Postnatal Pdzrn3 deficiency causes acute muscle atrophy without alterations in endplate morphology

• DOI: 10.1016/j.bbrc.2024.149542
• Publication Date: 2024-01-17T01:52:40Z
• Authors: Minako Kawai-Taka...; Yoshihiro Miyagawa; Takeshi Honda; Makoto Inui; Tohru Hosoyama
• Keywords: Muscle Atrophy

PDZ domain-containing RING finger family protein 3 (PDZRN3) is expressed in various tissues, including the skeletal muscle. Although PDZRN3 plays a crucial role terminal differentiation of myoblasts and synaptic growth/maturation myogenesis, this molecule postnatal muscles completely unknown despite its lifelong expression myofibers. In study, we aimed to elucidate function mature myofibers using myofiber-specific conditional knockout mice. After tamoxifen injection, deficiency was confirmed both fast slow Myf6-CreERT2; Pdzrn3flox/flox (Pdzrn3mcKO) Transcriptome analysis Pdzrn3mcKO mice identified differentially genes, muscle atrophy-related genes such as Smox, Amd1/2, Mt1/2, suggesting that involved homeostatic maintenance muscles. caused atrophy, predominantly fast-twitch (type II) myofibers, reduced strength. While did not influence endplate morphology or neuromuscular formation-related muscles, indicating relationship between junctions might be limited during development. Considering Pdzrn3 significantly lower aged than adult mice, speculated PDZRN3-mediated system associated with pathophysiology age-related decline, sarcopenia.