Myh7 regulates SDRC protein and biofilm formation to alleviate
osteomyelitis induced by Staphylococcus aureus
Abstract
SDRC is implicated in the pathogenesis of Staphylococcus aureus
osteomyelitis. However, the precise mechanism by which SDRC contributes
to the progression of this infection remains unclear. To explore SDRC’s
role in osteomyelitis, experiments were conducted on mouse models
infected with Staphylococcus aureus strains containing either the wild
type SDRC sequence or a knockout (KO-SDRC) sequence. Levels of
inflammatory factors like IL-6 and TNF-α were measured using Elisa.
Furthermore, changes in osteogenic indicators such as ALP, OST, and
Runx2 were detected using qPCR and Western blot analysis. Additionally,
transcriptome sequencing was employed to gain deeper insights into the
potential molecular mechanisms underlying SDRC’s promotion of
Staphylococcus aureus-induced osteomyelitis. The study revealed that the
ability of Staphylococcus aureus to form biofilms was significantly
weakened in strains where the SDRC protein was knocked out. Moreover,
mice infected with the KO-SDRC strain exhibited enhanced ossification
processes. Transcriptome sequencing demonstrated significant
overexpression of the Myh7 gene in the SDRC knockout osteomyelitis
mouse. Subsequent knockout of the Myh7 gene led to notable reductions in
mRNA and protein expressions of osteogenic indicators including Runx2,
ALP, OSX, and Osteocalcin. Overall, these findings suggest that SDRC
plays a crucial role in promoting the malignant progression of
osteomyelitis caused by Staphylococcus aureus. Its main mechanism
involves enhancing the formation of Staphylococcus aureus biofilms.
Conversely, Myh7 may exert an inhibitory effect on the SDRC protein,
reducing biofilm formation and mitigating the severity of osteomyelitis.
These findings offer novel insights into potential therapeutic targets
for the treatment of osteomyelitis.