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No renal phenotype in human phospholipid transfer protein transgenic apolipoprotein E deficient mice despite severe aortic atherosclerosis.

AbstractBACKGROUND:
Phospholipid transfer protein (PLTP) is an emerging cardiometabolic risk factor. Plasma PLTP is elevated in humans with end-stage kidney disease and glomerular proteinuria, but the contribution of systemic PLTP elevation to the development of renal damage is unknown. We tested whether human PLTP expression in ApoE deficient mice (an atherosclerosis-prone model) results in renal insufficiency, albuminuria, or glomerulosclerosis.
METHODS:
Serum creatinine, albuminuria, as well as kidney and aortic arch histology were determined in 6 male huPLTPtgApoE-/- mice and 8 similarly aged male wild type mice fed a regular chow diet.
RESULTS:
huPLTPtgApoE-/- mice (2- to 3-fold elevated PLTP activity) showed marked aortic atherosclerosis. However, serum creatinine (p = 0.11) and albuminuria (p = 0.87) were not increased, whereas renal arteriolar atherosclerosis and glomerulosclerosis were not evident in this PLTP transgenic model.
CONCLUSIONS:
High systemic PLTP expression does not contribute significantly to a renal phenotype despite being implicated in systemic atherosclerosis.
AuthorsRobin P F Dullaart, Rien Van Haperen, Jaap Van Den Born, Harry Van Goor, Rini De Crom, Arie Van Tol
JournalClinical laboratory (Clin Lab) Vol. 60 Issue 10 Pg. 1659-62 ( 2014) ISSN: 1433-6510 [Print] Germany
PMID25651711 (Publication Type: Journal Article)
Chemical References
  • Apolipoproteins E
  • PLTP protein, human
  • Phospholipid Transfer Proteins
Topics
  • Animals
  • Aorta, Thoracic (metabolism, pathology)
  • Aortic Diseases (genetics, metabolism, pathology)
  • Apolipoproteins E (deficiency, genetics)
  • Atherosclerosis (genetics, metabolism, pathology)
  • Disease Models, Animal
  • Genotype
  • Glomerulonephritis (genetics, metabolism, pathology)
  • Humans
  • Male
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Phenotype
  • Phospholipid Transfer Proteins (genetics, metabolism)
  • Proteinuria (genetics, metabolism, pathology)
  • Renal Insufficiency (genetics, metabolism, pathology)
  • Risk Factors
  • Severity of Illness Index
  • Up-Regulation

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