Biology subjects

Sheng, B.

Publications and source records attributed to Sheng, B..

5 recordsLinked to original sources

bioRxiv2026

Identification and experimental verification of key genes related to the Ras signaling pathway and the Hippo signaling pathway in osteoarthritis based on transcriptome data

BackgroundOsteoarthritis (OA) is a chronic degenerative joint disease characterized by the progressive deterioration of articular cartilage, significantly impacting the quality of life in middle-aged and elderly populations. The Ras and Hippo signaling pathways play critical roles in regulating cell proliferation, differentiation, and stress responses; however, their interactive mechanisms in OA remain unclear. This study aimed to identify key genes associated with these two pathways using bioinformatic approaches and to elucidate their potential mechanisms in OA. MethodsTranscriptomic data of OA along with Ras signaling pathway-related genes (RSPRGs) and Hippo signaling pathway-related genes (HSPRGs) were obtained from public databases. Differentially expressed genes (DEGs) were identified, and key genes were screened through machine learning, expression validation, and receiver operating characteristic (ROC) curve analysis. Functional insights were further explored via gene set enrichment analysis (GSEA), subcellular localization, immune infiltration analysis, regulatory network construction, and drug prediction. Finally, the expression of key genes was validated in clinical samples. ResultsKIT and CSF1R were identified as key genes. GSEA indicated their involvement in pathways such as the lysosome pathway. Subcellular localization predicted that KIT and CSF1R are distributed in the nucleus, extracellular region, and plasma membrane. Immune infiltration analysis revealed that KIT showed a positive correlation with eosinophils and a negative correlation with immature dendritic cells, while CSF1R was positively correlated with macrophages and negatively correlated with CD56 natural killer cells. Drug prediction suggested interactions between the key genes and several therapeutic agents, including avapritinib and IMC-CS4. Subsequently, we validated our findings in cartilage tissue samples and discovered that compared to the control group, both CSF1R mRNA and protein expression was significantly upregulated in OA tissue, while KIT expression was significantly downregulated.The same results were also validated in immunofluorescence staining of chondrocytes. ConclusionThis study identified KIT and CSF1R as key genes in OA, providing new theoretical insights and potential targets for mechanistic research and targeted therapy.

cell biology↗

bioRxiv2024

Have AI-Generated Texts from LLM Infiltrated the Realm of Scientific Writing? A Large-Scale Analysis of Preprint Platforms

Since the release of ChatGPT in 2022, AI-generated texts have inevitably permeated various types of writing, sparking debates about the quality and quantity of content produced by such large language models (LLM). This study investigates a critical question: Have AI-generated texts from LLM infiltrated the realm of scientific writing, and if so, to what extent and in what setting? By analyzing a dataset comprised of preprint manuscripts uploaded to arXiv, bioRxiv, and medRxiv over the past two years, we confirmed and quantified the widespread influence of AI-generated texts in scientific publications using the latest LLM-text detection technique, the Binoculars LLM-detector. Further analyses with this tool reveal that: (1) the AI influence correlates with the trend of ChatGPT web searches; (2) it is widespread across many scientific domains but exhibits distinct impacts within them (highest: computer science, engineering sciences); (3) the influence varies with authors who have different language speaking backgrounds and geographic regions according to the location of their affiliations (Italy, China, etc.); (4) AI-generated texts are used in various content types in manuscripts (most significant: hypothesis formulation, conclusion summarization); (5) AI usage has a positive influence on papers impact, measured by its citation numbers. Based on these findings, suggestions about the advantages and regulation of AI-augmented scientific writing are discussed.

scientific communication and education↗

bioRxiv2021

The genetic architecture of phenotypic diversity in the betta fish (Betta splendens)

The Betta fish displays a remarkable variety of phenotypes selected during domestication. However, the genetic basis underlying these traits remain largely unexplored. Here, we report a high-quality genome assembly and re-sequencing of 727 individuals representing diverse morphologies of the betta fish. We show that current breeds have a complex domestication history with extensive introgression with wild species. Using GWAS, we identify the genetic basis of multiple traits, including several coloration phenotypes, sex-determination which we map to DMRT1, and the long-fin phenotype which maps to KCNJ15. We identify a polygenic signal related to aggression with many similarities to human psychiatric traits, involving genes such as CACNB2 and DISC1. Our study provides a resource for developing the Betta fish as a genetic model for morphology and behavior in vertebrates.

genetics↗

bioRxiv2018

Regulatory T-cells are required for neonatal heart regeneration

Previous work has elegantly demonstrated that, unlike adult mammalian heart, the neonatal heart is able to regenerate after injury from postnatal day (P) 1 to 7. Recently, macrophages are found to be required in the repair process as depletion of which abolishes endogenous regenerative capability of the neonatal heart. Nevertheless, whether innate immunity alone is sufficient for neonatal heart regeneration is obscure. Here, we investigate a hitherto novel role of FOXP3+ regulatory T-cells (Treg) in neonatal heart regeneration. Unlike their wild type counterparts, NOD/SCID mice that are deficient for T-cells but innate immune cells including macrophages fail to regenerate their injured heart as early as P3. In wild type mice, both conventional CD4+ T-cells and Treg are recruited to cardiac muscle within the first week after injury. Treatment with the lytic anti-CD4 antibody that specifically depletes conventional CD4+ T-cells leads to reduced cardiac fibrosis; while treatment with the lytic anti-CD25 antibody that specifically depletes CD4+CD25hiFOXP3+ Treg contributes to increased fibrosis of the neonatal heart after injury. Moreover, adoptive transfer of Treg to NOD/SCID mice results in mitigated fibrosis and increased proliferation and function of cardiac muscle of the neonatal heart after injury. Mechanistically, single cell transcriptomic profiling reveals that Treg are a source of chemokines and cytokines that attract monocytes and macrophages previously known to drive neonatal heart regeneration. Furthermore, Treg directly promote proliferation of both mouse and human cardiomyocytes in a paracrine manner. Our findings uncover an unappreciated mechanism in neonatal heart regeneration; and offer new avenues for developing novel therapeutics targeting Treg-mediated heart regeneration.

developmental biology↗

bioRxiv2017

Protective effect of estrogen against intervertebral disc degeneration is attenuated by miR-221 through targeting estrogen receptor

Intervertebral disc degeneration (IDD) is a multifactorial disease that associates apoptosis, senescence and calcification of cartilage cells, inflammatory response and alterations in the extracellular matrix. Previous documents imply that estrogen and miR-221 may be involved in IDD. This study further investigated their regulatory mechanisms underlying IDD. Normal and degenerated cartilaginous endplates (CEP) tissues were isolated surgically from juvenile patients with idiopathic scoliosis and adult patients with IDD, respectively. PCR and western blot assays showed decreased aggrecan, Col2A1, TGF-{beta} and estrogen receptor (ER) levels in CEP, but increased MMP-3, adamts-5, IL-1{beta}, TNF-, IL-6 and miR-221 levels. CEP cells were harvested from degenerated CEP tissues and treated with doses of 17{beta}-E2. 17{beta}-E2 increased expression of aggrecan and Col2A1 levels in endplate chondrocytes and secretion of TGF-{beta}, but decreased IL-6 secretion. Moreover, 17{beta}-E2 inhibited the apoptosis and cell-cycle arrest in G0/G1, improving the cell viability. These data indicated estrogen confers protective effect against IDD. However, we found that ER was a target of miR-221 via luciferase assay. miR-221 up-regulation via the mimics or ER knockdown attenuated these protective effects conferred by estrogen, while intervention of miR-221 via the inhibitors promoted the protective effects. This study provided novel evidence that estrogen confers protective effects of CEP against IDD, however, up-regulated miR-221 in degenerated CEP decreased the protective effects via targeting ER, thus it may be an important cause for IDD.

cell biology↗