Downregulation of Genes for Skeletal Muscle Extracellular Matrix Components by Cisplatin

Biol Pharm Bull. 2024;47(11):1846-1850. doi: 10.1248/bpb.b24-00428.

Abstract

The extracellular matrix (ECM) in skeletal muscle is involved in a variety of physiological functions beyond the mechanical support of muscle tissue, nerves, and blood vessels; however, the role of the ECM in skeletal muscle remains unclear. There is little information regarding changes in the expression of factors comprising the ECM during cisplatin-induced muscle atrophy. In the present study, we examined the changes in gene expressions for skeletal muscle extracellular matrix components in skeletal muscle during cisplatin-induced muscle atrophy. Intraperitoneal administration of cisplatin caused muscle atrophy in mice and during this cisplatin-induced muscle atrophy, the expression of many procollagen genes (Col1a1, Col1a2, Col3a1, Col4a1, Col5a1, and Col5a2), elastin (Eln), fibronectin (Fn1), Laminin (Lama1, Lama2, and Lamb1) decorin (Dcn), heparan sulphate proteoglycans (Hspg2) and integrin (Itgb1) constituting the ECM was suppressed. Additional studies are needed to elucidate the pathological significance and mechanisms of reduced gene expression of ECM components associated with cisplatin-induced muscle atrophy.

Keywords: cisplatin; collagen; extracellular matrix; muscle atrophy; procollagen.

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Cisplatin* / toxicity
  • Down-Regulation* / drug effects
  • Extracellular Matrix Proteins / genetics
  • Extracellular Matrix Proteins / metabolism
  • Extracellular Matrix* / drug effects
  • Extracellular Matrix* / metabolism
  • Fibronectins / genetics
  • Fibronectins / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Muscle, Skeletal* / drug effects
  • Muscle, Skeletal* / metabolism
  • Muscular Atrophy / chemically induced
  • Muscular Atrophy / genetics
  • Muscular Atrophy / metabolism

Substances

  • Cisplatin
  • Extracellular Matrix Proteins
  • Antineoplastic Agents
  • Fibronectins