CELL BIOLOGY INTERNATIONAL
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2024
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IF 3.3
Jutao Li,Zhenming Gao
Breast cancer has become the leading cause of death in women. Membrane associated ring-CH-type finger 1 (MARCHF1) is associated with the development of various types of cancer, but the exact role of MARCHF1 in breast cancer remains unclear. In our study, the higher MARCHF1 expression was observed in tumor samples of patients with breast cancer and then the role of MARCHF1 in breast cancer was further evaluated. Overexpression of MARCHF1 contributed to proliferation of cancer cells and inhibition of oxidative stress. Knockdown of MARCHF1 reduced breast cancer cell proliferation, increased mitochondrial dysfunction induced by oxidative stress, eventually aggravating cell death. In vivo, MARCHF1 promoted the tumor growth and oppositely, MARCHF1 silencing suppressed the tumor development. Moreover, MARCHF1 interacted with repressor Element-1 silencing transcription factor (REST) and facilitated its ubiquitylation and degradation. Subsequently, REST negatively regulated the transcription of mitochondrial transcription factor A (TFAM). The subcutaneous tumor formation assay in nude mice also supported these conclusions. In details, knockdown of MARCHF1 upregulated the protein expression of REST and downregulated the mRNA level of TFAM. On the contrary, MARCHF1 overexpression exhibited opposite effects. Thus, MARCHF1 is conducive to the progression of breast cancer via promoting the ubiquitylation and degradation of RSET and then the transcription of TFAM. Downregulating MARCHF1 could provide a novel direction for treating breast cancer.
研究领域:
肿瘤学
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分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
Experimental and Therapeutic Medicine
·
2020
·Vol. 19
·期 3
·2326-2334
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IF 1.785
Zi‑Wen Chen,Chao‑Bao Peng,Zhong Pei,Meng‑Ruo Zhang,Tian‑Chan Yun,Zhi‑Min Yang,Fu‑Ping Xu
Insomnia is a common sleep disorder with a high prevalence and substantial adverse consequences. There is growing interest in identifying novel therapeutics from herbal medicine. Tenuifolin is a major constituent of the well‑known anti‑insomnia herb Radix Polygala. The present study investigated the neural activity in response to tenuifolin during rest/wake behaviour in zebrafish and identified the potential biological signalling pathways involved. An automatic video tracking system was used to monitor the behavioural response of zebrafish larvae for 24 h after treatment with tenuifolin. In total, six rest/wake parameters were measured and visualized with a behavioural fingerprint. Time series analysis was conducted by averaging the total rest and waking activity in 10 min intervals. A correlation analysis was performed between tenuifolin and well‑known compounds to analyse the underlying biological signalling pathways. Reverse transcription‑quantitative PCR was also performed to detect the effects of tenuifolin on the transcription of interesting genes associated with the signalling pathways that were potentially involved. The present results suggested tenuifolin significantly increased the total rest time during the dark phase, with a slight effect on the waking activity in zebrafish larvae. This behavioural phenotype induced by tenuifolin is similar to that of selective serotonin reuptake inhibitors and gamma‑aminobutyric acid (GABA) agonists. Furthermore, the expression levels of GABA transporter 1 were significantly increased after tenuifolin treatment. No significant difference was determined in other associated genes in untreated control and tenuifolin‑treated larvae. The present results suggested that tenuifolin caused sleep‑promoting activity in zebrafish and that these effects may be mediated by the serotoninergic systems and the GABAergic systems.
研究领域:
神经科学
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药理学
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中药学
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分子生物学
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DOI
PubMed
高影响因子
ACS Applied Materials & Interfaces
·
2024
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IF 8.3
He Zhao,Ling Zhang,Tianbo Deng,Chunzhong Li
Wearable sweat sensors have received considerable attention due to their great potential for noninvasive continuous monitoring of an individual’s health status applications. However, the low secretion rate and fast evaporation of sweat pose challenges in collecting sweat from sedentary individuals for noninvasive analysis of body physiology. Here, we demonstrate wearable textiles for continuous monitoring of sweat at rest using the combination of a heating element and a microfluidic channel to increase localized skin sweat secretion rates and combat sweat evaporation, enabling accurate and stable monitoring of trace amounts of sweat. The Janus sensing yarns with a glucose sensing sensitivity of 36.57 mA cm–2 mM–1 are embroidered into the superhydrophobic heated textile to collect sweat directionally, resulting in improved sweat collection efficiency of up to 96 and 75% retention. The device also maintains a highly durable sensing performance, even in dynamic deformation, recycling, and washing. The microfluidic sensing textile can be further designed into a wireless sensing system that enables sedentary-compatible sweat analysis for the continuous, real-time monitoring of body glucose levels at rest.
研究领域:
生物医学工程
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可穿戴设备
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健康监测
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DOI
PubMed
高影响因子
BIOSENSORS & BIOELECTRONICS
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2026
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IF 11.8
Jiaqi Liu,Jing Wang,Litong Chen,Yongxiang Ji,Benxing Su,Geng Zhong,Renfeng Dong,Tailin Xu
Androgens, comparable in importance to estrogens, are essential for female reproductive and physiological health. Polycystic ovary syndrome (PCOS), often caused by elevated testosterone (the primary androgen in females) is characterized by reproductive dysfunction, infertility, and metabolic abnormalities. However, current testosterone assays remain invasive, technically complex, and insufficiently sensitive, limiting their utility for early and noninvasive PCOS screening. This study developed a wearable molecularly imprinted (MIP) electrochemical sensor for highly sensitive in situ sweat testosterone monitoring, offering a new strategy for non-invasive PCOS screening. The sensor combines laser-induced graphene electrodes with graphene oxide/Prussian blue amplification and o-phenylenediamine imprinting, showing a linear response (R 2 = 0.9916) from 1 to 25 ng/ml with a detection limit of 0.75 ng/ml. The MIP sensor exhibited acceptable selectivity against structural analogs and major high-concentration interferents present in sweat. Sweat testosterone levels measured by the MIP sensor in an adult female presenting a part of PCOS symptoms demonstrated strong correlation with those measured by enzyme-linked immunosorbent assay (ELISA) (r = 0.8892). The integrated microfluidic platform, incorporating thermal stimulation and wireless transmission, establishes a streamlined “stimulate-collect-detect-transmit” workflow. This technology holds promise for future home-based endocrine screening, with the potential to integrate with luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which could significantly enhance the precision of PCOS diagnoses.
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PubMed
高影响因子
NEUROCHEMICAL RESEARCH
·
2021
·Vol. 47
·期 3
·713-722
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IF 3.996
Zhang Haiju,Yu Shiqian,Xia Liping,Peng Xia,Wang Shun,Yao Baozhen
Epilepsy (SE) is a common and serious neurological disease. NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome participates in the pathogenesis of SE, while its underlying mechanism is still unclear. Here, we attempted to explore the mechanism of action of NLRP3 inflammasome in SE. SE mouse model was constructed by administration of kainic acid (KA). Astrocytes were treated with KA to mimic SE cell model. MCC950 (NLRP3 inhibitor) and Z-YVAD-FMK (Caspase-1 inhibitor) were used to treat astrocytes to inhibit the activity of NLRP3 and Caspase-1. Nissl staining was performed to examine the morphology of neuron. Western blot, enzyme-linked immunosorbent assay and immunofluorescence staining were performed to assess protein expression. SE mouse model exhibited an increase of neuronal loss, and an up-regulation of Cleaved-Caspase-1, IL-1β and IL-18 in hippocampus. The levels of GFAP + ADK + cells were significantly increased in SE mice. MCC950 or Z-YVAD-FMK abolished these impacts conferred by KA in SE mice. Moreover, KA treatment enhanced the expression of NLRP3, Cleaved-Caspase-1, IL-1β and IL-18 in astrocytes, which was rescued by knockdown of NLRP3 or Caspase-1. Additionally, CREB, p-CREB, REST were up-regulated, and SP1 was down-regulated in the KA-treated SE mice and KA-treated astrocytes. Inhibition of NLRP3 or Caspase-1 rescued these proteins expression in KA-treated astrocytes. CREB or REST silencing reduced adenosine kinase (ADK) expression, while SP1 knockdown enhanced ADK expression in KA-treated astrocytes. In conclusion, NLRP3 inflammasome activation enhances ADK expression to accelerate SE in mice through regulating CREB/REST/SP1 signaling pathway. Thus, inhibition of NLRP3 inflammasome may be a treatment for SE.
研究领域:
神经科学
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免疫学
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药理学
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细胞生物学
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DOI
PubMed
高影响因子
Journal of Neuroinflammation
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2024
·Vol. 21
·期 1
·1-25
·
IF 9.3
Cheng Shimei,Lu Qiying,Liu Qiuli,Ma Yuanchen,Chen Jinshuo,Lu Di,Huang Mudan,Huang Yinong,Zhao Erming,Luo Jing,Zheng Haiqing
Background Neuronal death is the primary cause of poor outcomes in cerebral ischemia. The inflammatory infiltration in the early phase of ischemic stroke plays a vital role in triggering neuronal death. Either transplantation of mesenchymal stem cells (MSCs) derived from humans or repetitive transcranial magnetic stimulation (rTMS) have respectively proved to be neuroprotective and anti-inflammatory in cerebral ischemia. However, either treatment above has its limitations. Whether these two therapies have synergistic effects on improving neurological function and the underlying mechanisms remains unclear. This investigation aims to elucidate the synergistic effects and underlying mechanisms of MSCs combined with rTMS treatment on the neurological function recovery post-ischemia.Methods A Sprague-Dawley rat model of cerebral infarction was induced via transient middle cerebral artery occlusion (tMCAO). The rats were divided into five groups (n = 50): sham, tMCAO, rTMS, MSCs, and MSCs + rTMS groups. Transplantation of human umbilical cord MSCs and rTMS intervention were performed 24 h post-stroke. Neurological function was further assessed via several behavioral tests and the 2,3,5-triphenyltetrazolium chloride (TTC) staining companied with Nissl staining were used to assess neuronal survival. TUNEL staining, western blotting, immunofluorescence, immunohistochemistry, ELISA, and flow cytometry were employed to measure the levels of neuroinflammation and PANoptosis. The molecular mechanisms underlying the special role of rTMS in the combined therapy were distinguished with transcriptome sequencing via PC12 cells in oxygen-glucose deprivation/reoxygenation (OGD/R) conditions.Results The combined therapy efficiently reduced lesion volume and improved neuronal survival (P < 0.05), subsequently improving functional recovery after ischemic stroke. MSCs + rTMS treatment ameliorated the PANoptosis in neurons (P < 0.05), accompanied by decreased levels of inflammatory factors in the cerebral tissue and serum during the subacute phase of cerebral infarction. To further explore the roles of either therapy on synergistic effect, we found that the transplanted MSCs primarily localized in the spleen and reduced cerebral inflammatory infiltration after ischemia via suppressed splenic inflammation. Meanwhile, rTMS significantly protects neurons from PANoptosis in MSCs-inhibited inflammatory conditions by downregulating REST unveiled by transcriptome sequencing.Conclusion sOur study elucidates an unidentified mechanism by which the combination of MSCs and rTMS could synergistically promote neuronal survival and suppress neuroinflammation during the subacute phase of cerebral infarction, thus improving neurological outcomes. The downregulating REST induced by rTMS may potentially contribute to the neuroprotective effect against PANoptosis in MSCs-inhibited inflammatory conditions. These results are expected to provide novel insights into the mechanisms of MSCs and rTMS combination therapy in synergistically protecting against cerebral ischemia injury and potential targets underlying neuronal PANoptosis in the early phase of stroke.
研究领域:
神经科学
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干细胞生物学
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神经病学
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免疫学
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分子生物学
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DOI
PubMed
高影响因子
ANALYTICAL CHEMISTRY
·
2026
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IF 7.3
Jizhen Shang,Yan Zhang,Wenyuan Xu,Yangchun He,Guojia Tian,Yuchun Qiao,Xuecheng He,Hua Wang
Noninvasive monitoring of addictive substance biomarkers remains challenging due to the lack of autonomous sampling and portable analytical platforms suitable for resting conditions. Here, we present a fingertip-wearable sweat sensing platform that integrates osmotic sweat extraction with competitive lateral flow assay (LFA) for the simultaneous detection of cotinine and morphine in sweat. The device employs an ethylene glycol-modified poly(vinyl alcohol)–poly(acrylamide) (EG–PVA-PAAm) hydrogel to actively extract sweat from the fingertip and sustain capillary-driven transport toward a multichannel LFA detection zone. Gold nanoparticle-labeled monoclonal antibodies enable visual competitive immunochromatographic detection, where test-line intensity decreases with increasing analyte concentration. The LFA strips exhibit high specificity and wide linear detection ranges, with low limits of detection for cotinine and morphine and negligible cross-interference. Hydrogel-assisted osmotic pumping significantly enhances sweat collection compared to natural perspiration, ensuring sufficient sample delivery under resting conditions. In vitro evaluations in artificial sweat confirm concentration-dependent responses for both analytes, while on-skin studies successfully differentiate exposure levels between active smokers, passive and nonsmokers and allow dynamic monitoring of cotinine metabolism. This integrated wearable LFA system provides a portable and autonomous strategy for point-of-care testing (POCT) of addictive biomarkers in sweat.
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PubMed
高影响因子
JOURNAL OF AFFECTIVE DISORDERS
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2025
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IF 4.9
Huiying Xie,Yan Xue,Rui Deng,Liuxiang Chen,Yiyi Wang,Jia Xu,Hao Liu,Xingxing Li,Wei Cui,Jun-Fang Zhang
Background Stress is a significant trigger of depression, and miR-124 has been implicated in stress-induced depression, while the underlying molecular mechanisms remain unclear. Methods We established mouse depression models using chronic restraint stress (CRS) and chronic unpredictable mild stress (CUMS), and the HT-22 cell models with corticosterone (CORT) and glutamate (Glu). Depression-like behaviors were assessed using the forced swimming test, tail suspension test, and sucrose preference test. Adeno-associated viruses were employed to manipulate miR-124 and ubiquitin-specific protease 14 (USP14) expression. mRNA levels of miR-124 , Usp14 , and Rest were measured by qRT-PCR, the interaction between miR-124 and Usp14 mRNA was assessed by luciferase reporter assays, protein expression and interaction of USP14 and repressor element 1 silencing transcription factor (REST) were detected by western blotting, ubiquitination assay and co-immunoprecipitation. Immunofluorescence visualized altered REST expression in hippocampal neurons. Results CRS and CUMS robustly increased miR-124 levels in the hippocampus, while decreasing the USP14 and REST expression. Similar expression changes were seen in CORT- and Glu-treated HT-22 cells. Mice with miR-124 overexpression but not inhibition in the hippocampus exhibited notable depression-like behavior. Mechanistically, miR-124 directly targeted USP14, reduced USP14 binding to REST, thereby increasing REST ubiquitination and degradation. Inhibition of miR-124 produced antidepressant-like effects and restored the expression and interaction of USP14 and REST in the CRS and CUMS mice. Furthermore, overexpression of USP14 alleviated depression-like behaviors and low REST levels. Conclusion Hippocampal miR-124 mediates depression-like behavior under chronic stress via regulating the USP14/REST signaling pathway, highlighting its potential as a therapeutic target.
研究领域:
神经生物学
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分子精神病学
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信号转导
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表观遗传学
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应激生理学
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神经药理学
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DOI
PubMed
高影响因子
JOURNAL OF CHROMATOGRAPHY A
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2024
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IF 3.8
Chenglong Yu,Yuxuan Li,Xi-Ling Li,Chengqiang Han,Jing Li,Ri Jin,Jun Zhe Min
Monitoring changes in the content of chiral thiol compounds in the human body is crucial for the early diagnosis of oxidative stress-related diseases and the exploration of their pathogenesis. To address this, we synthesized a novel isotope mass spectrometry (MS) probe, denoted as ( R )-(5-(3-isothiocyanato ( 13 C) pyrrolidin-1-yl)-5-oxopentyl) triphenylphosphonium (N 13 CS-OTPP), with triphenylphosphine as its parent structure. In this study, we established a new ultra-high-performance liquid chromatography high-resolution mass spectrometry (UHPLC HRMS) relative quantitative method to monitor chiral thiol compounds in human urine under varying oxidative stress conditions. This method relies on the ratio of 12 C/ 13 C isotope-labeled peak areas. To assess the chiral separation efficiency of N 13 CS-OTPP, we employed three types of thiol compounds (D/L-GSH, D/L-Cys, and D/L-Hcy) and observed separation degrees (Rs) ranging from 1.82 to 1.89. We further validated the accuracy and feasibility of our relative quantitative methods using D/L-Cys-as a model compound. N 12 C/ 13 CS-OTPP-Cys-exhibited excellent linearity (R 2 = 0.9993–0.9994) across different molar ratios (D/L-Cys = 10:1, 4:1, 2:1, 1:1, 1:2, 1:4, 1:10) and achieved a low limit of detection (LOD) of 2.5 fmol. Additionally, we monitored the dynamic changes in urine D/L-Cys-and D/L-Hcy ratios in 12 healthy volunteers (six males and six females) under various oxidative stress states. We generated fitting curves and investigated the trends in chiral thiol compounds in vivo . This study introduces a novel method for the relative quantitative monitoring of chiral thiol compounds in different oxidative stress states within the human body. It also presents a new strategy for understanding the pathogenesis of related diseases resulting from the abnormal metabolism of thiol compounds.
研究领域:
分析化学
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生物医学
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代谢组学
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DOI
PubMed
高影响因子
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