4.7 Article

Disruption of Myosin 1e Promotes Podocyte Injury

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AMER SOC NEPHROLOGY
DOI: 10.1681/ASN.2007111172

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  1. American Heart Association [0335441T]
  2. American Diabetes Association [1-07-JF-39]
  3. National Institutes of Health [GM073823, DK 25387, HD32573]
  4. EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [P01HD032573] Funding Source: NIH RePORTER
  5. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R37DK025387, R01DK025387, R01DK062289] Funding Source: NIH RePORTER
  6. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM073823] Funding Source: NIH RePORTER

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Myosin 1e (Myo1e) is one of two Src homology 3 domain-containing long-tailed type I myosins in vertebrates, whose functions in health and disease are incompletely understood. Here, we demonstrate that Myo1e localizes to podocytes in the kidney. We generated Myo1e-knockout mice and found that they exhibit proteinuria, signs of chronic renal injury, and kidney inflammation. At the ultrastructural level, renal tissue from Myo1e-null mice demonstrates changes characteristic of glomerular disease, including a thickened and disorganized glomerular basement membrane and flattened podocyte foot processes. These observations suggest that Myo1e plays an important role in podocyte function and normal glomerular filtration.

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