Biology subjects

Nie, D.

Publications and source records attributed to Nie, D..

5 recordsLinked to original sources

bioRxiv2025

Structural and temporal dynamics analysis on PANoptosis in sepsis: a bibliometric analysis

PANoptosis, as a new type of programmed cell death, is characterized by pyroptosis, apoptosis and necroptosis, and is a key mechanism causing a variety of inflammatory diseases. Despite the growing number of studies indicating the crucial role of PANoptosis in sepsis, there has been no bibliometric analysis of the research hotspots and trends in this field. Therefore, this study aims to explore the history, research hotspots and emerging trends of PANoptosis in sepsis related research in the past 20 years from the perspective of structure and temporal dynamics. The articles related to PANoptosis in sepsis were retrieved from the Web of Science Core Collection (WoSCC) database from 2000 to 2024. CiteSpace and HistCite were used to analyse the historical features, the evolution of active topics, and emerging trends about PANoptosis in sepsis. 6165 original articles and reviews on PANoptosis in sepsis were included in the bibliometric analysis. In the last 20 years, the number of published documents is increasing year by year and reaches a peak in 2022. At the same time, many activation themes have emerged at different times, as evidenced by a total of 96 categories, 865 keywords and 629 reference bursts. Keyword clustering anchored eight emerging research subfields, namely 0# oxidative stress, 1#pyroptosis, 2#sepsis-associated encephalopathy, 3#acute kidney injury, 4#immunosuppression, 5#necroptosis, 7#lung injury and 8#extracellular vesicles. The keyword alluvial map shows that the most persistent research concepts in this field are phosphatase. And the emerging keywords are toll_like_receptors, regulatory T cells, recognition, etc. In a timeline visualization based on the time span of the citations, we find five relevant emerging topics, namely 1# immunosuppression, 2# sepsis-induced cardiomyopathy, 3# pyroptosis, 4# acute kidney injury, and 13# COVID-19. Our study provides a comprehensive bibliometric analysis and summary about the current status and trends on PANoptosis in sepsis, which will aid researchers in conducting further scientific research in this field.

bioinformatics↗

bioRxiv2025

Mutations in ASH1L cause a neurodevelopmental disorder with sex differences in epilepsy and autism

To understand brain phenotypes associated with ASH1L, we performed both studies in mouse models and clinical phenotyping of human subjects. We found in mice that ASH1L mutations result in seizures, microcephaly, and also less complex dendritic morphology. When we analyzed human subjects based for epilepsy, intellectual disability, and ASD, we found sex differences in epilepsy and autism, with epilepsy predominantly in female and ASD in male subjects. To understand the cellular and molecular mechanisms of the sex-difference, we performed whole cell patch clamp electrophysiology in mice and found hyperexcitability in female compared with male hippocampal CA1 neurons. We report the identification of sex-specific transcriptomic signatures resulting from ASH1L haploinsufficiency. Differentially expressed genes in female mice showed distinct association with epileptic encephalopathy, postnatal microcephaly and autistic behaviors. Thus, the role of ASH1L in specific circuits may be sex-dependent leading to sexual dimorphic effects from disruption of this gene.

neuroscience↗

bioRxiv2024

A peptide targeting outer membrane protein A of Acinetobacter baumannii exhibits antibacterial activity by reducing bacterial pathogenicity

The World Health Organization has classified multidrug-resistant (MDR) Acinetobacter baumannii as a significant threat to human health, necessitating the urgent discovery of new antibacterial drugs to combat bacterial resistance. Outer membrane protein A of A. baumannii (AbOmpA) is an outer membrane-anchored {beta}-barrel-shaped pore protein that plays a critical role in bacterial adhesion, invasion, and biofilm formation. Therefore, AbOmpA is considered a key virulence factor of A. baumannii. Herein, we screened three phage display peptide libraries targeting AbOmpA and identified several peptides. Among them, P92 (amino acid sequence: QMGFMTSPKHSV) exhibited the highest binding affinity with AbOmpA, with a KD value of 7.84 nM. In vitro studies demonstrated that while P92 did not directly inhibit bacterial growth, it significantly reduced the invasion and adhesion capabilities of multiple clinical isolates of MDR A. baumannii and concentration-dependently inhibited biofilm formation by acting on OmpA. Furthermore, the polymerase chain reaction results confirmed a significant positive correlation between the antibacterial effect of P92 and OmpA expression levels. Encouragingly, P92 also displayed remarkable therapeutic efficacy against A. baumannii infection in various models, including an in vitro cell infection model, a mouse skin infection model, and a mouse sepsis model. These results highlight P92 as a novel and highly effective antimicrobial molecule specifically targeting the virulence factor AbOmpA. IMPORTANCEDifferent from the action mechanism of traditional antibiotics, antibacterial strategies aimed at targeting bacterial virulence factors can effectively reduce bacterial pathogenicity without compromising bacterial growth and reproduction, making it a crucial research direction in combating bacterial drug resistance. Despite the influence of various factors on the expression of bacterial virulence factors, specific and consistently expressed virulence factors in certain bacteria can still serve as viable targets for drug development. In this study, we focused on outer membrane protein A, a key virulence factor of A. baumannii, and successfully identified a highly specific antimicrobial peptide P92 through screening processes. Furthermore, our findings demonstrate its efficacy in various dynamic models for anti-infective therapy. These results validate that antibacterial agents targeting bacterial virulence factors possess relatively or absolutely narrow spectrum antimicrobial properties, enabling precise antibacterial action without inducing bacterial resistance.

microbiology↗

bioRxiv2020

Moderate and intensive mechanical loading differentially modulate the phenotype of tendon stem/progenitor cells in vivo

To examine the differential mechanobiological responses of specific resident tendon cells, we developed an in vivo model of whole-body irradiation followed by injection of either tendon stem/progenitor cells (TSCs) expressing green fluorescent protein (GFP-TSCs) or mature tenocytes expressing GFP (GFP-TNCs) into the patellar tendons of wild type C57 mice. Injected mice were subjected to moderate treadmill running (MTR) and intensive treadmill running (ITR). In MTR mice, both GFP-TSC and GFP-TNC injected tendons maintained normal cell morphology with elevated expression of tendon related markers collagen I and tenomodulin. In ITR mice injected with GFP-TNCs, cells also maintained an elongated shape similar to the shape found in normal/untreated control mice, as well as elevated expression of tendon related markers. However, ITR mice injected with GFP-TSCs showed typical tendinopathic changes, such as cell morphology transitioning to a round shape, elevated chondrogenic differentiation, and increased gene expression of non-tenocyte related genes LPL, Runx-2, and SOX-9. Increased gene expression data was supported by immunostaining showing elevated expression of SOX-9, Runx-2, and PPAR{gamma}. This study provides evidence that while MTR maintains tendon homeostasis by promoting the differentiation of TSCs into tenocytes, ITR may cause the development of tendinopathy by inducing non-tenocyte differentiation of TSCs, thus leading to the presence of non-tendinous tissues in tendon.

cell biology↗

bioRxiv2019

HMGB1 mediates the development of tendinopathy due to mechanical overloading

Mechanical overloading is a major cause of tendinopathy, but the underlying pathogenesis of tendinopathy is unclear. Here we report that high mobility group box1 (HMGB1) is released to the tendon extracellular matrix and initiates an inflammatory cascade in response to mechanical overloading in a mouse model. Moreover, administration of glycyrrhizin (GL), a naturally occurring triterpene and a specific inhibitor of HMGB1, the tendons inflammatory reactions. Also, while prolonged mechanical overloading in the form of long-term intensive treadmill running induces Achilles tendinopathy in mice, administration of GL completely blocks the tendinopathy development. Additionally, mechanical overloading of tendon cells in vitro induces HMGB1 release to the extracellular milieu, thereby eliciting inflammatory and catabolic responses as marked by increased production of prostaglandin E2 (PGE2) and matrix metalloproteinase-3 (MMP-3) in tendon cells. Application of GL abolishes the cellular inflammatory/catabolic responses. Collectively, these findings point to HMGB1 as a key molecule that is responsible for the induction of tendinopathy due to mechanical overloading placed on the tendon.

cell biology↗