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2018 ; 6
(ä): e5192
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High expression of SLC26A6 in the kidney may contribute to renal calcification
via an SLC26A6-dependent mechanism
#MMPMID30002986
Jiang H
; Pokhrel G
; Chen Y
; Wang T
; Yin C
; Liu J
; Wang S
; Liu Z
PeerJ
2018[]; 6
(ä): e5192
PMID30002986
show ga
BACKGROUND: Solute-linked carrier 26 gene family 6 (SLC26A6), which is mainly
expressed in intestines and kidneys, is a multifunctional anion transporter
crucial in the transport of oxalate anions. This study aimed to investigate the
role of kidney SLC26A6 in urolithiasis. METHODS: Patients were divided into two
groups: stone formers and nonstone formers. Samples were collected from patients
following nephrectomy. Lentivirus with Slc26a6 (lentivirus-Slc26a6) sequence and
lentivirus with siRNA-Slc26a6 (lentivirus-siRNA-Slc26a6) sequence were
transfected into rats' kidneys respectively and Slc26a6 expression was detected
using Western blot and immunohistochemical analyses. After administering ethylene
glycol, oxalate concentration and prevalence of stone formation between the
transgenic and control groups were measured using 24-h urine analysis and Von
Kossa staining, respectively. RESULTS: Immunohistochemical and Western blot
analyses indicated that stone formers had a significantly higher level of
expression of SLC26A6 in the kidney compared with the control group. After
lentivirus infection, the urinary oxalate concentration and rate of stone
formation in lentivirus-Slc26a6-tranfected rats increased remarkably, while
lentivirus-siRNA-Slc26a6-transfected rats showed few crystals. CONCLUSION: The
results showed that high expression levels of renal SLC26A6 may account for
kidney stone formation. Downregulating the expression of SLC26A6 in the kidney
may be a potential therapeutic target to prevent or treat urolithiasis.