Human amniotic epithelial cells suppress relapse of corticosteroid-remitted experimental autoimmune disease

Accelerated senescence of renal tubular epithelial cells is associated with disease progression of patients with immunoglobulin A (IgA) nephropathyLiu, J., Yang, J., He, Y., Cai, G., Zhang, J., Lin, L., Zhan, J., , Xiao, H.(2012). Accelerated senescence of renal tubular epithelial cells is associated with disease progression of patients with immunoglobulin A (IgA) nephropathy. Translational Research,159(6), 454463.Julie Nieva D. Sianquita3Bio5College of Science, Department of Biological SciencesUniversity of Santo Tomas

Disease: Immunoglobin A nephropathy (IgNA)Bergers diseaseKidney disease that occurs when an antibody called Immunoglobin A (IgA) lodges in the kidney.Result in local inflammation that, over time, may hamper the kidneys ability to filter waste, excess water and electrolytes from the blood.

Affecting Cells: Renal Tubular Epithelial Cellsepithelial cells, usually larger than granulocytes, contain a large round or oval nucleus and normally slough into the urine in small numbers.with nephrotic disease the number sloughed is increased.Suggested that its accelerated senescence may contribute to the progression of IgNA

Studyblue.comImage of a RTECMethodologyMethodologyMethodologyMethodologyResultsThe expression of senescence-associated markers, such as SA--gal, p21, p16 were significantly in patients with grade I-II IgAN compared with normal controls.A linear correlation analysis revealed that the expression of senescence-associated markers was associated significantly with blood pressure and renal dysfunction but not with patient age, BMI, LDL cholesterol level, or 24-h urinary protein value.Percentages of p16 and p21- positive RTECs and SA--gal positivity were associated closely with glomerular sclerosis, interstitial fibrosis, and vessel lesion.ConclusionThe results indicated that renal tubular epithelial cells (RTECs) in immunoglobulin A nephropathy (IgAN) patients exhibited features of accelerated senescence, which were unrelated to mechanisms associated with normal aging. Observations indicated that IgAN could induce the accelerated senescence of RTECs, and cellular senescence might contribute to disease progression.Insufficient supply of blood in renal interstitium might be associated with the accelerated senescence or RTECs.This study indicates that the accelerated senescence of RTECs might contribute to the progression of IgAN by trigerring inflammatory response and the deposition ofepeithelial cell matrix protein.