PhD Scientific Days 2026

Molecular Medicine 3.

Decorin-Mediated ECM Remodeling in DSS-Induced Intestinal Inflammation

Előadó neve

Mógor, Fruzsina, MSc

Neptune code

BTO2ZZ

Előadó munkahelye

Semmelweis University Department of Anatomy, Histology and Embryology

Előadó telefonszáma

06303255823

Előadó e-mail címe

mogor.fruzsina@gmail.com

Az előadás címe

Decorin-Mediated ECM Remodeling in DSS-Induced Intestinal Inflammation

Szerző(k) neve és munkahelye

Fruzsina Mógor¹, Dr. Dávid Dóra¹, Brigitta Roskó¹, Emad Ben Dahman¹, Aleksei Krupyshev¹

1: Semmelweis University Department of Anatomy, Histology and Embryology

Bemutatás módja

Szóbeli

Szekció

Molecular Medicine 3.

Language of the presentation

English

Preferred session

Molecular Medicine

Összefoglaló szövege

Introduction
The extracellular matrix (ECM) is an active regulator of intestinal homeostasis. Decorin (DCN), a small leucine-rich proteoglycan (SLRP), organizes collagen fibrils and modulates TGF-β, MMP, and growth factor signaling. Its role in ECM remodeling during intestinal inflammation remains poorly understood.
Aims
To characterize DCN expression and its cellular source in DSS-induced colitis, assess its functional relevance using DCN knockout (KO) mice, and define the stromal ECM remodeling landscape using single-cell RNA sequencing (scRNA-seq).
Methods
Colitis was induced in wild-type (WT) and DCN KO C57BL/6 mice with 3% DSS. DCN expression was quantified by qPCR and validated by RNAscope in situ hybridization and the microscopic pictures were analysed with custom imageJ macro. Cell-type–specific expression was resolved by in silico scRNA-seq analysis. CellChat v2 was applied to infer intercellular signaling.
Results
DCN KO mice showed more severe intestinal inflammation and higher mortality than WT controls. DCN mRNA was markedly elevated in inflamed WT colon; RNAscope confirmed an increased number of DCN-expressing cells due to DSS. scRNA-seq identified mesothelial cells and a colonic crypt fibroblast subpopulation (cCF2) as primary DCN sources. DSS induced upregulation of MMP3, ADAMTS4, TIMP1, and TIMP3. CellChat v2 revealed elevated TGF-β, FN1, and IGF signaling in stroma. Longitudinal scRNA-seq (Data source: Ho et al., 2021) uncovered a paradoxical ECM collapse: fibroblasts upregulated TIMP1/TIMP3 yet downregulated the entire SLRP network (LUM, OGN, ASPN) and key structural components (FN1, Col14a1, FBN1, POSTN, CTGF), indicating scaffold failure despite active protease inhibition.
Conclusion
DCN is upregulated during intestinal inflammation and produced by a defined stromal subpopulation. DCN KO mice exhibit catastrophic ECM disorganization consistent with SLRP network collapse in scRNA-seq data. These findings identify DCN and the SLRP family as essential gatekeepers of ECM integrity during colonic inflammation.
Funding
„SUPPORTED BY THE EKÖP-2025-2.1.1. NEW NATIONAL EXCELLENCE PROGRAM OF THE MINISTRY FOR CULTURE AND INNOVATION FROM THE SOURCE OF THE NATIONAL RESEARCH, DEVELOPMENT AND INNOVATION FUND.”

University

Semmelweis University

Supervisor

Dr. Dávid Dóra

Publication of my abstract

I give consent to the publication of my abstract on the website of the congress.

phd.section.field

in doctoral studies after complex exam (PhD)

Kind

Szabad

Status

elfogadva

Accepted presentation method

szóbeli

Előadás fájl jóváhagyás

nem hagyta jóvá

Előadó

9173

Start

10:00

End

10:10