABI, hemoglobin, and albumin) were consistent between the two groups, EOLA1 was expressed highly in the skin tissues of the acute wound in DFU but lowly in those of the chronic wound. On the contrary, the expression of some important molecules (e.g., NF- κ B and IL-6) in inflammatory activation pathways was higher in the CW group than in the AW group, which is consistent with the previous studies [8, 9]. This suggests that EOLA1 may be involved in the negative regulation of local chronic inflammatory response in DFU.…”

Section: Discussionsupporting

confidence: 91%

“…EOLA1 is weakly expressed in leukocytes and endothelial cells under a resting state, and such expression can be significantly increased after stimulation with lipopolysaccharide (LPS). EOLA1 has the functions of promoting cell growth, inhibiting apoptosis, and downregulating the secretion of immune-inflammatory factors such as intracellular interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1) [8, 9]. In addition, EOLA1 is associated with cell growth, and the growth of ECV304 cells is significantly slowed down after the inhibition of EOLA1 expression [10].…”

Section: Introductionmentioning

confidence: 99%

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The Reduced Expression of EOLA1 May Be Related to Refractory Diabetic Foot Ulcer

Leng

Pan

et al. 2019

Mediators of Inflammation

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Background. Chronic diabetic foot ulcer (DFU) is one of the most intractable complications of diabetes mellitus (DM). Its pathogenesis is complex, and uncontrolled chronic inflammation is an important factor. Endothelial overexpressed lipopolysaccharide-associated factor 1 (EOLA1) discovered in our laboratory is an intracellular protein with the function of inflammatory regulation. This study was aimed at observing the expression of EOLA1 in DFU skin tissues and its relationship with inflammation and at exploring the possible role of EOLA1 in DFU and its mechanism. Methods. The patients with DFU were divided into 2 groups based on the formation time of ulcer: the acute wound (AW) group with the course of disease≤4 weeks and the chronic wound (CW) group with the course of disease>4 weeks. The relevant clinical data of patients were collected, and the skin tissues around the ulcer were used for immunofluorescence detection and immunohistochemical staining to observe inflammation. The expression levels of EOLA1, metallothionein 2A (MT2A), nuclear factor-κB (NF-κB), and interleukin-6 (IL-6) were detected by western blot. Results. A total of 79 patients were enrolled in the study. The results of immunofluorescence and immunohistochemistry showed that EOLA1 was expressed in the epithelial tissues of DFU. However, the expression of EOLA1 in the CW group was significantly lower than that in the AW group (P<0.05), and the expression of NF-κB and IL-6 was obviously increased (P<0.05). Conclusion. The refractory wounds in patients with DFU may be closely related to the uncontrolled activation of inflammatory pathways in cells caused by the reduced expression of negative regulators of inflammation (e.g., EOLA1), and such decreased expression may be also strongly linked to the persistent state of inflammation.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

The Reduced Expression of EOLA1 May Be Related to Refractory Diabetic Foot Ulcer

Leng

Pan

et al. 2019

Mediators of Inflammation

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“…MT2A could regulate cell inflammatory response through inhibition of nuclear factor-κB (NF-κB) [ 55 ], and endothelial-overexpressed LPS-associated factor-1 (EOLA1) [ 56 ]. Inflammatory cytokines are released by oxidative stress [ 57 ], whereas MT2A could inhibit the activation of pro-inflammatory cytokines, such as IL-6, IL-12 and TNF-α [ 15 ].…”

Section: Mt2a Functionmentioning

confidence: 99%

Mammalian Metallothionein-2A and Oxidative Stress

Ling

Wei

Wang

et al. 2016

IJMS

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Mammalian metallothionein-2A (MT2A) has received considerable attention in recent years due to its crucial pathophysiological role in anti-oxidant, anti-apoptosis, detoxification and anti-inflammation. For many years, most studies evaluating the effects of MT2A have focused on reactive oxygen species (ROS), as second messengers that lead to oxidative stress injury of cells and tissues. Recent studies have highlighted that oxidative stress could activate mitogen-activated protein kinases (MAPKs), and MT2A, as a mediator of MAPKs, to regulate the pathogenesis of various diseases. However, the molecule mechanism of MT2A remains elusive. A deeper understanding of the functional, biochemical and molecular characteristics of MT2A would be identified, in order to bring new opportunities for oxidative stress therapy.

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“…EOLA1 was reported to mediate the expression of several proteins such as IL-6 and VCAM-1 under the stimulus of LPS [10,25]. Previously, a fraction of ASCH proteins were speculated to conduct transcriptional or translational roles [11], and the nuclease activity of Zm ASCH was suggested to be involved in the removal of cellular RNAs, and thus, regulation of transcriptional and translational processes [14].…”

Section: Discussionmentioning

confidence: 99%

Crystal Structure of Human EOLA1 Implies Its Possibility of RNA Binding

Kim

Park

et al. 2019

Molecules

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Human endothelial-overexpressed lipopolysaccharide-associated factor 1 (EOLA1) has been suggested to regulate inflammatory responses in endothelial cells by controlling expression of proteins, interleukin-6 and vascular cell adhesion molecule-1, and by preventing apoptosis. To elucidate the structural basis of the EOLA1 function, we determined its crystal structure at 1.71 Å resolution and found that EOLA1 is structurally similar to an activating signal cointegrator-1 homology (ASCH) domain with a characteristic β-barrel fold surrounded by α-helices. Despite its low sequence identity with other ASCH domains, EOLA1 retains a conserved ‘GxKxxExR’ motif in its cavity structure. The cavity harbors aromatic and polar residues, which are speculated to accommodate nucleotide molecules as do YT521-B homology (YTH) proteins. Additionally, EOLA1 exhibits a positively charged cleft, similar to those observed in YTH proteins and the ASCH protein from Zymomonas mobilis that exerts ribonuclease activity. This implies that the positively charged cleft in EOLA1 could stabilize the binding of RNA molecules. Taken together, we suggest that EOLA1 controls protein expression through RNA binding to play protective roles against endothelial cell injuries resulting from lipopolysaccharide (LPS)-induced inflammation responses.

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EOLA1 Inhibits Lipopolysaccharide-Induced Vascular Cell Adhesion Molecule-1 Expression by Association with MT2A in ECV304 Cells

Cited by 7 publications

References 16 publications

The Reduced Expression of EOLA1 May Be Related to Refractory Diabetic Foot Ulcer

The Reduced Expression of EOLA1 May Be Related to Refractory Diabetic Foot Ulcer

Mammalian Metallothionein-2A and Oxidative Stress

Crystal Structure of Human EOLA1 Implies Its Possibility of RNA Binding

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