Genomics

Dataset Information

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Osteopontin Deficiency Amerliorates Alport Kindey Pathology


ABSTRACT: Kidneys were snap frozen from 2 month old wild type, Col4a3-/-, or Col4a3-/-OPN-/- mice. RNA was isolated using Mirvana Paris kit. Overall design: Kidneys were snap frozen from 2 month old wild type (n=2), Col4a3-/- (n=3), or Col4a3-/-OPN-/- (n=3) mice. RNA was isolated using Mirvana Paris kit.

INSTRUMENT(S): [MoGene-2_0-st] Affymetrix Mouse Gene 2.0 ST Array [transcript (gene) version]

SUBMITTER: Lina A Shehadeh  

PROVIDER: GSE109777 | GEO | 2018-01-30

REPOSITORIES: GEO

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Publications

Osteopontin deficiency ameliorates Alport pathology by preventing tubular metabolic deficits.

Ding Wen W   Yousefi Keyvan K   Goncalves Stefania S   Goldstein Bradley J BJ   Sabater Alfonso L AL   Kloosterboer Amy A   Ritter Portia P   Lambert Guerline G   Mendez Armando J AJ   Shehadeh Lina A LA  

JCI insight 20180322 6


Alport syndrome is a rare hereditary renal disorder with no etiologic therapy. We found that osteopontin (OPN) is highly expressed in the renal tubules of the Alport mouse and plays a causative pathological role. OPN genetic deletion ameliorated albuminuria, hypertension, tubulointerstitial proliferation, renal apoptosis, and hearing and visual deficits in the Alport mouse. In Alport renal tubules we found extensive cholesterol accumulation and increased protein expression of dynamin-3 (DNM3) an  ...[more]

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