Extracellular Matrix Microstructures Modulate Hepatic Methionine Cycle and Methylations

The field of mechanobiology has grown in the past decade, but limited studies investigate how the extracellular matrix affects the cell metabolome. The methionine cycle involves the catabolism and regeneration of methionine through the donation and recovery of a single methyl group; this methyl group can methylate DNA, RNA, and proteins to alter gene expression and protein-protein interactions. Through studying cells cultured on fibrous (mimicking healthy extracellular matrice (ECM)) and flat (mimicking severely fibrotic ECM) substrates, we observed an increase in methionine cycle enzyme expression in cells on the flat substrate. We also present how the methionine cycle is modulated by the ECM through transmembrane protein integrin β1. By inhibiting integrin activation through the ligand-mimicking peptide RGD, we observed that the methionine cycle was protected from alteration. The results presented provide insight into possible therapeutic targets for fibrotic diseases and knowledge of mechanisms by which the ECM alters cell processes.

Authors

Institutions

Publication Details

Journal
Biomacromolecules
Published
2025-04-29
DOI
https://doi.org/10.1021/acs.biomac.4c01748
Primary Topic
Pancreatic function and diabetes
Type
article
Field-Weighted Citation Impact
0.00

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Extracellular Matrix Microstructures Modulate Hepatic Methionine Cycle and Methylations

Chengpeng Chen, John A. Terrell
Biomacromolecules
Pancreatic function and diabetes
article

Extracellular Matrix Microstructures Modulate Hepatic Methionine Cycle and Methylations

Chengpeng Chen, John A. Terrell
article en

Abstract

The field of mechanobiology has grown in the past decade, but limited studies investigate how the extracellular matrix affects the cell metabolome. The methionine cycle involves the catabolism and regeneration of methionine through the donation and recovery of a single methyl group; this methyl group can methylate DNA, RNA, and proteins to alter gene expression and protein-protein interactions. Through studying cells cultured on fibrous (mimicking healthy extracellular matrice (ECM)) and flat (mimicking severely fibrotic ECM) substrates, we observed an increase in methionine cycle enzyme expression in cells on the flat substrate. We also present how the methionine cycle is modulated by the ECM through transmembrane protein integrin β1. By inhibiting integrin activation through the ligand-mimicking peptide RGD, we observed that the methionine cycle was protected from alteration. The results presented provide insight into possible therapeutic targets for fibrotic diseases and knowledge of mechanisms by which the ECM alters cell processes.

BiomacromoleculesVol. 26(6)
University of Maryland, Baltimore County (US)
National Institute of General Medical Sciences
Zero hunger
Openalex Percentile: Top 84%
Pancreatic function and diabetes
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.

Extracellular Matrix Microstructures Modulate Hepatic Methionine Cycle and Methylations — Chengpeng Chen, John A. Terrell · Biomacromolecules (2025) | TGRS Research Map | TGRS