cell rna seq dataset  (Broad Clinical Labs)

Journal: Frontiers in Immunology

Article Title: Identification of mitochondria-related biomarkers in liver fibrosis via interpretable machine learning and WGCNA: transcriptomic analysis and In Vivo validation

doi: 10.3389/fimmu.2026.1705706

Figure Lengend Snippet: Single-cell transcriptomic analysis of liver fibrosis. (A) Quality control metrics before cell filtering, including the distribution of gene counts (nFeature_RNA), UMI counts (nCount_RNA), and the percentages of mitochondrial and hemoglobin genes across samples. (B) Cell clustering of liver fibrosis samples. (C) Cell-type annotation of single-cell RNA-seq data. (D) Cell cycle analysis of single-cell transcriptomic data. (E) Proportional changes of different cell types between normal and fibrotic groups. (F) Expression distribution of Acot9, Aldh1b1, and Pck2 across different cell types.

Article Snippet: Single-cell RNA sequencing (scRNA-seq) datasets were obtained from GSE145086 and GSE233084 , both generated using the 10X Genomics platform ( , ).

Techniques: Single Cell, Control, RNA Sequencing, Cell Cycle Assay, Expressing

Journal: Nature Communications

Article Title: MerTK-triggered TGFβ1 autocrine signal regulates microglial response to neurodegeneration

doi: 10.1038/s41467-026-69189-3

Figure Lengend Snippet: A – J 8-week-old Cx3cr1 CreER/+ ; Mertk fl/fl and control Cx3cr1 CreER/+ ; Mertk +/+ female mice were subjected to the 4-hydroxytamoxifen-induced Cre-recombinase activity and then utilized for the model of optic nerve injury. Microglial expression of PU.1 ( A ) or IRF8 ( B ) in the optic nerves at 3 days post-injury was assessed by co-immunostaining with CD11b, and representative images are shown. Arrowheads exemplify the PU.1 + microglia. Note that IRF8 is a transcription factor with nuclear staining, and the green-channel fluorescence signal on the boundary of optic nerves was non-specific staining. C mRNA levels of Mertk in the optic nerves at 3 days post-injury were determined by qPCR. n = 3 mice per condition, mean ± SEM, two-way ANOVA test. Microglia densities ( D ), PU.1 + microglia ( E ), and IRF8 + microglia ( F ) were quantified. n = 5 mice per condition, mean ± SEM, two-way ANOVA test. G – J Microglia were FACS-sorted from the optic nerves and analyzed by RNA-seq. Pooled RNA-seq data from 4 mice per condition are shown. G GO enrichment analysis of microglia from the injured optic nerves of control Cx3cr1 CreER/+ ; Mertk +/+ versus Cx3cr1 CreER/+ ; Mertk fl/fl mice. Expression levels of homeostatic markers ( H ), signature genes for microglial response to neurodegenerative insults ( I ), and proinflammatory cytokines and chemokines ( J ) in microglia of the indicated conditions.

Article Snippet: The single-cell RNA sequencing (scRNA-seq) datasets of the Human Protein Atlas showed MERTK as the highest expressed one among central components of phagocytosis pathways in human brain microglia.

Techniques: Control, Activity Assay, Expressing, Immunostaining, Staining, Fluorescence, RNA Sequencing

Journal: Nature Communications

Article Title: MerTK-triggered TGFβ1 autocrine signal regulates microglial response to neurodegeneration

doi: 10.1038/s41467-026-69189-3

Figure Lengend Snippet: A – C 8-week-old Cx3cr1 CreER/+ ; Tgfbr1 fl/fl and control Cx3cr1 CreER/+ ; Tgfbr1 +/+ female mice were subjected to the 4-hydroxytamoxifen-induced Cre-recombinase activity and then utilized for the model of optic nerve injury. Microglial phospho-SMAD2 (p-SMAD2) in the optic nerves at 3 days post-injury was assessed by co-immunostaining with CD11b. A Representative images are shown. Microglia densities ( B ) and p-SMAD2 + microglia ( C ) were quantified. n = 3 mice per condition, mean ± SEM, two-way ANOVA test. D 8-week-old Cx3cr1 CreER/+ ; Tgfb1 fl/fl , Cx3cr1 CreER/+ ; Tgfbr1 fl/fl , and control Cx3cr1 CreER/+ female mice were subjected to the 4-hydroxytamoxifen-induced Cre-recombinase activity and then utilized for the model of optic nerve injury. Microglia were FACS-sorted from the injured optic nerves and analyzed by RNA-seq. Pooled RNA-seq data from 4 mice per condition are shown for GO enrichment analysis of microglia from the injured optic nerves of control Cx3cr1 CreER/+ versus Cx3cr1 CreER/+ ; Tgfb1 fl/fl mice and control Cx3cr1 CreER/+ versus Cx3cr1 CreER/+ ; Tgfbr1 fl/fl mice. E – G 8-week-old Cx3cr1 CreER/+ ; Irf8 fl/fl , Cx3cr1 CreER/+ ; Tgfb1 fl/fl , Cx3cr1 CreER/+ ; Tgfbr1 fl/fl , and control Cx3cr1 CreER/+ female mice were subjected to the 4-hydroxytamoxifen-induced Cre-recombinase activity and then utilized for the model of optic nerve injury. Microglia were FACS-sorted from the optic nerves and analyzed by RNA-seq. Pooled RNA-seq data from 4 mice per condition are shown. Expression levels of homeostatic markers ( E ), signature genes for microglial response to neurodegenerative insults ( F ), and proinflammatory cytokines and chemokines ( G ) in microglia of the indicated conditions.

Article Snippet: The single-cell RNA sequencing (scRNA-seq) datasets of the Human Protein Atlas showed MERTK as the highest expressed one among central components of phagocytosis pathways in human brain microglia.

Techniques: Control, Activity Assay, Immunostaining, RNA Sequencing, Expressing