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Tytuł pozycji:

Progressive glomerular and tubular damage in sickle cell trait and sickle cell anemia mouse models.

Tytuł:
Progressive glomerular and tubular damage in sickle cell trait and sickle cell anemia mouse models.
Autorzy:
Saraf SL; Division of Hematology & Oncology, Department of Medicine, Comprehensive Sickle Cell Center, University of Illinois at Chicago, Chicago, Illinois. Electronic address: .
Sysol JR; Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois.
Susma A; Department of Pathology, University of Illinois at Chicago, Chicago, Illinois.
Setty S; Department of Pathology, University of Illinois at Chicago, Chicago, Illinois.
Zhang X; Division of Hematology & Oncology, Department of Medicine, Comprehensive Sickle Cell Center, University of Illinois at Chicago, Chicago, Illinois.
Gudehithlu KP; Division of Nephrology, Department of Medicine, John H. Stroger, Jr Hospital of Cook County, Chicago, Illinois.
Arruda JAL; Division of Nephrology, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois.
Singh AK; Division of Nephrology, Department of Medicine, John H. Stroger, Jr Hospital of Cook County, Chicago, Illinois.
Machado RF; Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois.
Gordeuk VR; Division of Hematology & Oncology, Department of Medicine, Comprehensive Sickle Cell Center, University of Illinois at Chicago, Chicago, Illinois.
Źródło:
Translational research : the journal of laboratory and clinical medicine [Transl Res] 2018 Jul; Vol. 197, pp. 1-11. Date of Electronic Publication: 2018 Feb 02.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural
Język:
English
Imprint Name(s):
Original Publication: New York, N.Y. : Elsevier, [2006]-
MeSH Terms:
Disease Progression*
Anemia, Sickle Cell/*pathology
Kidney Glomerulus/*pathology
Kidney Tubules/*pathology
Sickle Cell Trait/*pathology
Anemia, Sickle Cell/blood ; Anemia, Sickle Cell/genetics ; Animals ; Disease Models, Animal ; Gene Expression Regulation ; Hypertrophy ; Kidney Glomerulus/ultrastructure ; Kidney Tubules/ultrastructure ; Mice, Transgenic ; Sickle Cell Trait/blood ; Sickle Cell Trait/genetics
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Grant Information:
K23 HL125984 United States HL NHLBI NIH HHS; R01 HL111656 United States HL NHLBI NIH HHS; R01 HL127342 United States HL NHLBI NIH HHS
Entry Date(s):
Date Created: 20180225 Date Completed: 20181029 Latest Revision: 20190701
Update Code:
20240105
PubMed Central ID:
PMC6003843
DOI:
10.1016/j.trsl.2018.01.007
PMID:
29476712
Czasopismo naukowe
Homozygosity for the hemoglobin (Hb) S mutation (HbSS, sickle cell anemia) results in hemoglobin polymerization under hypoxic conditions leading to vaso-occlusion and hemolysis. Sickle cell anemia affects 1:500 African Americans and is a strong risk factor for kidney disease, although the mechanisms are not well understood. Heterozygous inheritance (HbAS; sickle cell trait) affects 1:10 African Americans and is associated with an increased risk for kidney disease in some reports. Using transgenic sickle mice, we investigated the histopathologic, ultrastructural, and gene expression differences with the HbS mutation. Consistent with progressive glomerular damage, we observed progressively greater urine protein concentrations (P = 0.03), glomerular hypertrophy (P = 0.002), and glomerular cellularity (P = 0.01) in HbAA, HbAS, and HbSS mice, respectively. Ultrastructural studies demonstrated progressive podocyte foot process effacement, glomerular basement membrane thickening with reduplication, and tubular villous atrophy with the HbS mutation. Gene expression studies highlighted the differential expression of several genes involved in prostaglandin metabolism (AKR1C18), heme and iron metabolism (HbA-A2, HMOX1, SCL25A37), electrolyte balance (SLC4A1, AQP6), immunity (RSAD2, C3, UBE2O), fatty acid metabolism (FASN), hypoxia hall-mark genes (GCK, SDC3, VEGFA, ETS1, CP, BCL2), as well as genes implicated in other forms of kidney disease (PODXL, ELMO1, FRMD3, MYH9, APOA1). Pathway analysis highlighted increased gene enrichment in focal adhesion, extracellular matrix-receptor interaction, and axon guidance pathways. In summary, using transgenic sickle mice, we observed that inheritance of the HbS mutation is associated with glomerular and tubular damage and identified several candidate genes and pathways for future investigation in sickle cell trait and sickle cell anemia-related kidney disease.
(Copyright © 2018 Elsevier Inc. All rights reserved.)

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