PMID- 25406076
OWN - NLM
STAT- MEDLINE
DCOM- 20160104
LR  - 20181113
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 9
IP  - 11
DP  - 2014
TI  - Role of moesin in renal fibrosis.
PG  - e112936
LID - 10.1371/journal.pone.0112936 [doi]
LID - e112936
AB  - BACKGROUND: Renal fibrosis is the final common pathway of chronic kidney disease 
      (CKD). Moesin is a member of Ezrin/Radixin/Moesin (ERM) protein family but its 
      role in renal fibrosis is not clear. METHOD: Human proximal tubular cells (HK-2) 
      were stimulated with or without TGF-beta1. Moesin and downstream target genes were 
      examined by real-time PCR and western blot. Phosphorylation of moesin and related 
      signaling pathway was investigated as well. Rat model of unilateral ureteral 
      obstruction (UUO) was established and renal moesin was examined by 
      immunohistochemistry. Moesin in HK-2 cells were knocked down by siRNA and change 
      of downstream genes in transfected HK-2 cells was studied. All animal experiments 
      were reviewed and approved by the Ethics Committee for animal care of Ruijin 
      Hospital. RESULT: HK-2 cells stimulated with TGF-beta1 showed up-regulated level of 
      alpha-SMA and down-regulated level of E-Cadherin as well as elevated mRNA and protein 
      level of moesin. In rat model of UUO, renal moesin expression increased in 
      accordance with severity of tubulointerestital fibrosis in the kidneys with 
      ureteral ligation while the contralateral kidneys were normal. Further study 
      showed that TGF-beta1 could induce phosphorylation of moesin which depended on Erk 
      signaling pathway and Erk inhibitor PD98059 could block moesin phosphorylation. 
      Effects of TGF-beta1 on moesin phosphorylation was prior to its activation to total 
      moesin. RNA silencing studies showed that knocking down of moesin could attenuate 
      decrease of E-Cadherin induced by TGF-beta1. CONCLUSION: We find that moesin might 
      be involved in renal fibrosis and its effects could be related to interacting 
      with E-Cadherin.
FAU - Chen, Yong-Xi
AU  - Chen YX
AD  - Department of nephrology, Ruijin Hospital, Shanghai Jiaotong University, school 
      of medicine, Shanghai, PR China.
FAU - Zhang, Wen
AU  - Zhang W
AD  - Department of nephrology, Ruijin Hospital, Shanghai Jiaotong University, school 
      of medicine, Shanghai, PR China.
FAU - Wang, Wei-Ming
AU  - Wang WM
AD  - Department of nephrology, Ruijin Hospital, Shanghai Jiaotong University, school 
      of medicine, Shanghai, PR China.
FAU - Yu, Xia-Lian
AU  - Yu XL
AD  - Department of nephrology, Ruijin Hospital, Shanghai Jiaotong University, school 
      of medicine, Shanghai, PR China.
FAU - Wang, Yi-Mei
AU  - Wang YM
AD  - Department of nephrology, Ruijin Hospital, Shanghai Jiaotong University, school 
      of medicine, Shanghai, PR China.
FAU - Zhang, Min-Jun
AU  - Zhang MJ
AD  - Animal Experiment and Research Center, Ruijin Hospital, Shanghai Jiaotong 
      University, school of medicine, Shanghai, PR China.
FAU - Chen, Nan
AU  - Chen N
AD  - Department of nephrology, Ruijin Hospital, Shanghai Jiaotong University, school 
      of medicine, Shanghai, PR China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141118
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (ACTA2 protein, human)
RN  - 0 (Actins)
RN  - 0 (Cadherins)
RN  - 0 (Microfilament Proteins)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 144131-77-1 (moesin)
SB  - IM
MH  - Actins/metabolism
MH  - Analysis of Variance
MH  - Animals
MH  - Blotting, Western
MH  - Cadherins/*metabolism
MH  - Cell Line
MH  - Fibrosis/metabolism
MH  - Humans
MH  - Immunohistochemistry
MH  - Microfilament Proteins/*metabolism
MH  - Phosphorylation
MH  - RNA, Small Interfering/genetics
MH  - Rats
MH  - Real-Time Polymerase Chain Reaction
MH  - Renal Insufficiency, Chronic/*metabolism/*pathology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/*physiology
MH  - Transforming Growth Factor beta1
PMC - PMC4236084
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2014/11/19 06:00
MHDA- 2016/01/05 06:00
PMCR- 2014/11/18
CRDT- 2014/11/19 06:00
PHST- 2014/06/01 00:00 [received]
PHST- 2014/10/17 00:00 [accepted]
PHST- 2014/11/19 06:00 [entrez]
PHST- 2014/11/19 06:00 [pubmed]
PHST- 2016/01/05 06:00 [medline]
PHST- 2014/11/18 00:00 [pmc-release]
AID - PONE-D-14-24417 [pii]
AID - 10.1371/journal.pone.0112936 [doi]
PST - epublish
SO  - PLoS One. 2014 Nov 18;9(11):e112936. doi: 10.1371/journal.pone.0112936. 
      eCollection 2014.