PMID- 20299783
OWN - NLM
STAT- MEDLINE
DCOM- 20101012
LR  - 20161125
IS  - 1421-9670 (Electronic)
IS  - 0250-8095 (Linking)
VI  - 31
IP  - 5
DP  - 2010
TI  - Suppressor of cytokine signaling-1 ameliorates expression of MCP-1 in diabetic 
      nephropathy.
PG  - 380-8
LID - 10.1159/000286559 [doi]
AB  - BACKGROUND: Janus kinase (JAK)/signal transducers and activators of transcription 
      (STAT) contribute to diabetic nephropathy. Suppressor of cytokine signaling-1 
      (SOCS-1) is one of the negative feedback regulators of JAK/STAT signaling. This 
      study investigated the effect of SOCS-1 on the JAK/STAT pathway and MCP-1 
      expression in diabetic nephropathy. METHODS: Streptozotocin-induced diabetic mice 
      received pEF-FLAG-I/mSOCS-1 plasmid or pEF-FLAG-I vector for 4 weeks and were 
      compared with age-matched nondiabetic mice. Functional and pathologic markers, 
      expression of monocyte chemoattractant protein-1 (MCP-1) and TGF-beta1 and 
      phosphorylation of STAT1 and STAT3 were assessed. The effect of SOCS-1 on the 
      expression of MCP-1 in mesangial cells under high glucose conditions was also 
      examined. RESULTS: Urine albumin excretion and renal hypertrophy were alleviated 
      in diabetic mice by overexpression of SOCS-1. The expression of TGF-beta1 and 
      MCP-1 and the activation of STAT1 and STAT3 were significantly inhibited in 
      diabetic kidney by gene delivery of SOCS-1. In cultured mesangial cells, 
      overexpression of SOCS-1 markedly suppressed high glucose-induced MCP-1 
      expression. CONCLUSIONS: This study suggests that SOCS-1 may attenuate renal 
      damage by ameliorating MCP-1 expression and regulation of the phosphorylation of 
      JAK/STAT in diabetic mice.
CI  - 2010 S. Karger AG, Basel.
FAU - Shi, Yonghong
AU  - Shi Y
AD  - Department of Pathology, Hebei Medical University, Shijiazhuang, PR China.
FAU - Du, Chunyang
AU  - Du C
FAU - Zhang, Yanling
AU  - Zhang Y
FAU - Ren, Yunzhuo
AU  - Ren Y
FAU - Hao, Jun
AU  - Hao J
FAU - Zhao, Song
AU  - Zhao S
FAU - Yao, Fang
AU  - Yao F
FAU - Duan, Huijun
AU  - Duan H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100319
PL  - Switzerland
TA  - Am J Nephrol
JT  - American journal of nephrology
JID - 8109361
RN  - 0 (Blood Glucose)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (SOCS1 protein, human)
RN  - 0 (STAT1 Transcription Factor)
RN  - 0 (Socs1 protein, mouse)
RN  - 0 (Stat1 protein, mouse)
RN  - 0 (Suppressor of Cytokine Signaling 1 Protein)
RN  - 0 (Suppressor of Cytokine Signaling Proteins)
RN  - 0 (Transforming Growth Factor beta1)
SB  - IM
MH  - Animals
MH  - Blood Glucose/metabolism
MH  - Chemokine CCL2/*metabolism
MH  - Diabetes Mellitus, Experimental/*blood/therapy
MH  - Diabetic Nephropathies/*blood/*therapy
MH  - Humans
MH  - Immunohistochemistry/methods
MH  - Male
MH  - Mice
MH  - Phosphorylation
MH  - STAT1 Transcription Factor/metabolism
MH  - Suppressor of Cytokine Signaling 1 Protein
MH  - Suppressor of Cytokine Signaling Proteins/*metabolism
MH  - Transforming Growth Factor beta1/biosynthesis
EDAT- 2010/03/20 06:00
MHDA- 2010/10/13 06:00
CRDT- 2010/03/20 06:00
PHST- 2009/11/18 00:00 [received]
PHST- 2010/02/03 00:00 [accepted]
PHST- 2010/03/20 06:00 [entrez]
PHST- 2010/03/20 06:00 [pubmed]
PHST- 2010/10/13 06:00 [medline]
AID - 000286559 [pii]
AID - 10.1159/000286559 [doi]
PST - ppublish
SO  - Am J Nephrol. 2010;31(5):380-8. doi: 10.1159/000286559. Epub 2010 Mar 19.