Level of Autophagy in Lichen Planus: Role of Endoplasmic Reticulum Stress Proteins | ||
| Egyptian Academic Journal of Biological Sciences. C, Physiology and Molecular Biology | ||
| Article 23, Volume 14, Issue 1, June 2022, Pages 265-275 PDF (592.07 K) | ||
| Document Type: Original Article | ||
| DOI: 10.21608/eajbsc.2022.228646 | ||
| Authors | ||
| Taha Azouz1; Laila Rashed1; Salwa Fayez1; Rania Mounir2; Yasmin Elwan1 | ||
| 1The Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Cairo University, Egypt. | ||
| 2The Department of Dermatology, Faculty of Medicine, Cairo University, Egypt. | ||
| Abstract | ||
| Lichen Planus (LP) is a common T cell-mediated chronic inflammatory disease affecting skin & or mucous membranes. Also, T cell-induced autophagy is involved in the immunopathogenesis of the oral type of lichen planus (OLP). Beclin-1 is an autophagy marker with a critical role in the autophagic process. Heat shock proteins (HSP) synthesis increases in response to many stressors being the molecular chaperones. HSP has an important role in the Endoplasmic reticulum stress (ER stress) process. HSPs are assumed to be involved in the initiation and probably continuation of lichen planus through the autoimmune lymphocytic response. GRP78 (Glucose-regulated protein 78) is one of the HSPs that may play a substantial role in LP. ATF6 (activated transcription factor6) is one of ER stress pathway sensors that may link ER stress and autophagy. The study was conducted on 40 lichen planus patients and 20 healthy control subjects. GRP78, ATF6 and Beclin-1 gene expressions were estimated by real-time PCR. Patients with oral and cutaneous lichen planus showed a significant increase in GRP78, ATF6 and Beclin-1 compared to the normal control group. Conclusion; the results conduct an increase in autophagy and endoplasmic reticulum stress markers with lichen planus which may represent an inductive or protective mechanism for lichen planus. | ||
| Keywords | ||
| lichen planus; ER stress; autophagy; GRP78; ATF6; Beclin-1 | ||
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