Mouse bone marrow fibrosis LC-MS/MS

ABSTRACT: Bone marrow fibrosis (BMF) disrupts normal blood cell production, and excessive activation of the TGF-β signaling pathway is considered a key factor in the progression of the disease. Therefore, regulating TGF-β secretion is crucial for reversing fibrotic conditions. Histone deacetylase inhibitors (HDACis) are one such potential regulator, as they can influence TGF-β expression. In a previous study, we developed a selective HDAC6 inhibitor, J22352, targeting pulmonary fibrosis, but its effects on BMF were not previously examined. This study aimed to evaluate J22352's impact on bone marrow-derived myofibroblasts. We found that J22352 significantly reduced cell viability, triggered apoptosis, and suppressed extracellular matrix (ECM) accumulation. Through liquid chromatography-tandem mass spectrometry (LC-MS/MS), we identified 334 differentially expressed proteins (DEPs) linked to apoptosis, programmed cell death, ECM deposition, and collagen formation. These findings indicate that J22352 effectively mitigates BMF by inducing apoptosis and reducing ECM buildup. This study highlights J22352 as a promising selective HDAC6 inhibitor that could potentially slow BMF progression, offering new possibilities for clinical applications.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Fibroblast, Bone Marrow

SUBMITTER: Chiao-Hsu Ke  

LAB HEAD: Chen-Si Lin

PROVIDER: PXD055276 | Pride | 2025-08-25

REPOSITORIES: Pride