Exosomal ATF3 RNA Attenuates Pro‐Inflammatory Gene MCP‐1 Transcription in Renal Ischemia‐Reperfusion

Chen, Hsi Hsien; Lai, Pei Fang; Lan, Yi; Cheng, Ching Feng; Zhong, Wen; Lin, Yuh Feng; Chen, Tzen‐Wen; Lin, Heng

doi:10.1002/jcp.24554

Cited by 70 publications

(65 citation statements)

References 39 publications

(56 reference statements)

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“…For example, ATF1 is involved in wound healing and gingival inflammation [65]. ATF3 attenuates transcription of the proinflammatory gene MCP-1 in renal ischemia-reperfusion injury [14] and may significantly influence inflammatory processes in the central nervous system (CNS) that are related to the frequency of epileptic seizures [66]. Recent evidence suggests a role for ATF2 in inflammation.…”

Section: Functional Involvement Of Atf2 In Inflammationmentioning

confidence: 99%

The Regulatory Role of Activating Transcription Factor 2 in Inflammation

Bian³

et al. 2014

Mediators of Inflammation

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Activating transcription factor 2 (ATF2) is a member of the leucine zipper family of DNA-binding proteins and is widely distributed in tissues including the liver, lung, spleen, and kidney. Like c-Jun and c-Fos, ATF2 responds to stress-related stimuli and may thereby influence cell proliferation, inflammation, apoptosis, oncogenesis, neurological development and function, and skeletal remodeling. Recent studies clarify the regulatory role of ATF2 in inflammation and describe potential inhibitors of this protein. In this paper, we summarize the properties and functions of ATF2 and explore potential applications of ATF2 inhibitors as tools for research and for the development of immunosuppressive and anti-inflammatory drugs.

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Section: Functional Involvement Of Atf2 In Inflammationmentioning

confidence: 99%

The Regulatory Role of Activating Transcription Factor 2 in Inflammation

Bian³

et al. 2014

Mediators of Inflammation

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“…Hence, urine exosome is an interesting source of urine biomarkers [17–19]. Activating transcription factor 3 (ATF3) is one of the transcriptional factor protected inside urine exosome which expressed in urine of AKI in patients and animal models [20, 21]. Renal ATF3 is activated in mouse models of ischemic reperfusion injury and cisplatin induced nephrotoxicity [22, 23].…”

Section: Introductionmentioning

confidence: 99%

“…Renal ATF3 is activated in mouse models of ischemic reperfusion injury and cisplatin induced nephrotoxicity [22, 23]. Interestingly, ATF3 downstream functions are anti-apoptosis and anti-inflammation through the attenuation of pro-inflammatory mediators and the alteration of the chromatin binding site in transcriptional factors [21, 22, 24, 25]. Hence, ATF3 should be involved in the pathophysiology of sepsis, AKI and sepsis-AKI.…”

Section: Introductionmentioning

confidence: 99%

“…Hence, ATF3 should be involved in the pathophysiology of sepsis, AKI and sepsis-AKI. Unfortunately, ATF3 detection in total urine and non-exosomal urine fraction is inconsistent [20, 21] due, in part, to the degradation of transcriptional factor in urine [26]. But ATF3 seems to be protected inside exosome membrane and allow easier detection [20].…”

Section: Introductionmentioning

confidence: 99%

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Urinary exosomal activating transcriptional factor 3 as the early diagnostic biomarker for sepsis-induced acute kidney injury

Chancharoenthana

Somparn

et al. 2017

BMC Nephrol

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BackgroundAn early sepsis-induced acute kidney injury (sepsis-AKI) biomarker is currently in needed. Urinary neutrophil gelatinase-associated lipocalin (uNGAL) is a candidate of sepsis-AKI biomarker but with different cut-point values. Urinary exosomal activating transcriptional factor 3 (uATF3) has been mentioned as an interesting biomarker.MethodsWe conducted experiments in mice and a prospective, multicenter study in patients as a proof of concept that urine exosome is an interesting biomarker. An early expression of ATF3 in kidney of CD-1 mice at 6 h after cecal ligation and puncture implied the possibility of uATF3 as an early sepsis-AKI biomarker. Increase serum creatinine (Scr) ≥0.3 mg/dL from the baseline was used as an AKI diagnosis and urine was analyzed for uATF3 and uNGAL. Patients with baseline Scr at admission ≥1.5 mg/dL were excluded.ResultsThe analysis showed higher Scr, uNGAL and uATF3 in patients with sepsis-AKI in comparison with patients with sepsis-non-AKI and healthy volunteers. A fair correlation, r2 = 0.47, between uATF3 and uNGAL was showed in sepsis-AKI group with Scr ≥2 mg/dL. To see if uATF3 could be an early sepsis-AKI biomarker, urine sample was collected daily during the first week of the admission. In sepsis-AKI and sepsis-non-AKI groups, uNGAL were 367 ± 43 ng/mL and 183 ± 23 ng/mL, respectively; and uATF3 were 19 ± 4 ng/mL and 1.4 ± 0.8 ng/mL, respectively. With the mean value of uNGAL and uATF3 in sepsis AKI as a cut-off level, AUROC of uNGAL and uATF3 were 64% (95% CI 0.54 to 0.74) and 84% (95% CI 0.77 to 0.91), respectively.ConclusionsUrine exosome is an interesting source of urine biomarker and uATF3 is an interesting sepsis-AKI biomarker.

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“…The miRNA content of these vesicles seems to have a positive effect on renal tubular epithelial cells, reducing apoptosis and promoting cell proliferation [130]. Chen et al [131] probed, in a mouse model, that injection of exosomal transcriptional repressor activating transcription factor 3 (ATF3), which has an anti-apoptotic effect and inhibits inflammatory responses, is able to reduce ischemia-reperfusion kidney injury. Similarly, the effect of liver stem cell EVs in the regeneration of renal-tubule injury has been suggested in the study of Herrera Sánchez et al [132], who demonstrated the inhibitory effect of these vesicles on renal-tubular cell apoptosis in a murine model of acute kidney injury.…”

Section: Future Researchmentioning

confidence: 99%

Molecular and Genetic Mechanisms Involved in the Pathogenesis of Cardiorenal Cross Talk

Virzì

Clementi²,

Brocca³

et al. 2016

Pathobiology

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The term ‘cardiorenal syndrome' (CRS) encloses a scenario of clinical interactions in which cardiac and renal dysfunctions coexist. The cross talk between the heart and the kidney is clearly evidenced but not fully understood. Indeed, different factors have been shown to be involved in the pathogenesis of CRS, such as systemic inflammation, oxidative stress, apoptosis and immune dysregulation. Recently, considerable attention has been paid to the role of new alternative mechanisms which may be implicated in the pathogenesis of cardiorenal cross talk. In this review, we will focus on epigenetics, prenatal programming, small noncoding RNAs and extracellular vesicles, aiming to elucidate their possible role in heart and kidney diseases.

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Exosomal ATF3 RNA Attenuates Pro‐Inflammatory Gene MCP‐1 Transcription in Renal Ischemia‐Reperfusion

Cited by 70 publications

References 39 publications

The Regulatory Role of Activating Transcription Factor 2 in Inflammation

The Regulatory Role of Activating Transcription Factor 2 in Inflammation

Urinary exosomal activating transcriptional factor 3 as the early diagnostic biomarker for sepsis-induced acute kidney injury

Molecular and Genetic Mechanisms Involved in the Pathogenesis of Cardiorenal Cross Talk

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