The association between expression of IFIT1 in podocytes of MRL/lpr mice and the renal pathological changes it causes: An animal study.
Renal damage is the major cause of SLE associated mortality, and IFIT1expression was elevated in SLE cases in accordance of previous studies. Therefore, we conducted an animal study to identify the role of IFIT1 expression in renal pathological changes.18 female MRL/lpr mice and same number of female BALB/c mice were enrolled in present study. Quantitative analysis of urine protein, Complement C3 and C4, and anti-ds DNA antibody were conducted. HE and PAS staining and TEM analysis were employed to observe the pathological changes in renal tissue. Significant elevation on urine protein and anti-dsDNA and reduction on Complement C3 and C4 were observed in MRL/lpr mice when comparing the controls in same age. Staining and TEM analysis observed several pathological changes in glomerulus among MRL/lpr mice, including cellular enlargement, basement membrane thickening, and increased cellularcasts. The linear regression analysis found the optical density of IFIT1 was inversely associated with F-actin, Nephrin, and Podocin, but not Synatopodin. In summary, IFIT1 expression is associated with podocytes damage, and capable of suppressing some proteins essential to glomerular filtration.
Rheumatism Department, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, China.
Weiping
W
Hu
Rheumatism Department, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, China.
Guodong
G
Niu
Rheumatism Department, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, China.
Hongbo
H
Li
Rheumatism Department, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, China.
Hanyuan
H
Gao
Rheumatism Department, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, China.
Rudian
R
Kang
Rheumatism Department, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, China.
Xiaoqing
X
Chen
Rheumatism Department, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, China.
Ling
L
Lin
D048868:Adaptor Proteins, Signal Transducing; D000818:Animals; D000974:Antibodies, Antinuclear / Q000097:blood / Q000276:immunology; D015415:Biomarkers; D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism; D003165:Complement System Proteins / Q000276:immunology / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D005455:Fluorescent Antibody Technique; D008181:Lupus Nephritis / Q000235:genetics* / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D051379:Mice; D019463:Mice, Inbred MRL lpr; D050199:Podocytes / Q000378:metabolism*; D011507:Proteinuria / Q000378:metabolism; D016601:RNA-Binding Proteins
D048868:Adaptor Proteins, Signal Transducing; D000974:Antibodies, Antinuclear; D015415:Biomarkers; D002352:Carrier Proteins; C092573:Ifit1 protein, mouse; D016601:RNA-Binding Proteins; D003165:Complement System Proteins
IFIT1; Immune response; Immunity; Immunology and Microbiology Section; animal study; lupus nephritis; podocytes; renal pathological changes