Non-histone nuclear protein HMGN2 differently regulates the urothelium barrier function by altering expression of antimicrobial peptides and tight junction protein genes in UPEC J96-infected bladder epithelial cell monolayer.

Abstract:

:The urinary tract is vulnerable to frequent challenges from environmental microflora. Uropathogenic Escherichia coli (UPEC) makes a major contribution to urinary tract infection (UTI). Previous studies have characterized positive roles of non-histone nuclear protein HMGN2 in lung epithelial innate immune response. In the study presented here, we found HMGN2 expression was up-regulated in UPEC J96-infected urothelium. Surprisingly, over-expression of HMGN2 promoted disruption of BECs 5637 cells' intercellular junctions by down-regulating tight junction (TJs) components' expression and physical structure under J96 infection. Further investigation showed that BECs 5637 monolayer, in which HMGN2 was over-expressed, had significantly increased permeability to J96. Our study systemically explored the regulatory roles of HMGN2 in BECs barrier function during UPEC infection and suggested different modulations of intracellular and paracellular routes through which UPEC invades the bladder epithelium.

journal_name

Acta Biochim Pol

journal_title

Acta biochimica Polonica

authors

Tian H,Miao J,Zhang F,Xiong F,Zhu F,Li J,Wang X,Chen S,Chen J,Huang N,Wang Y

doi

10.18388/abp.2017_1622

subject

Has Abstract

pub_date

2018-01-01 00:00:00

pages

93-100

issue

1

eissn

0001-527X

issn

1734-154X

pii

1622

journal_volume

65

pub_type

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