Muscle regeneration therapy using dedifferentiated fat cell (DFAT) for anal sphincter dysfunction
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In brief
In brief
This preclinical study demonstrates that dedifferentiated fat cells (DFAT) promote muscle regeneration and functional recovery in a rat model of anal sphincter injury. DFAT-treated animals showed accelerated restoration of anal resting pressure and enhanced formation of mature muscle tissue, suggesting a promising cell-based therapy for fecal incontinence and sphincter dysfunction.
- DFAT-conditioned medium enhances myogenic differentiation markers (MyoD, Myogenin) in C2C12 myoblast cells in vitro.
- Local DFAT administration accelerates anal sphincter pressure recovery in rat models with CTX-induced sphincter injury.
- Histological analysis shows increased mature muscle cells in DFAT-treated rats by days 14-21 post-injury.
- DFAT therapy demonstrates both functional and structural muscle repair potential for anorectal sphincter dysfunction.
- This preclinical study supports DFAT as a novel regenerative cell therapy for sphincter injury treatment.
Written by the GCMD Library team from the article.
Abstract
Purpose
We investigated the effects of mouse-derived DFAT on the myogenic differentiation of a mouse-derived myoblast cell line (C2C12) and examined the therapeutic effects of rat-derived DFAT on anal sphincter injury using a rat model.
Methods
C2C12 cells were cultured using DMEM and DFAT-conditioned medium (DFAT-CM), evaluating MyoD and Myogenin gene expression via RT-PCR. DFAT was locally administered to model rats with anorectal sphincter dysfunction 3 days post-CTX injection. Therapeutic effects were assessed through functional assessment, including anal pressure measurement using solid-state manometry pre/post-CTX, and on days 1, 3, 7, 10, 14, 17, and 21 post-DFAT administration. Histological evaluation involved anal canal excision on days 1, 3, 7, 14, and 21 after CTX administration, followed by hematoxylin–eosin staining.
Results
C2C12 cells cultured with DFAT-CM exhibited increased MyoD and Myogenin gene expression compared to control. Anal pressure measurements revealed early recovery of resting pressure in the DFAT-treated group. Histologically, DFAT-treated rats demonstrated an increase in mature muscle cells within newly formed muscle fibers on days 14 and 21 after CTX administration, indicating enhanced muscle tissue repair.
Conclusion
DFAT demonstrated the potential to enhance histological and functional muscle tissue repair. These findings propose DFAT as a novel therapeutic approach for anorectal sphincter dysfunction treatment.