PMID- 30454893
OWN - NLM
STAT- MEDLINE
DCOM- 20190517
LR  - 20190517
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 507
IP  - 1-4
DP  - 2018 Dec 9
TI  - Interleukin-7 stimulation inhibits nephrin activation and induces podocyte 
      injury.
PG  - 100-105
LID - S0006-291X(18)32361-1 [pii]
LID - 10.1016/j.bbrc.2018.10.173 [doi]
AB  - The glomerular podocytes control filtration barrier permeability in the kidney, 
      and their disturbance underlies the pathogenesis of idiopathic nephrotic syndrome 
      (INS), a kidney disease that predominantly occurs in children. In this study, we 
      found that the interleukin-7 receptor (IL-7R) was induced in the glomeruli of 
      adriamycin (ADR)-induced mouse nephropathy, a rodent model of nephrotic syndrome. 
      In addition, IL-7R was also induced by ADR in mouse podocytes cultured in vitro. 
      Functionally, we discovered that IL-7R activation through the stimulation of 
      recombinant IL-7 induced apoptosis of podocytes, and moreover, IL-7 stimulation 
      inhibited nephrin activation and caused actin cytoskeleton disorganization, 
      indicating that IL-7 stimulation induces podocyte injury. Furthermore, IL-7 
      stimulation impaired the filtration barrier function of podocyte monolayer. 
      Together, these results identify IL-7 and its receptor IL-7R as potential 
      regulators of podocyte function, which might offer a novel therapeutic target in 
      the treatment of INS.
CI  - Copyright (c) 2018. Published by Elsevier Inc.
FAU - Zhai, Shubo
AU  - Zhai S
AD  - Department of Pediatric Nephropathy, The First Hospital of Jilin University, 
      China.
FAU - Zhao, Lengyue
AU  - Zhao L
AD  - Department of Pediatric Nephropathy, The First Hospital of Jilin University, 
      China.
FAU - Zhang, Yan
AU  - Zhang Y
AD  - Department of Pediatric Nephropathy, The First Hospital of Jilin University, 
      China.
FAU - Ma, Qingshan
AU  - Ma Q
AD  - Department of Pediatric Nephropathy, The First Hospital of Jilin University, 
      China. Electronic address: maqs7121@163.com.
LA  - eng
PT  - Journal Article
DEP - 20181116
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Albumins)
RN  - 0 (Interleukin-7)
RN  - 0 (Membrane Proteins)
RN  - 0 (Receptors, Interleukin-7)
RN  - 0 (nephrin)
RN  - 80168379AG (Doxorubicin)
SB  - IM
MH  - Actin Cytoskeleton/drug effects
MH  - Albumins/metabolism
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Cell Line
MH  - Doxorubicin
MH  - Interleukin-7/*pharmacology
MH  - Kidney Diseases/chemically induced/pathology
MH  - Male
MH  - Membrane Proteins/*metabolism
MH  - Mice, Inbred BALB C
MH  - Podocytes/drug effects/*metabolism/*pathology
MH  - Receptors, Interleukin-7/metabolism
MH  - Up-Regulation/drug effects
OTO - NOTNLM
OT  - Idiopathic nephrotic syndrome
OT  - Interleukin-7
OT  - Nephrin activation
OT  - Podocyte
EDAT- 2018/11/21 06:00
MHDA- 2019/05/18 06:00
CRDT- 2018/11/21 06:00
PHST- 2018/10/19 00:00 [received]
PHST- 2018/10/28 00:00 [accepted]
PHST- 2018/11/21 06:00 [pubmed]
PHST- 2019/05/18 06:00 [medline]
PHST- 2018/11/21 06:00 [entrez]
AID - S0006-291X(18)32361-1 [pii]
AID - 10.1016/j.bbrc.2018.10.173 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2018 Dec 9;507(1-4):100-105. doi: 
      10.1016/j.bbrc.2018.10.173. Epub 2018 Nov 16.