GEO series

CD5L Promotes Efferocytosis and Resolution of Retinal Ischemic Injury

GSE301077 Mus musculus (mouse) RNA-seq (gene expression) 18 samples Submitted 2026/03/19 Platform GPL13112

At a glance

RNA-seq (gene expression) · mouse · 18 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Mus musculus (mouse)
Samples: 18 samples: 6 conditions, mostly in triplicateGroups are read from the sample names, not from the paper. Check the list below.
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper: CD5L promotes efferocytosis and resolution of retinal ischemic injuryCell death & disease · 2026

Summary (written by the submitters)

Ischemia-induced retinopathy is a defining characteristic of prevalent ocular conditions such as diabetic retinopathy and central retinal artery and vein occlusions. Current therapeutic interventions for ischemic retinopathies have shown limited efficacy, highlighting the need for a better understanding of the underlying mechanisms. Histone deacetylase 3 (HDAC3) is a member of the class I histone deacetylase enzyme family, which participates in regulating gene expression by removing acetyl groups from histone proteins.

Read the full summary ↓

We have recently uncovered the role of myeloid HDAC3 as a potential key inhibitor of efferocytosis following retinal ischemia, the process by which myeloid cells clear dead cells to facilitate tissue repair. Here, we investigated the underlying mechanism by which HDAC3 inhibits efferocytosis through regulating the CD5 antigen-like (CD5L)/cluster of differentiation 36 (CD36) axis, which was identified through RNA-sequencing. We utilized myeloid-specific HDAC3 knockout (KO) mice in our in vivo studies and in vitro macrophage efferocytosis assays. To assess the role of CD5L in retinal injury, we subjected CD5L KO mice to ischemia-reperfusion (IR) and treated wild-type (WT) mice with recombinant CD5L. We evaluated retinal injury outcomes through retinal imaging, neurovascular assessments, and functional tests conducted in vivo. Additionally, we conducted in vitro studies to investigate the underlying mechanisms. RNA sequencing data identified CD5L as a pro-efferocytic molecule that is upregulated in HDAC3 knockout macrophages after exposure to apoptotic cells in vitro. Similarly, CD5L is also upregulated in the retinas of myeloid HDAC3 knockout mice following IR injury, where it colocalized with myeloid cells. HDAC3 suppresses CD5L transcription in an LXR-dependent manner. Experiments conducted with CD5L KO mice and treatment involving recombinant CD5L protein demonstrated a protective role for CD5L against retinal ischemic injury. Additionally, we found that CD36, a receptor for CD5L that facilitates the clearance of apoptotic cells, is upregulated in the retina myeloid cells following IR injury. In vitro experiments indicated that CD5L mediates efferocytosis via CD36.

Published in

CD5L promotes efferocytosis and resolution of retinal ischemic injury

Shahror RA, Zaman B, Chuesiang P et al. · Cell death & disease 2026 · PMID 42009635 · doi:10.1038/s41419-026-08752-8

This dataset

Open GSE301077 in finder → Find more mouse RNA-seq datasets →

Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE301077_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1283228 and SRA study SRP595650. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42009635) ↗

Study design

6 conditions, mostly in triplicate

WT-NO Treatment, ×3 WT-NAC, ×3 WT-AC, ×3 HDAC3 KO-NO Treatment, ×3 HDAC3 KO-NAC, ×3 HDAC3 KO-AC, ×3

Supports a between-group comparison across 18 samples.

How we read this: 6 replicated groups read from 18 sample titles; they account for 18 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

GSM9074743 WT-NO Treatment, bio rep 1 WT-NO Treatment,
GSM9074744 WT-NO Treatment, bio rep 2 WT-NO Treatment,
GSM9074745 WT-NO Treatment, bio rep 3 WT-NO Treatment,
GSM9074746 WT-NAC, bio rep 1 WT-NAC,
GSM9074747 WT-NAC, bio rep 2 WT-NAC,
GSM9074748 WT-NAC, bio rep 3 WT-NAC,
GSM9074749 WT-AC, bio rep 1 WT-AC,
GSM9074750 WT-AC, bio rep 2 WT-AC,
GSM9074751 WT-AC, bio rep 3 WT-AC,
GSM9074752 HDAC3 KO-NO Treatment, bio rep 1 HDAC3 KO-NO Treatment,
GSM9074753 HDAC3 KO-NO Treatment, bio rep 2 HDAC3 KO-NO Treatment,
GSM9074754 HDAC3 KO-NO Treatment, bio rep 3 HDAC3 KO-NO Treatment,
GSM9074755 HDAC3 KO-NAC, bio rep 1 HDAC3 KO-NAC,
GSM9074756 HDAC3 KO-NAC, bio rep 2 HDAC3 KO-NAC,
GSM9074757 HDAC3 KO-NAC, bio rep 3 HDAC3 KO-NAC,
GSM9074758 HDAC3 KO-AC, bio rep 1 HDAC3 KO-AC,
GSM9074759 HDAC3 KO-AC, bio rep 2 HDAC3 KO-AC,
GSM9074760 HDAC3 KO-AC, bio rep 3 HDAC3 KO-AC,

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