About

Wen-Tse Lin is a Clinical Assistant Professor of General Dentistry at the Henry M. Goldman School of Dental Medicine. He earned his DMD, MSD in Oral Biology, and CAGS in Periodontology from the Henry M. Goldman School of Dental Medicine, completing these degrees in 2017, 2012, and 2012 respectively. He also holds a DDS from Kaohsiung Medical University in Taiwan, obtained in 2005. His academic and professional focus is within the field of general dentistry, with an emphasis on preventive and restorative dentistry. As a faculty member, he contributes to the educational mission of the dental school, supporting student training and patient care at the institution's state-of-the-art clinical facilities.

Research topics

• Biology
• Genetics
• Computational biology
• Cell biology
• Computer Science
• Ecology
• Bioinformatics

Selected publications

• Progressive Remodeling of Global Protein Interaction Networks in a Mouse Model of Tauopathy

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-07-06 · 2 citations

  preprintOpen access1st author

  Neurodegenerative disease is marked not just by loss of proteins or cells, but by dynamic rewiring of macromolecular interaction networks that precede and drive pathology. Here, we present the first temporally resolved, systems-scale map of multi-protein complex remodeling in a tauopathy model, integrating co-fractionation mass spectrometry, quantitative phosphoproteomics, and machine learning to decode phosphorylation-dependent shifts in protein interactomes across disease progression. This interactomic atlas identifies functionally validated assemblies-including MAPT-Dpysl2 and Cyfip1-actin complexes-that modulate early disease phenotypes in vivo. By revealing how phosphorylation tunes macromolecular complex architecture and function, this work reframes tauopathy as a disease of dynamic network instability, and establishes a generalizable framework for early detection and mechanistic dissection of neurodegeneration.

  PublisherOA PDFDOI

• Multiomics identify the gene expression signature of the spinal cord during aging process

  Communications Biology · 2025-02-07 · 4 citations

  articleOpen access

  Age-related long-term disability is attracting increasing attention due to the growing ageing population worldwide. However, the current understanding of the senescent spinal cord remains insufficient. Bulk RNA sequencing reveals that 526 genes are upregulated and 300 genes are downregulated in senescent spinal cords. Pathway enrichment analysis of differentially expressed genes shows that senescence in spinal cords is related to phagosome function, neuroinflammation, ferroptosis, and necroptosis. Prediction of upstream transcription factors and interactome analysis identify Spi1 as a transcription factor that potentially plays a core role in senescent spinal cords. Spatial transcriptomics illustrates the spatial distribution of the transcriptomic landscape in both young and senescent spinal cords and identifies distinct neuronal and glial subtypes. The ferroptosis-associated gene Fth1 is upregulated in aged spinal cords. Flow cytometry reveals increased accumulation of free Fe2+ and ROS in senescent mixed glial cells; however, CCK-8 assays reveal that these cells are resistant to ferroptosis. SiRNA and lentivirus experiments indicate that the overexpression of Fth1 in normal mixed glial cells reduces their sensitivity to ferroptosis, whereas Fth1 knockdown increases their sensitivity to ferroptosis. In summary, spatial and bulk transcriptomics elucidate the transcriptional characteristics of young versus senescent spinal cords, thus highlighting the role of Fth1 in mediating ferroptosis resistance in senescent mixed glial cells. Multiomics sheds light on the gene expression signature of the spinal cord during the ageing process-resistance to ferroptosis via the upregulation of Fth1.

  PublisherOA PDFDOI

• Numerical acceleration method for static and dynamic analysis of deepwater laying pipelines

  Ocean Engineering · 2025-07-01

  article
  PublisherDOI

• Numerical Acceleration Method for Static and Dynamic Analysis of Deepwater Laying Pipelines

  SSRN Electronic Journal · 2025-01-01

  preprintOpen access
  PublisherDOI

• Phase-programmed immunoengineering: dual-functional nanofibrous scaffold with spatiotemporal Cu-Mg release for anti-infection to pro-repair transition in wounds

  Materials & Design · 2025-08-05 · 1 citations

  articleOpen access

  Schematic illustration of PLLA@CM for treating infected wounds. (A) Fabrication of PLLA@CM via coaxial electrospinning. (B) Stage-specific functionality of PLLA@CM under ultrasound stimulation. (C) Differential regulatory effects of copper and magnesium ions on macrophages. • Developed an innovative bioactive wound dressing that synergistically combines immunomodulation and antibacterial functions for enhanced infected wound healing. • Systematically characterized the immunoregulatory effects of PLLA@CM in polarizing macrophages and modulating the wound microenvironment. • Uncovered the underlying therapeutic mechanisms of PLLA@CM in promoting infected wound repair at cellular and molecular levels. • Engineered a novel core–shell nanofiber biomaterial with controlled ion release and piezoelectric properties for comprehensive wound management. Infected wounds present formidable clinical challenges, where microbial clearance and tissue regeneration demand spatiotemporally coordinated immune responses. Conventional therapeutic strategies often fail to reconcile antimicrobial efficacy with immunomodulatory precision, exacerbating risks of chronic inflammation or delayed repair. Here, a hierarchical electrospun membrane integrating copper- and magnesium-doped bioactive glass nanoparticles (Cu-BGns/Mg-BGns) within poly (L-lactic acid) (PLLA) is engineered to dynamically regulate macrophage polarization and synergize piezoelectric-driven antibacterial activity. The membrane features a core–shell architecture that sequentially releases Cu 2+ (outer layer) to activate M1 macrophages for pathogen clearance during the infection phase, followed by Mg 2+ (inner layer) to promote M2 polarization for tissue repair. Under ultrasound stimulation, the piezoelectric PLLA matrix generates hydroxyl radicals (•OH), amplifying antibacterial efficacy via reactive oxygen species (ROS)-mediated bacterial membrane disruption. In a murine full-thickness infected wound model, the membrane accelerates healing by 1.6-fold compared to controls, demonstrating enhanced angiogenesis, collagen deposition, and immune coordination. RNA sequencing confirms temporal regulation of inflammatory pathways (TNF/NOD-like receptor), aligning macrophage phenotypes with healing stages. This biphasic immunomodulatory strategy offers a blueprint for advanced wound dressings that dynamically harmonize antimicrobial defense and regenerative processes.

  PublisherDOI

• Distinct age- and pathology-dependent epitranscriptome and translational dysfunction in a tauopathy mouse model

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-20

  preprintOpen access

  Abstract Chronic neurodegenerative diseases, such as tauopathies, cause major metabolic changes in the brain affecting gene expression at both the transcriptional and translational levels. Our understanding of how regulation of translation changes with disease has focused on mRNA and its translational regulatory factors, RNA binding proteins, and microRNAs, despite clear evidence for translational and post-translational dysfunction in ADRD and tauopathies. The neurobiology of tRNA has only recently begun to be studied, but the impact of chronic neurodegenerative diseases on tRNA biology and translational dysfunction is largely unknown. We have previously shown that the tRNA pool and tRNA modifications behave as a system to regulate the cellular stress response by undergoing stress-specific reprogramming and causing selective translation of mRNAs from codon-biased stress response genes. Here we tested this stress-induced tRNA reprogramming and codon-biased translation system in the response to mutant tau expression by performing mass spectrometric quantification of ∼8500 proteins and 49 tRNA modifications, AQRNA-seq analysis of 222 cytosolic and mitochondrial tRNAs and other small RNAs, and informatic analysis of codon usage patterns in >23,000 protein-coding genes. Analysis of these datasets revealed that aging and tauopathy elicit major adaptation of the tRNA transcriptome and epitranscriptome as well as corresponding evidence of a program of translation of families of codon-biased genes for aging and disease responsive proteins. The mitochondrial tRNA transcriptome showed a strong response to aging and disease with 21 of the 22 mt-tRNAs showing age and disease-linked increases in expression, accompanied by mitochondria-specific modifications such as ms2i6A and f5C. Surprisingly, there were few significant changes in the 203 cytosolic tRNA isodecoders. However, a 10-fold increase tRNA isodecoder tRNA-Arg-TCT-5-1 was accompanied by increased translation of proteins encoded by genes highly enriched in its AGA cognate codon. These changes in tRNA biology are mirrored by strongly biased use of synonymous codons among the most highly upregulated and downregulated proteins in the P301S MAPT mice. Taken together these findings suggest the aging and disease brain produces an integrated response for translational control that is highly integrated with changes in tRNA biology.

  PublisherOA PDFDOI

• Piezoelectric and bactericidal effects of GaSe-loaded poly-L-lactic acid fibrous dressings under ultrasound stimulation for improved MRSA-infected wound healing

  Colloids and Surfaces B Biointerfaces · 2025-09-25

  article
  PublisherDOI

• Phosphoproteomic Analysis Reveals Differences in Intercellular Spread Among Feline Herpesvirus Type 1 Mutants

  Veterinary Sciences · 2025-12-11

  articleOpen access1st author

  Feline herpesvirus-1 (FHV-1) is taxonomically classified within the family Herpesviridae, subfamily Alphaherpesvirinae, genus Varicellovirus, and species Felid alphaherpesvirus 1. The genome of FHV-1 is 135,797 bp in length and encodes 74 proteins. Among these proteins, serine/threonine protein kinase (pK) and thymidine kinase (TK) have been identified as potential virulence factors in alphaherpesviruses, although these kinases are dispensable for viral replication. As kinases, regulating phosphorylation modification is one of their functions, while the mechanism by which phosphorylation modification affects cell physiological functions and thereby influences viral replication remains unclear. In this study, we generated pK- and TK-deficient FHV-1 mutants by CRISPR/Cas9-mediated homologous recombination. The pK-deficient virus produced significantly smaller plaques than the TK-deficient virus. The replication kinetics of the pK-deficient virus were attenuated in multistep growth compared to the TK-deficient virus. These results indicate that deletion of the pK gene markedly reduces the replicative capacity of FHV-1. We applied data-independent acquisition (DIA) quantitative proteomics to profile changes in global protein expression and phosphorylation in F81 cells upon infection with TK−, pK−, and wild-type FHV-1 strain. The pK-deficient virus exhibited 3632 differentially phosphorylated proteins containing 11,936 modification sites; the TK-deficient virus showed 4529 differentially phosphorylated proteins with 19,225 phosphorylation sites. Functional characterization through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses identified significant involvement of phosphoproteins in spliceosome pathways in pK-deficient virus and ATP-dependent chromatin remodeling pathway in TK-deficient virus. Notably, several splicing regulators—including Ess-2 and CDK13, which modulate host spliceosomal function—displayed significantly reduced phosphorylation levels in pK-deficient viruses. A significant enrichment of ATP-dependent factors, such as SMARCA5 and RSF1, was observed in the TK-deficient virus. To our knowledge, this is the first investigation into the effects of FHV-1 infection on the host cell phosphoproteome. These data offer new insights into the phosphoregulatory circuits and signaling networks triggered by FHV-1 and may enhance our understanding of the FHV-1 replication mechanism.

  PublisherOA PDFDOI

• Corrigendum: Integrated metabolomics and proteomics reveal biomarkers associated with hemodialysis in end-stage kidney disease

  Frontiers in Pharmacology · 2024-02-09

  erratumOpen access1st author

  [This corrects the article DOI: 10.3389/fphar.2023.1243505.].

  PublisherOA PDFDOI

• Impacts of Nutlin-3a and exercise on murine double minute 2–enriched glioma treatment

  Neural Regeneration Research · 2024-03-01 · 9 citations

  articleOpen access

  JOURNAL/nrgr/04.03/01300535-202504000-00029/figure1/v/2024-07-06T104127Z/r/image-tiff Recent research has demonstrated the impact of physical activity on the prognosis of glioma patients, with evidence suggesting exercise may reduce mortality risks and aid neural regeneration. The role of the small ubiquitin-like modifier (SUMO) protein, especially post-exercise, in cancer progression, is gaining attention, as are the potential anti-cancer effects of SUMOylation. We used machine learning to create the exercise and SUMO-related gene signature (ESLRS). This signature shows how physical activity might help improve the outlook for low-grade glioma and other cancers. We demonstrated the prognostic and immunotherapeutic significance of ESLRS markers, specifically highlighting how murine double minute 2 (MDM2), a component of the ESLRS, can be targeted by nutlin-3. This underscores the intricate relationship between natural compounds such as nutlin-3 and immune regulation. Using comprehensive CRISPR screening, we validated the effects of specific ESLRS genes on low-grade glioma progression. We also revealed insights into the effectiveness of Nutlin-3a as a potent MDM2 inhibitor through molecular docking and dynamic simulation. Nutlin-3a inhibited glioma cell proliferation and activated the p53 pathway. Its efficacy decreased with MDM2 overexpression, and this was reversed by Nutlin-3a or exercise. Experiments using a low-grade glioma mouse model highlighted the effect of physical activity on oxidative stress and molecular pathway regulation. Notably, both physical exercise and Nutlin-3a administration improved physical function in mice bearing tumors derived from MDM2-overexpressing cells. These results suggest the potential for Nutlin-3a, an MDM2 inhibitor, with physical exercise as a therapeutic approach for glioma management. Our research also supports the use of natural products for therapy and sheds light on the interaction of exercise, natural products, and immune regulation in cancer treatment.

  PublisherDOI

Frequent coauthors

• Yisheng Chen

  Huashan Hospital

  32 shared

• Andrew Emili

  Boston University

  32 shared

• Feng Luo

  Sichuan University

  27 shared

• Jiehua Li

  Sichuan University

  26 shared

• Hongbin Liu

  Chinese People's Liberation Army

  25 shared

• Liping Chen

  Wuhan University

  25 shared

• Manhua Liu

  25 shared

• Jun You

  25 shared

Education

• Other

  Henry M. Goldman School of Dental Medicine

  2017

• Other, Oral Biology

  Henry M. Goldman School of Dental Medicine

  2012

• Other, Periodontology

  Henry M. Goldman School of Dental Medicine

  2012

• Other

  Kaohsiung Medical University (Taiwan)

  2005