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Updated: Jun 17, 2026

Isolation of Myofibroblasts from Mouse and Human Esophagus
Published on: January 18, 2015
Smooth-to-striated muscle transition in human esophagus: an immunohistochemical study using fetal and adult materials
Yukio Katori1, Baik Hwan Cho, Chang Ho Song
1Department of Otolaryngology & Head and Neck Surgery, Tohoku University Graduate School of Medicine, Sendai, Japan. yukatori@concerto.plala.or.jp
Background:
A craniocaudal transition from smooth to striated muscle occurs in the fetal mouse esophagus muscularis propria, until finally the entire muscle component becomes striated. Although no such investigation has been conducted using human fetuses, the transition appears to be incomplete.
Methods:
In horizontal sections of 10 human fetuses between 9 and 16 weeks of gestation, we identified immunoreactivity for smooth muscle actin (SMA), striated muscle myosin heavy chain (MyH), desmin, PGP9.5, S100 protein, c-kit, and CD68 in the thoracic esophagus. The TUNEL method was used to identify apoptosis. For comparison, the same immunohistochemistry was conducted using 10 adult esophaguses.
Results:
In fetuses at all stages examined, a transition zone was found in the upper thoracic esophagus that was attached to the middle one-third of the trachea. In the transition zone, the MyH-positive longitudinal muscle fibers were surrounded by flat, SMA-positive cells, whereas the MyH-positive circular fibers were sometimes located adjacent to the SMA-positive fibers. However, in adults, smooth muscle tended to be clearly separated from striated muscle. The distribution of cells showing immunoreactivity for PGP9.5, S100 or c-kit did not differ between the oral and anal sides of the transition zone. Desmin was positive in the muscularis propria, but negative in the muscularis mucosae. Neither CD68-positive macrophages nor TUNEL-positive cells were present in the esophagus.
Conclusions:
In the human esophagus, the smooth-to-striated muscle transition appears to stop at the mid-thoracic level. Cell death or transdifferentiation of smooth muscle appears unlikely, but phenotypic transformation into desmin-positive myofibroblasts is a possibility.
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