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2015 ; 26
(6
): 1402-13
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Renal glycosphingolipid metabolism is dysfunctional in lupus nephritis
#MMPMID25270066
Nowling TK
; Mather AR
; Thiyagarajan T
; Hernández-Corbacho MJ
; Powers TW
; Jones EE
; Snider AJ
; Oates JC
; Drake RR
; Siskind LJ
J Am Soc Nephrol
2015[Jun]; 26
(6
): 1402-13
PMID25270066
show ga
Nearly one half of patients with lupus develop glomerulonephritis (GN), which
often leads to renal failure. Although nephritis is diagnosed by the presence of
proteinuria, the pathology of nephritis can fall into one of five classes defined
by different forms of tissue injury, and the mechanisms involved in pathogenesis
are not completely understood. Glycosphingolipids are abundant in the kidney,
have roles in many cellular functions, and were shown to be involved in other
renal diseases. Here, we show dysfunctional glycosphingolipid metabolism in
patients with lupus nephritis and MRL/lpr lupus mice. Specifically, we found that
glucosylceramide (GlcCer) and lactosylceramide (LacCer) levels are significantly
higher in the kidneys of nephritic MRL/lpr lupus mice than the kidneys of
non-nephritic lupus mice or healthy controls. This elevation may be, in part,
caused by altered transcriptional regulation and/or activity of LacCer synthase
(GalT5) and neuraminidase 1, enzymes that mediate glycosphingolipid metabolism.
We show increased neuraminidase 1 activity early during the progression of
nephritis (before significant elevation of GlcCer and LacCer in the kidney).
Elevated levels of urinary LacCer were detected before proteinuria in lupus mice.
Notably, LacCer levels were higher in the urine and kidneys of patients with
lupus and nephritis than patients with lupus without nephritis or healthy
controls. Together, these results show early and significant dysfunction of the
glycosphingolipid metabolic pathway in the kidneys of lupus mice and patients
with lupus nephritis and suggest that molecules in this pathway may serve as
early markers in lupus nephritis.
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