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2014 ; 92
(12
): 1245-56
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Urinary semaphorin 3A correlates with diabetic proteinuria and mediates diabetic
nephropathy and associated inflammation in mice
#MMPMID25249008
Mohamed R
; Ranganathan P
; Jayakumar C
; Nauta FL
; Gansevoort RT
; Weintraub NL
; Brands M
; Ramesh G
J Mol Med (Berl)
2014[Dec]; 92
(12
): 1245-56
PMID25249008
show ga
Semaphorin 3A (sema3A) was recently identified as an early diagnostic biomarker
of acute kidney injury. However, its role as a biomarker and/or mediator of
chronic kidney disease (CKD) related to diabetic nephropathy is unknown. We
examined the expression of sema3A in diabetic animal models and in humans and
tested whether sema3A plays a pathogenic role in the development of diabetic
nephropathy. The expression of sema3A was localized to podocytes and epithelial
cells in distal tubules and collecting ducts in control animals, and its
expression was increased following the induction of diabetes. Quantification of
sema3A urinary excretion in three different diabetic mouse models showed that
excretion was increased as early as 2 weeks after the induction of diabetes and
increased over time, in conjunction with the development of nephropathy.
Consistent with the mouse data, increased sema3A urinary excretion was detected
in diabetic patients with albuminuria, particularly in those with
macroalbuminuria. Genetic ablation of sema3A or pharmacological inhibition with a
novel sema3A inhibitory peptide was protected against diabetes-induced
albuminuria, kidney fibrosis, inflammation, oxidative stress, and renal
dysfunction. We conclude that sema3A is both a biomarker and a mediator of
diabetic kidney disease and could be a promising therapeutic target in diabetic
nephropathy. Key messages Diabetes induced sema3A excretion in urine. Increased
semaphorin 3A was associated with severity of albuminuria. Seme3A-mediated
diabetes induced glomerulosclerosis. Peptide-based inhibition of semaphorin3A
suppressed diabetic nephropathy.
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