Abstract
Lupus nephritis (LN) is one of the most common and severe complications of lupus. However, the mechanisms for renal damage have not been well elucidated. There are evidences show that glomerular endothelial cells (GECs) are damaged in LN. Immune complexes can deposit in subendothelial area and could affect GEC functions. In the present study, we used heat-aggregated gamma globulin (HAGG) to simulate immune complexes and investigated their effects on GEC functions. Our results revealed that HAGG impaired different aspect of the GEC functions. HAGG changed cell morphology, upregulated the expression of active caspase-3, inhibited angiogenesis, and increased NO production in GECs. These results provide new clues for the mechanisms of renal damage and the pathology of LN.
Highlights
Lupus nephritis (LN) is one of the most common and severe complications of lupus
In the present study, we further investigated on a series of glomerular endothelial cells (GECs) functions under the stimulation of heat-aggregated gamma globulin (HAGG) in vitro and found that cell morphology, cell death, angiogenesis, and intracellular nitric oxide production were impaired, which shed lights on the mechanisms of renal damage and the pathology of LN
Cell morphology is commonly used as a measurement of the outcomes of various stimulations [20]
Summary
Lupus nephritis (LN) is one of the most common and severe complications of lupus. Renal involvement is a leading predictor of poor prognosis in lupus patients [1]. Numerous factors (genetic, environmental, infectious, hormonal, and immune) contribute to this complex pathogenesis [2,3]. The precise mechanisms for renal impairment are not thoroughly understood. The glomerular filtration membrane (GFM) is the structural and functional foundation of the kidney, consisting of glomerular endothelial cells (GECs), podocytes, and glomerular basement membrane [4]. Impairment in any component of the GFM can injure renal functions. The role of GECs in LN has not been well elucidated
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