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Downregulation of exocyst Sec10 accelerates kidney tubule cell recovery through enhanced cell migration.

Abstract：

:Migration of surviving kidney tubule cells after sub-lethal injury, for example ischemia/reperfusion (I/R), plays a critical role in recovery. Exocytosis is known to be involved in cell migration, and a key component in exocytosis is the highly-conserved eight-protein exocyst complex. We investigated the expression of a central exocyst complex member, Sec10, in kidneys following I/R injury, as well as the role of Sec10 in wound healing following scratch injury of cultured Madin-Darby canine kidney (MDCK) cells. Sec10 overexpression and knockdown (KD) in MDCK cells were used to investigate the speed of wound healing and the mechanisms underlying recovery. In mice, Sec10 decreased after I/R injury, and increased during the recovery period. In cell culture, Sec10 OE inhibited ruffle formation and wound healing, while Sec10 KD accelerated it. Sec10 OE cells had higher amounts of diacylglycerol kinase (DGK) gamma at the leading edge than did control cells. A DGK inhibitor reversed the inhibition of wound healing and ruffle formation in Sec10 OE cells. Conclusively, downregulation of Sec10 following I/R injury appears to accelerate recovery of kidney tubule cells through activated ruffle formation and enhanced cell migration.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Noh MR,Jang HS,Song DK,Lee SR,Lipschutz JH,Park KM,Kim JI

doi

10.1016/j.bbrc.2018.01.013

subject

Has Abstract

pub_date

2018-02-05 00:00:00

pages

309-315

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(18)30013-5

journal_volume

496

pub_type

杂志文章

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