Macrophage migration inhibitory factor is a possible candidate for the induction of microalbuminuria in diabetic db/db mice.
Biol Pharm Bull
; 36(5): 741-7, 2013.
Article
en En
| MEDLINE
| ID: mdl-23649333
ABSTRACT
Preventing the onset of microalbuminuria in diabetic nephropathy is a problem that needs urgent rectification. The use of a mouse model for diabetes is vital in this regard. For example, db/db mice exhibit defects in the leptin receptor Ob-Rb sub-type, while the ob/ob strain exhibits defects in the leptin ligand. These mouse strains demonstrate type 2 diabetes, either with or without microalbuminuria, respectively. The purpose of the present study was to use DNA microarray technology to screen for the gene responsible for the onset of diabetic microalbuminuria. Using Affymetrix Mouse Gene ST 1.0 arrays, microarray analysis was performed using total RNA from the kidneys of ob control, ob/ob, db/m, and db/db mice. Microarray and quantitative reverse transcription-polymerase chain reaction (RT-PCR) indicated that transcription of the macrophage migration inhibitory factor (MIF) gene was significantly enhanced in the kidneys of db/db mice. Western blotting showed that levels of MIF protein was enhanced in the kidneys of both diabetic db/db and ob/ob mice. On the other hand, elevation of urinary MIF excretion detected by enzyme-linked immunosorbent assay (ELISA) was only in db/db mice and preceded the onset of microalbuminuria. Immunofluorescence studies revealed that MIF was expressed in mouse kidney glomeruli. While MIF expression was enhanced in the diabetic kidneys of both mouse strains, the elevated secretion from db/db mouse kidneys may be responsible for initiating the onset of microalbuminuria in diabetic nephropathy.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Factores Inhibidores de la Migración de Macrófagos
/
Oxidorreductasas Intramoleculares
/
Diabetes Mellitus Tipo 2
/
Nefropatías Diabéticas
/
Albuminuria
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Biol Pharm Bull
Asunto de la revista:
BIOQUIMICA
/
FARMACOLOGIA
Año:
2013
Tipo del documento:
Article
País de afiliación:
Japón