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Published on: July 25, 2022
Caspase-9 expression is increased in endothelial cells of active Behçet's disease patients
Pinar Oztaş1, Neşe Lortlar, Muhterem Polat
1First Dermatology Department, Ankara Numune Education and Research Hospital, Gazi University School of Medicine, Ankara, Turkey. poztas@yahoo.com
Insights
Caspase-9 expression is significantly increased in the endothelial cells of patients with active Behçet
Area of Science:
- Immunology
- Cell Biology
- Dermatology
Background:
- Behçet's disease is a multisystem disorder with unknown causes.
- Caspase-9 plays a critical role in initiating apoptosis.
- Understanding molecular mechanisms in Behçet's disease is crucial for treatment.
Purpose of the Study:
- To investigate the expression of caspase-9 in endothelial and perivascular cells in active Behçet's disease.
- To determine if caspase-9 levels differ between patients with Behçet's disease and control groups.
Main Methods:
- Oral and skin biopsies were collected from 15 active Behçet's disease patients, 9 healthy controls, and 18 psoriasis patients.
- Immunohistochemical analysis was performed using a primary antibody for caspase-9.
- Statistical analysis was conducted to compare caspase-9 expression levels.
Main Results:
- Significantly higher caspase-9 expression was observed in endothelial cells of active Behçet's disease patients compared to healthy controls (P=0.049).
- Endothelial cell caspase-9 staining was also significantly higher in Behçet's disease patients versus inflammatory controls (P=0.006).
- No significant difference in caspase-9 expression was found in dermal perivascular cells among the groups (P=0.407).
Conclusions:
- Endothelial cells are implicated in the pathogenesis of Behçet's disease.
- Increased caspase-9 expression in endothelial cells suggests a role in the disease process.
- Further research into endothelial cell apoptosis pathways in Behçet's disease is warranted.
Background:
Behçet's disease is a multisystem disease of unknown etiology. Caspase-9 is responsible for initiating the caspase activation cascade during apoptosis. The aim of this study was to examine caspase-9 expression in both endothelial and perivascular infiltrates of patients with active Behçet's disease.
Methods:
Fifteen patients with active Behçet's disease, attending the First Dermatology Department, Ankara Numune Hospital, Ankara, Turkey between June 2003 and December 2005, were included in the study. Oral biopsy specimens from nine healthy volunteers were taken as the healthy control group, and skin biopsies from 18 psoriasis patients were used as the inflammatory control group. The specimens were examined with caspase-9 primary antibody. Statistical analyses were performed using SPSS 11.5.
Results:
The mean caspase-9-positive endothelial cell counts were 7.17 +/- 2.45 in active Behçet's disease, 4.81 +/- 0.76 in healthy controls, and 4.35 +/- 1.34 in inflammatory controls. The difference between Behçet's disease and healthy controls was statistically significant, with increased endothelial staining in active Behçet's disease (P = 0.049). The difference between Behçet's disease and inflammatory controls was also statistically significant; the rate of staining was higher in Behçet's disease (P = 0.006). The mean caspase-9-positive dermal perivascular cell counts were 5.15 +/- 2.32 in Behçet's disease, 3.32 +/- 0.82 in healthy controls, and 5.54 +/- 4.95 in inflammatory controls. These values did not show any statistically significant difference (P = 0.407).
Conclusion:
Endothelial cells are one of the key cells in Behçet's disease, and our findings support the role of endothelial cells in the etiopathogenesis of Behçet's disease.
