High Sensitivity Determination of TNF-α for Early Diagnosis of Neonatal Infections with a Novel and Reusable Electrochemical Sensor

Li, Liangliang; Li, Miaomiao; Wang, Wenwen; Zhang, Qian; Liu, Dongyun; Li, Xianghong; Jiang, Hong

doi:10.3390/s17050992

Cited by 14 publications

(5 citation statements)

References 36 publications

(35 reference statements)

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“…[2][3][4][5][6] This view has been substantiated largely by studies in which elevated TNFα levels have been reported in patients with cancer treated with DOX. [7][8][9] However, the relationship between TNFα and DOX cardiotoxicity remains cryptic. TNFα can drive innate signaling by pathogen-activated molecular programs, as well as damage-activated molecular programs.…”

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confidence: 99%

Proteasomal Degradation of TRAF2 Mediates Mitochondrial Dysfunction in Doxorubicin-Cardiomyopathy

et al. 2022

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Background: Cytokines such as tumor necrosis factor-α (TNFα) have been implicated in cardiac dysfunction and toxicity associated with doxorubicin (DOX). Although TNFα can elicit different cellular responses, including survival or death, the mechanisms underlying these divergent outcomes in the heart remain cryptic. The E3 ubiquitin ligase TRAF2 (TNF receptor associated factor 2) provides a critical signaling platform for K63-linked polyubiquitination of RIPK1 (receptor interacting protein 1), crucial for nuclear factor-κB (NF-κB) activation by TNFα and survival. Here, we investigate alterations in TNFα–TRAF2–NF-κB signaling in the pathogenesis of DOX cardiotoxicity. Methods: Using a combination of in vivo (4 weekly injections of DOX 5 mg·kg −1 ·wk −1 ) in C57/BL6J mice and in vitro approaches (rat, mouse, and human inducible pluripotent stem cell–derived cardiac myocytes), we monitored TNFα levels, lactate dehydrogenase, cardiac ultrastructure and function, mitochondrial bioenergetics, and cardiac cell viability. Results: In contrast to vehicle-treated mice, ultrastructural defects, including cytoplasmic swelling, mitochondrial perturbations, and elevated TNFα levels, were observed in the hearts of mice treated with DOX. While investigating the involvement of TNFα in DOX cardiotoxicity, we discovered that NF-κB was readily activated by TNFα. However, TNFα-mediated NF-κB activation was impaired in cardiac myocytes treated with DOX. This coincided with loss of K63- linked polyubiquitination of RIPK1 from the proteasomal degradation of TRAF2. Furthermore, TRAF2 protein abundance was markedly reduced in hearts of patients with cancer treated with DOX. We further established that the reciprocal actions of the ubiquitinating and deubiquitinating enzymes cellular inhibitors of apoptosis 1 and USP19 (ubiquitin-specific peptidase 19), respectively, regulated the proteasomal degradation of TRAF2 in DOX-treated cardiac myocytes. An E3-ligase mutant of cellular inhibitors of apoptosis 1 (H588A) or gain of function of USP19 prevented proteasomal degradation of TRAF2 and DOX-induced cell death. Furthermore, wild-type TRAF2, but not a RING finger mutant defective for K63-linked polyubiquitination of RIPK1, restored NF-κB signaling and suppressed DOX-induced cardiac cell death. Last, cardiomyocyte-restricted expression of TRAF2 (cardiac troponin T–adeno-associated virus 9–TRAF2) in vivo protected against mitochondrial defects and cardiac dysfunction induced by DOX. Conclusions: Our findings reveal a novel signaling axis that functionally connects the cardiotoxic effects of DOX to proteasomal degradation of TRAF2. Disruption of the critical TRAF2 survival pathway by DOX sensitizes cardiac myocytes to TNFα-mediated necrotic cell death and DOX cardiotoxicity.

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confidence: 99%

Proteasomal Degradation of TRAF2 Mediates Mitochondrial Dysfunction in Doxorubicin-Cardiomyopathy

et al. 2022

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“…Then, SiNWs were immersed in an aqueous solution of HF and AgNO 3 under the optimal conditions found in our previous study devoted for rhodamine 6G detection [26]. The AgNPs/SiNWs were further functionalized with a densely packed self-assembled layer of hexanethiol, to avoid nonspecific binding of the analyte on the surface, by incubating the SERS substrate in 10 -3 M of MCH [29,30]. Since the arrangement of the thiolated DNA on sensor surfaces has a deep impact on molecular recognition [31], the thiol-terminated DNA aptamer (anti-PSA) was tethered to the surface by exchanging with already adsorbed thiols through immersing MCH/AgNPs/SiNWs substrate (11 cm 2 wafer) in 2 mL of 1 µM of anti-PSA aptamer dissolved in PBS for 4, 8, 12 and 16h at RT.…”

Section: Bioplatform Assembly and Operationmentioning

confidence: 99%

Functionalized SERS substrate based on silicon nanowires for rapid detection of prostate specific antigen

Ouhibi

Raouafi

Lorrain

et al. 2021

Sensors and Actuators B: Chemical

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Owing to its high sensitivity, surface-enhanced Raman spectroscopy (SERS) is largely used in biosensing as an efficient optical technique. In this work, we report the elaboration of a novel SERS substrate based aptasensor for ultra-sensitive and selective detection of prostate specific antigen (PSA). The SERS substrate is based on silicon nanowires (SiNWs) as transducer surface coated by silver nanoparticules (AgNPs). The silver nanoparticles have two purposes : a) aptamer immobilization via thiol chemistry and b) Raman signal enhancement. The presence of PSA induces the appearance of amide vibration modes only if the aptamer is present on the surface of SiNWs. The platform is highly sensitive, selective and specific to PSA in a wide range of concentrations from 0.1 to 20 µg.L -1 with a detection limit of 0.1 µg.L -1 , which encompasses the blood serum range of healthy subjects and ill patients. This optical biosensor shows a great stability and it is successfully validated in human blood serum samples showing very good results.

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“…Platinum, which is often alloyed with Iridium, is commonly used for clinical applications and is recognized to be durable and safe over long periods of time. Platinum however, has a relatively low CIC (Leung et al, 2015 ), other emerging materials such as various forms of Iridium Oxide and poly (3,4-ethylenedioxythiophene) (PEDOT) have CIC values of roughly 20x to 100x (respectively) as that of Platinum (Cogan, 2008 ), and are good candidates for the microelectrodes required for accessing targets in mice. Validation of the durability of these materials is ongoing (Straka et al, 2018 ; Dijk et al, 2019 ).…”

Section: Technical Challengesmentioning

confidence: 99%

Closed-loop neuromodulation will increase the utility of mouse models in Bioelectronic Medicine

Datta-Chaudhuri

2021

Bioelectron Med

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Mouse models have been of tremendous benefit to medical science for the better part of a century, yet bioelectronic medicine research using mice has been limited to mostly acute studies because of a lack of tools for chronic stimulation and sensing. A wireless neuromodulation platform small enough for implantation in mice will significantly increase the utility of mouse models in bioelectronic medicine. This perspective examines the necessary functionality of such a system and the technical challenges needed to be overcome for its development. Recent progress is examined and the outlook for the future of implantable devices for mice is discussed.

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High Sensitivity Determination of TNF-α for Early Diagnosis of Neonatal Infections with a Novel and Reusable Electrochemical Sensor

Cited by 14 publications

References 36 publications

Proteasomal Degradation of TRAF2 Mediates Mitochondrial Dysfunction in Doxorubicin-Cardiomyopathy

Proteasomal Degradation of TRAF2 Mediates Mitochondrial Dysfunction in Doxorubicin-Cardiomyopathy

Functionalized SERS substrate based on silicon nanowires for rapid detection of prostate specific antigen

Closed-loop neuromodulation will increase the utility of mouse models in Bioelectronic Medicine

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