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Engineered amphiregulin promotes tissue healing via multiple mechanisms following acute injury

ABSTRACT: Amphiregulin (AREG), a growth factor expressed by immune cells, has emerged as an important mediator of tissue healing; however, its therapeutic potential remains elusive. Here, we engineered an optimized AREG (eAREG) that promotes robust skin repair and muscle regeneration in murine models. We found that eAREG improves tissue healing following acute injury via multiple synergistic mechanisms. These pro-regenerative effects were preserved in diabetic mice with elevated inflammation and impaired healing. Together, these findings identify eAREG as a promising regenerative biologic for multiple injury types.

ORGANISM(S): Homo sapiens

PROVIDER: GSE328352 | GEO | 2026/05/28

REPOSITORIES: GEO

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Engineered amphiregulin promotes tissue healing via multiple mechanisms following acute injury

Project description:Engineered amphiregulin promotes tissue healing via multiple mechanisms following acute injury

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Amphiregulin mediates non-cell-autonomous effect of senescence on reprogramming

Project description:Cellular senescence is an irreversible growth arrest with a highly dynamic secretome, termed the senescence-associated secretory phenotype (SASP). Senescence has been implicated in somatic reprogramming to pluripotency. The cell-intrinsic proliferation arrest is a barrier for reprogramming, whereas the SASP facilitates the cell fate conversion in nonsenescent cells. However, the mechanisms by which reprogramming-induced senescence regulates cell plasticity are not well understood. Here, we have further investigated how the heterogeneity of paracrine senescence impacts reprogramming. We show that senescence promotes in vitro reprogramming in a stress-dependent manner. We identified a catalog of SASP factors and pathways potentially involved in the cell fate conversion using an unbiased proteomic analysis. Amphiregulin (AREG), a growth factor frequently secreted by the senescent cells, promotes in vitro reprogramming by accelerating proliferation and MET via the EGFR signaling pathway. Of note, AREG treatment diminished the negative effect of donor age on reprogramming. Finally, AREG enhances in vivo reprogramming in the skeletal muscle. Hence, senescence could facilitate cellular plasticity via various SASP factors to promote reprogramming and tissue repair.

2022-07-28 | PXD028590 | Pride

An amphiregulin reporter mouse enables transcriptional and clonal expansion analysis of reparative lung Treg cells

Project description:Treg cells play critical roles in tissue repair processes, certain of which are mediated by production of the growth factor amphiregulin (Areg). We developed a knock-in mouse model for detection of Areg production in live Treg cells, inserting a Thy1a (Thy1.1) construct into the endogenous Areg locus, such that for every transcript of Areg that is translated, a Thy1.1 transcript is also translated and trafficked separately to the cell surface. We used this mouse model to sort for Thy1.1- or Thy1.1+ (Areg-producing or -non-producing) lung Treg cells in models of lung damage (influenza A virus infection and bleomycin acute lung injury), and used them for assessment of gene expression and clonal expansion of these populations.

2025-05-14 | GSE292440 | GEO

Radiation-induced amphiregulin drives tumor metastases

Project description:In this study, we demonstrate that radiation induces the epidermal growth factor receptor (EGFR) ligand amphiregulin (AREG) in tumor cells, which stimulates distant metastasis proliferation in both patients and pre-clinical murine tumor models. Using single-cell RNAseq (sc-RNAseq), we characterized the effects of AREG-induction on immune cells in the lung metastatic microenvironment of B6 mice.

2025-02-27 | GSE250375 | GEO

An amphiregulin reporter mouse enables transcriptional and clonal expansion analysis of reparative lung Treg cells [scRNA-Seq]

2025-05-14 | GSE277256 | GEO

An amphiregulin reporter mouse enables transcriptional and clonal expansion analysis of reparative lung Treg cells [RNA-Seq]

2025-05-14 | GSE277226 | GEO

Amphiregulin Switches Progenitor Cell Fate for Lineage Commitment During Gastric Mucosal Regeneration

Project description:Background & Aims: Isthmic progenitors, tissue-specific stem cells in the stomach corpus, maintain mucosal homeostasis by balancing between proliferation and differentiation to gastric epithelial lineages. The progenitor cells rapidly adopt an active state in response to mucosal injury. However, it remains unclear how the isthmic progenitor cell niche is controlled during the regeneration of damaged epithelium. Methods: We recapitulated tissue recovery process after acute mucosal injury in the mouse stomach. BrdU incorporation was utilized to trace newly generated cells during the injury and recovery phases. To define epithelial lineage commitment process during recovery, we performed single cell RNA-sequencing on epithelial cells from the mouse stomachs. We validated the effects of amphiregulin (AREG) on the mucosal recovery, utilizing recombinant AREG treatment or AREG deficient mice. Results: We determined that an EGFR ligand, AREG, can control progenitor cell lineage commitment. Based on the identification of lineage-committed subpopulations in the corpus epithelium through single cell RNA-sequencing and BrdU incorporation, we showed that isthmic progenitors give rise to epithelial cell lineages through an ordered paradigm during mucosal regeneration. During recovery, AREG treatment promotes repopulation with parietal cells, while suppressing surface cell commitment of progenitors. In contrast, TGF-alpha did not alter parietal cell regeneration but did induce expansion of surface cell populations. AREG deficiency impairs parietal cell regeneration, but increases surface cell commitment. Conclusions: These data demonstrate that different EGF receptor ligands can distinctly regulate isthmic progenitor-driven mucosal regeneration and lineage commitment.

2026-03-12 | GSE316067 | GEO

The EGF Receptor Ligand Amphiregulin Controls Cell Division via FoxM1

Project description:We analyzed the effect of tetracycline (Tet)-inducible amphiregulin (AREG) silencing on the transcriptome of immortalized human N/TERT keratinocytes in the presence or absence of exogenous rhEGF. Tetracycline-mediated AREG silencing significantly altered the expression of 2,331 genes, 623 of which were not normalized towards normal by treatment with EGF. Genes irreversibly up-regulated by suppression of AREG overlapped with genes involved in keratinocyte differentiation. A significant proportion of the irreversibly down-regulated genes featured upstream binding sites recognized by FoxM1

2016-06-23 | GSE70230 | GEO

Effect of Amphiregulin on global gene expression in injured skeletal muscle in the presence or absence of CD4+Foxp3+ regulatory T cells (Tregs).

Project description:Global gene expression analysis of injured skeletal muscle showed that amphiregulin (Areg), a growth factor over-expressed by muscle Treg cells, enhances muscle regeneration both in the presence and in the absence of Tregs. Foxp3-DTR+ and Foxp3-DTR- mice were injured with cardiotoxin in TA muscle at day 0 and treated with diphtheria toxin every other day from day 0 until dissection. Amphiregulin or PBS were administered im on day 0 and ip every other day until dissection. TA muscle was flash-frozen and RNA was extracted using Trizol. RNA from whole tissue samples was amplified, labeled, and hybridized to Affymetrix Mouse Gene 1.0 ST Arrays.

2013-12-15 | E-GEOD-50097 | biostudies-arrayexpress

Amphiregulin Upregulated in Esophageal Squamous Cell Carcinoma Cells upon Direct Contact with Cancer-Associated Fibroblasts

Project description:Cancer-associated fibroblasts (CAFs) are a pivotal component of the tumor microenvironment, significantly contributing to the progression of esophageal squamous cell carcinoma (ESCC). Direct co-culture of human bone marrow-derived mesenchymal stem cells (MSCs), one of the origins of CAFs, with ESCC cell line, led to increased amphiregulin (AREG) expression and secretion in the ESCC cells. Consequently, the expression and phosphorylation of the AREG receptor EGFR were upregulated in co-cultured ESCC cells. Moreover, AREG treatment enhanced ESCC cell survival and migration through the EGFR-Erk/p38 signaling pathway. Immunohistochemical analysis of AREG using human ESCC tissues showed a positive correlation between the intensity of AREG expression in tumor invasive front and the expression level of the CAF marker FAP. Furthermore, bioinformatics database analysis confirmed a significant upregulation of AREG expression in ESCC tissues compared to normal tissues. These findings suggest that AREG is involved in CAF-mediated ESCC progression and could be a novel therapeutic target for ESCC.

2024-12-04 | GSE274064 | GEO

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