Regeneration of Panniculus Carnosus Muscle in Fetal Mice Is Characterized by the Presence of Actin Cables

Mammalian skin, including human and mouse skin, does not regenerate completely after injury; it is repaired, leaving a scar. However, it is known that skin wounds up to a certain stage of embryonic development can regenerate. The mechanism behind the transition from regeneration to scar formation is...

Full description

Saved in:
Bibliographic Details
Published inBiomedicines Vol. 11; no. 12; p. 3350
Main Authors Hamada, Mariko, Takaya, Kento, Wang, Qi, Otaki, Marika, Imbe, Yuka, Nakajima, Yukari, Sakai, Shigeki, Okabe, Keisuke, Aramaki-Hattori, Noriko, Kishi, Kazuo
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 01.12.2023
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Mammalian skin, including human and mouse skin, does not regenerate completely after injury; it is repaired, leaving a scar. However, it is known that skin wounds up to a certain stage of embryonic development can regenerate. The mechanism behind the transition from regeneration to scar formation is not fully understood. Panniculus carnosus muscle (PCM) is present beneath the dermal fat layer and is a very important tissue for wound contraction. In rodents, PCM is present throughout the body. In humans, on the other hand, it disappears and becomes a shallow fascia on the trunk. Fetal cutaneous wounds, including PCM made until embryonic day 13 (E13), regenerate completely, but not beyond E14. We visualized the previously uncharacterized development of PCM in the fetus and investigated the temporal and spatial changes in PCM at different developmental stages, ranging from full regeneration to non-regeneration. Furthermore, we report that E13 epidermal closure occurs through actin cables, which are bundles of actomyosin formed at wound margins. The wound healing process of PCM suggests that actin cables may also be associated with PCM. Our findings reveal that PCM regenerates through a similar mechanism.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:2227-9059
2227-9059
DOI:10.3390/biomedicines11123350