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06:59
Isolation of Primary Myofibroblasts from Mouse and Human Colon Tissue
Published on: October 12, 2013
CAM5.2-positive subserosal myofibroblasts in appendicitis
Tadashi Hamauzu1, Naoto Kuroda, Limei Guo
1Department of Pathology, Program of Bioregulation and Genetics, Kochi Medical School, Kochi University, Kochi, Japan.
Medical Molecular Morphology
|December 26, 2006
Summary
Myofibroblasts accumulate around appendicitis perforations, originating from submesothelial or mesothelial cells. These cells, identified by specific markers, replace absent CD34-positive stromal cells in the affected area.
Area of Science:
- Gastroenterology
- Surgical Pathology
- Cell Biology
Background:
- Appendicitis perforation leads to significant tissue changes.
- The role of myofibroblasts in appendicitis complications is not fully understood.
- Understanding stromal cell origin is crucial for tissue repair mechanisms.
Purpose of the Study:
- To investigate the distribution and origin of myofibroblasts in appendicitis perforations.
- To characterize stromal cell populations in normal and perforated appendices.
- To identify potential cellular sources of myofibroblasts in appendicitis.
Main Methods:
- Immunohistochemistry on 45 appendicitis cases.
- Analysis of stromal cells using markers like alpha-smooth muscle actin (ASMA), CD34, cytokeratin CAM5.2, cytokeratin 5, and HBME-1.
- Double immunostaining to assess coexpression of markers.
Main Results:
- Myofibroblasts were found in the subserosal area around appendicitis perforations, particularly with abscess and granulation tissue.
- CD34-positive stromal cells were absent in the perforation's subserosal area.
- Coexpression of ASMA and cytokeratin CAM5.2, and cytokeratin 5 and cytokeratin CAM5.2, was observed in stromal cells.
Conclusions:
- Myofibroblasts in the subserosal area of appendicitis perforations likely originate from submesothelial or mesothelial cells.
- These findings highlight a distinct cellular response in appendicitis complications.
- The study provides insights into the cellular dynamics of wound healing in appendicitis.
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