# The Contribution of CD26-Negative Fibroblasts to Endometrial Scarring

## TL;DR

This study explores how CD26-negative fibroblasts in the endometrium may prevent scarring during healing.

## Contribution

The study identifies CD26-negative fibroblasts as a potential factor in the endometrium's ability to heal without scarring.

## Key findings

- CD26-negative fibroblasts showed increased wound healing and COL1A1 secretion when treated with IL1α.
- CD26 inhibition reduced IL1α-induced effects, suggesting a regulatory role in scar formation.
- CD26 was not expressed in stromal cells but was abundant in endometrial glands.

## Abstract

The human endometrium is unique in that it has a high potential for regeneration after menstruation without scarring. Although growth factors are thought to be responsible for scar formation, it has recently been shown for foetal skin that CD26-negative fibroblasts are essential. Thus, we investigated whether CD26 might be involved in scar formation. Primary human endometrial stromal cells (HPESCs) were stimulated with interleukin-1 alpha (IL1α) to induce CD26 protein expression, and secretion of the scar-associated proteins collagen 1 alpha 1 (COL1A1) and TGF-β3 was measured using ELISAs. The contribution of CD26 to wound closure was analysed using a wound healing assay. The CD26 inhibitor diprotin A (DPA) was used to attenuate CD26 activity. Immunohistochemistry of human uterine samples showed negligible stromal staining of CD26, but CD26 was abundant in the endometrial glands. Treatment of CD26-negative HPESCs with IL1α induced CD26 protein expression, strongly stimulated wound healing in vitro, and increased secretion of COL1A1, but decreased TGF-β3 secretion. DPA effectively attenuated all IL1α-induced effects. We suggest that the stromal non-expression of the scar-associated protein CD26 might contribute to non-scarring during endometrial wound healing.