Maha Alhelf - Biotechnology School, Nile University, Giza, Egypt.
Laila Rashed - Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Cairo University,Cairo, Egypt.
Sahar Ahmed - Rheumatologyand Immunology Unit, Internal Medicine Department, Faculty ofMedicine, Cairo University, Cairo, Egypt.
Mohamed Mohamed - Endocrinology Unit, Internal Medicine Department, Faculty of Medicine, Cairo University, Cairo, Egypt.
Marwa Abdelgwad - Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Cairo University,Cairo, Egypt.

Background: Systemic lupus erythematosus (SLE) is an autoimmune disease with inflammatory nature. One of the leading causes of death in SLE patients is cardiovascular (CVS) morbidity. MiRNA-۲۴ is highly expressed in vascular endothelial cells (VECs). This dysregulated expression pattern is associated with dysfunction or even damage of VECs and leads to the occurrence of cardiovascular diseases. YKL- ۴۰ is an inflammatory glycoprotein involved in the pathogenesis of endothelial dysfunction and thereby atherosclerosis. In this work, we aimed at illustrating the possible role of miR-۲۴ and its target YKL-۴۰ in the pathogenesis of the CVS morbidity associated with SLE. Methods: This work was conducted on ۴۰ SLE patients and ۴۰ healthy controls. Quantitative realtime PCR (qPCR) was done to estimate the expression level of miRNA-۲۴ in serum. In addition, we measured the serum level of YKL-۴۰ using ELISA. Results: miR-۲۴-fold change was found to be down-regulated, whereas serum YKL- ۴۰ was upregulated among SLE patients with observed significant and negative correlation between the two parameters. Conclusions: Our study provided an insight about the role of miR-۲۴ and its target serum YKL-۴۰ protein in the development of SLE-related inflammation and atherosclerosis.

miRNA-۲۴, SDC-۱, SLE, VCAM, YKL-۴۰.