PhD Scientific Days 2026

Poster Session 2.C - Molecular Medicine

Enteric Neural Crest Cells Pave Their Way with Collagen I

Name of the presenter

Soós, Ádám

Institute/workplace of the presenter

Department of Anatomy, Histology and Embryology

Authors

Helga-Hajnalka Botyánszki-Farkas¹, Nándor Nagy¹, Ádám Soós¹
1: Department of Anatomy, Histology and Embryology, Semmelweis University

Text of the abstract

Introduction: The enteric nervous system (ENS) is part of the autonomic nervous system and regulates numerous functions of the gastrointestinal tract. The neural network in the gut is composed of neurons and glial cells. In terms of embryonic origin, the ENS derives from neural crest-derived neural stem cells (NCCs), which originate from the dorsal part of the neural tube and colonize the layers of the gut tube. The migration of NCCs is regulated by the extracellular matrix (ECM) produced in their mesenchymal environment. The ECM may be permissive, supporting cell migration, or inhibitory, preventing NCC migration.
Aims and Methods: During transcriptomic analysis of NCCs migrating in the gut, we found that migrating cells in the hindgut of early embryos produce type I collagen, which is characteristic of connective tissue. According to previous knowledge, this property had been described only in cranial NCCs. The main aims of our experimental work were to: 1) characterize collagen I expression by NCCs in the embryonic and postnatal colon; and 2) determine collagen I-positive expression in vitro and in ex vivo 3D collagen gel organ cultures.
Results: Using immunocytochemical staining of hindgut segments isolated from chicken embryos at stages E7, E8, E10, E12, and E16 (n = 4/stage), we demonstrated that Hsp47, which directs collagen I secretion, is expressed only in undifferentiated NCCs migrating in the hindgut of 7-day-old embryos. NCC colonization of the hindgut is completed on embryonic day 8. In subsequent developmental stages, N-cadherin-positive NCCs no longer express Hsp47; type I collagen remains present only in the mesenchymal cells of the gut. This observation was also confirmed in in vitro and ex vivo gut cultures.
Conclusion: Our experimental data indicate that NCCs colonizing the intestinal tract produce ECM during their migration. Our results raise the possibility that the expression of collagens supporting cell migration is essential for the normal development of the enteric nervous system in the colon. This is supported by our preliminary finding that when collagen I synthesis was inhibited with dimethyloxalyl glycine, NCCs failed to colonize the hindgut, resulting in an aganglionic colon.
Funding: NKFI K-138664