Biomedical subjects

Jialiang Li

Publications and source records attributed to Jialiang Li.

3 recordsLinked to original sources

PubMed2026

DOT1L-mediated H3K79me3 of ITCH promotes AURKA ubiquitination to suppress ECM degradation in osteoarthritis.

As a prevalent chronic joint disorder, osteoarthritis (OA) is characterized by degenerative changes, primarily driven by the pathological degradation of the chondrocyte extracellular matrix (ECM). Current therapies lack efficacy in halting ECM degradation, making elucidation of its regulatory mechanisms crucial for developing novel OA treatments. This study investigated the role of the DOT1L/ITCH/AURKA axis in ECM degradation during OA development. An in vitro OA model was established by treating rat chondrocytes with 10 ng/mL IL-1β for 24 h. TNF-α and IL-6 secretion was measured by ELISA. ECM content was assessed via alcian blue staining. RT-qPCR, western blot, and immunofluorescence staining analyzed associated molecule expression. Co-IP verified ITCH-AURKA interaction and AURKA ubiquitination. ChIP detected DOT1L and H3K79me3 enrichment at the ITCH promoter. An anterior cruciate ligament transection (ACL-T)-induced OA rat model with intra-articular injection of DOT1L-overexpressing lentivirus was further established, followed by HE staining, safranin O-fast green staining, and IHC analysis. IL-1β stimulation upregulated AURKA but downregulated DOT1L and ITCH expression in rat chondrocytes. ITCH promoted AURKA ubiquitination and degradation, thereby attenuating IL-1β-stimulated degradation of ECM in rat chondrocytes. DOT1L upregulated ITCH expression by mediating H3K79me3 modification at its promoter. DOT1L-dependent H3K79me3 enrichment at the ITCH promoter downregulated AURKA, ultimately inhibiting IL-1β-induced ECM degradation in rat chondrocytes. In vivo, DOT1L overexpression alleviated ACL-T-induced cartilage degeneration and reversed the ACL-T-induced downregulation of ITCH and upregulation of AURKA and ADAMTS5. Collectively, our findings identify the DOT1L/ITCH/AURKA axis as a key epigenetic and post-translational regulatory mechanism that protects against ECM degradation in OA.

Animals↗

PubMed2026

Beyond species trees: pervasive gene flow limits phylogenomic resolution in the diversification of Juniperus from the Qinghai-Tibet Plateau.

Understanding how lineages diversify despite persistent ancestral polymorphism and recurrent gene flow remains a central challenge in evolutionary biology. Juniperus distributed across the Qinghai-Tibet Plateau provide an ideal system for addressing this question because repeated geological uplift and climatic oscillations have likely promoted cycles of lineage divergence, range shifts, and secondary contact. Here, we combined approximately 1.08 million genome-wide SNPs from 164 individuals representing thirteen Juniperus lineages with phylogenomic datasets comprising 3,381 nuclear single-copy genes and nearly complete plastomes. We detected extensive phylogenomic discordance and cytonuclear incongruence across genomic datasets. Topology weighting, coalescent simulations, quartet-based tests, and analyses of gene flow and reticulation collectively support the interpretation that these patterns were shaped by the combined effects of prolonged incomplete lineage sorting and gene flow during lineage diversification. Ecological niche analyses further provide a spatial and climatic context in which environmentally similar lineages may have had greater opportunities for secondary contact during historical range shifts. Collectively, our results reveal that the evolutionary history of Qinghai-Tibet Plateau Juniperus is characterized by reticulate diversification rather than strictly bifurcating evolution, and demonstrate how genome-wide discordance can provide biological insights into the evolutionary processes underlying lineage diversification.

Gene Flow↗

PubMed2025

Immune Cell Type-Specific DNA Methylation Regions Associate With 24-Hour Blood Pressure Regulation in Black People.

BACKGROUND: DNA methylation and immune cells have been linked to blood pressure (BP) regulation and the development of hypertension. However, the immune cell profiles and the cell type-specific DNA methylation associated with BPs remain unclear. METHODS: This study evaluates the 19 cell type deconvolution algorithms using reduced representation bisulfite sequencing data, comparing them to in silico mixtures derived from whole-genome bisulfite sequencing. The top-performing algorithm, Epigenetic Dissection of Intra-Sample Heterogeneity (EpiDISH)-Robust Partial Correlations, was applied to 281 Black inpatients with 24-hour BP monitoring. The immune cell profiles and cell type-specific DNA methylation regions associated with these BP phenotypes were further investigated using regression analysis. RESULTS: In patients with hypertension, B-cell and CD4 effector memory T-cell abundances were significantly elevated. Monocyte and CD8 effector memory T-cell fractions positively correlated with nighttime BP, and CD3 T cells were inversely associated with office BP. These associations remained robust after covariate adjustments and were partially validated in the Medical Information Mart for Intensive Care-IV cohort. For the first time, we identified several cell type-specific DNA methylation regions as being associated with BP phenotypes and patterns across 13 immune cells, with approximately one third predominantly found in effector CD8 T cells. CONCLUSIONS: These findings provide novel insights into the epigenetically regulated immune mechanisms underlying BP regulation and identify potential targets for hypertension management.

Humans↗