Changes in nascent chromatin structure regulate activation of the pro-fibrotic transcriptome and myofibroblast emergence in organ fibrosis.

Authors

• Morgan D Basta
• Svetlana Petruk
• Ross Summer
• Joel Rosenbloom
• Peter J Wermuth
• Edward Macarak
• Alex V Levin
• Alexander Mazo
• Janice L Walker

Publication/Presentation Date

5-19-2023

Abstract

Cell reprogramming to a myofibroblast responsible for the pathological accumulation of extracellular matrix is fundamental to the onset of fibrosis. Here, we explored how condensed chromatin structure marked by H3K72me3 becomes modified to allow for activation of repressed genes to drive emergence of myofibroblasts. In the early stages of myofibroblast precursor cell differentiation, we discovered that H3K27me3 demethylase enzymes UTX/KDM6B creates a delay in the accumulation of H3K27me3 on nascent DNA revealing a period of decondensed chromatin structure

Volume

26

Issue

5

First Page

106570

Last Page

106570

ISSN

2589-0042

Published In/Presented At

Basta, M. D., Petruk, S., Summer, R., Rosenbloom, J., Wermuth, P. J., Macarak, E., Levin, A. V., Mazo, A., & Walker, J. L. (2023). Changes in nascent chromatin structure regulate activation of the pro-fibrotic transcriptome and myofibroblast emergence in organ fibrosis. iScience, 26(5), 106570. https://doi.org/10.1016/j.isci.2023.106570

Disciplines

Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods

PubMedID

37250334

Department(s)

Administration and Leadership

Document Type

Article