Glucose Induces IL-1α-Dependent Inflammation and Extracellular Matrix Proteins Expression and Deposition in Renal Tubular Epithelial Cells in Diabetic Kidney Disease.
Adult
Aged
Biomarkers
Cell Line, Tumor
Diabetic Nephropathies
/ etiology
Epithelial Cells
/ metabolism
Extracellular Matrix Proteins
/ genetics
Female
Fluorescent Antibody Technique
Gene Expression Regulation
Glucose
/ metabolism
Humans
Immunohistochemistry
Interleukin-1alpha
/ genetics
Kidney Tubules
/ metabolism
Male
Middle Aged
alarmins
diabetic nephropathy (DN)
extracellular matrix
inflammation
interleukin 1
kidney
stressorin
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2020
2020
Historique:
received:
21
09
2019
accepted:
19
05
2020
entrez:
1
8
2020
pubmed:
1
8
2020
medline:
13
4
2021
Statut:
epublish
Résumé
Diabetes mellitus is linked with metabolic stress that induces cellular damage and can provoke renal inflammation and fibrotic responses that eventually lead to chronic kidney disease. Because the inflammasome, interleukin 1 (IL-1), IL-1α/IL-β, and IL-1R are central elements of kidney inflammation and pharmacological IL-1R antagonist (IL-1Ra) was shown to prevent or even reverse diabetic nephropathy (DN) in animal models, we explored the intrinsic expression of IL-1 molecules in kidney tissue of DN patients as regulators of renal inflammation. We used biopsies taken from DN patients and controls and show a high level of IL-1α expression in renal tubular epithelial cells, whereas both IL-1 agonistic molecules (i.e., IL-1α and IL-1β) were devoid of the glomeruli. Human proximal tubular kidney HK-2 cells exposed to high glucose (HG) gradually increase the expression of IL-1α but not IL-1β and induce the expression and deposition of extracellular matrix (ECM) proteins. We further demonstrate that
Identifiants
pubmed: 32733443
doi: 10.3389/fimmu.2020.01270
pmc: PMC7358427
doi:
Substances chimiques
Biomarkers
0
Extracellular Matrix Proteins
0
IL1A protein, human
0
Interleukin-1alpha
0
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1270Informations de copyright
Copyright © 2020 Salti, Khazim, Haddad, Campisi-Pinto, Bar-Sela and Cohen.
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