Association of Circulating Levels of Hypoxia-Inducible Factor-1α and miR-210 with Photosensitivity in Systemic Lupus Erythematosus Patients

Abstract

Background: miR-210, a key HypoxamiR, regulates the hypoxia and inflammation-linked hypoxia. Systemic lupus erythematosus (SLE), a chronic autoimmune disease, responsible for many pathological disorders, including photosensitivity. Objective: Finding the correlation between the circulating miR-210/HIF-1α levels and photosensitivity in SLE patients and other SLE-associated pathological complications, in a single-center case control study. Methods: Study population of 104 SLE Egyptian patients with photosensitivity, 32 SLE patients without photosensitivity, and 32 healthy subjects. SLE activity was assessed for all patients by SLE Disease Activity Index (SLEDAI). The clinical complications/manifestations and the hematological/serological analyses were recorded. HIF-α concentration was investigated by ELISA and miR-210 expression was analyzed by qRT-PCR. Results: The results revealed that circulating miR-210 was significantly increased in SLE/photosensitivity than SLE and controls. The additional occurrence of malar rash, oral ulcers, renal disorders or hypertension resulted in a higher expression of miR-210. SLEDAI activity status showed no effect on miR-210. Erythrocyte sedimentation rate, white blood cells, hemoglobin, platelets, the patients age and the disease duration were positively correlated with circulatory miR-210. HIF-α concentration was significantly induced in SLE/photosensitivity than SLE and controls. In SLE/photosensitivity, presence of renal disorders and hypertension resulted in highest HIF-α concentrations. A strong positive correlation was recorded between HIF-α concentration and circulatory miR-210 in SLE/photosensitivity patients (r = 0.886). Conclusion:: The dysregulation of circulating miR-210/ HIF-1α levels in SLE/photosensitivity‎ patients is controlled by the presence of additional pathological complications and supposed that hypoxia pathway might interact positively with the pathogenesis and illness progress of SLE.