Journal of Neurogastroenterology and Motility : eISSN 2093-0887 / pISSN 2093-0879

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Fig. 3. Smooth muscle phenotype is altered in achalasia, with no evidence of ongoing smooth muscle proliferation. (A-C) Representative images of esophageal circular smooth muscle (CSM) from control and achalasia showing antibody staining for the smooth muscle marker proteins, transgelin (SM22) (A), α-smooth muscle actin (SMA) (B), and smoothelin (SMOO) (C) expression. Scale bar, 20 µm. (D) Antibody staining for the proliferation marker Ki-67 showing staining in positive control tissue (esophageal mucosa) but absence from control and achalasia esophageal CSM. Scale bar, 20 µm. (E) Image analysis showing staining intensity of SMA, SM22 and SMOO in CSM biopsies from achalasia patients (Ach) relative to control (Con). *P < 0.05 vs control. (F) Staining intensities of SMA relative to control in the 3 subtypes of achalasia. *P < 0.05 vs control.
J Neurogastroenterol Motil 2024;30:166~176
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