PMID- 28390948
OWN - NLM
STAT- MEDLINE
DCOM- 20181127
LR  - 20181127
IS  - 0925-4439 (Print)
IS  - 0925-4439 (Linking)
VI  - 1863
IP  - 6
DP  - 2017 Jun
TI  - Relationship of angiotensin I-converting enzyme (ACE) and bradykinin B2 receptor 
      (BDKRB2) polymorphism with diabetic nephropathy.
PG  - 1264-1272
LID - S0925-4439(17)30114-X [pii]
LID - 10.1016/j.bbadis.2017.04.002 [doi]
AB  - PURPOSE: To determine whether ACE(2) I/D and BDKRB2(3) +9/-9 polymorphism 
      causatively affect diabetic nephropathy progression RESULTS: STZ-induced 
      metabolic disorder, as well as inflammatory responses, was significantly 
      aggravated in ACE II-B2R(4)+9bp, ACE DD-B2R+9bp, or ACE DD-B2R-9bp diabetic mice 
      but not ACE II-B2R-9bp, indicating the genetic susceptibility of ACE DD or 
      B2R+9bp to diabetic nephropathy. Furthermore, ACE II-B2R+9bp, ACE DD-B2R+9bp, or 
      ACE DD-B2R-9bp rather than ACE II-B2R-9bp, worsened renal performance and 
      enhanced pathological alterations induced by STZ. Markedly elevated monocyte 
      chemoattractant protein-1(MCP-1), podocin, osteopontin (OPN), transforming growth 
      factor-beta1 (TGF-beta1), and reduced nephrin, podocin were also detected both in 
      diabetic mice and podocytes under hyperglycemic conditions in response to ACE 
      II-B2R+9bp, ACE DD-B2R+9bp, or ACE DD-B2R-9bp, versus ACE II-B2R-9bp. In 
      addition, high glucose-induced mitochondrial oxidative stress and cell apoptosis 
      were observably increased in response to ACE II-B2R+9bp, ACE DD-B2R+9bp, or ACE 
      DD-B2R-9bp but not ACE II-B2R-9bp. CONCLUSIONS: We provide first evidence 
      indicating the causation between ACE DD or B2R+9bp genotype and the increased 
      risk for diabetic nephropathy, broadening our horizon about the role of genetic 
      modulators in this disease.
CI  - Copyright (c) 2017 Elsevier B.V. All rights reserved.
FAU - Zou, Honghong
AU  - Zou H
AD  - Medical Center of the Graduate School, Nanchang University, Nanchang, China.
FAU - Wu, Guoqing
AU  - Wu G
AD  - Department of Nephrology, the Affiliated Hospital of Jiangxi University of 
      Traditional Chinese Medicine, Nanchang, China.
FAU - Lv, Jinlei
AU  - Lv J
AD  - Department of Nephrology, the First Affiliated Hospital of Nanchang University, 
      No.17, Yongwai Street, Donghu District, Nanchang, China.
FAU - Xu, Gaosi
AU  - Xu G
AD  - Department of Nephrology, the Second Affiliated Hospital of Nanchang University, 
      No. 1, Minde Road, Donghu District, Nanchang, China. Electronic address: 
      gaosi_xu@126.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170405
PL  - Netherlands
TA  - Biochim Biophys Acta Mol Basis Dis
JT  - Biochimica et biophysica acta. Molecular basis of disease
JID - 101731730
RN  - 0 (Receptor, Bradykinin B2)
RN  - EC 3.4.15.1 (Peptidyl-Dipeptidase A)
SB  - IM
EIN - Biochim Biophys Acta. 2017 Dec 26;:. PMID: 29288064
MH  - Animals
MH  - *Diabetic Nephropathies/genetics/metabolism/pathology
MH  - Mice
MH  - *Peptidyl-Dipeptidase A/genetics/metabolism
MH  - Podocytes/*metabolism/pathology
MH  - *Polymorphism, Genetic
MH  - *Receptor, Bradykinin B2/genetics/metabolism
OTO - NOTNLM
OT  - ACE I/D polymorphism
OT  - BDKRB2 +9/-9 polymorphism
OT  - Diabetic nephropathy
OT  - Mitochondrial oxidative stress
EDAT- 2017/04/10 06:00
MHDA- 2018/11/28 06:00
CRDT- 2017/04/10 06:00
PHST- 2017/01/16 00:00 [received]
PHST- 2017/03/21 00:00 [revised]
PHST- 2017/04/04 00:00 [accepted]
PHST- 2017/04/10 06:00 [pubmed]
PHST- 2018/11/28 06:00 [medline]
PHST- 2017/04/10 06:00 [entrez]
AID - S0925-4439(17)30114-X [pii]
AID - 10.1016/j.bbadis.2017.04.002 [doi]
PST - ppublish
SO  - Biochim Biophys Acta Mol Basis Dis. 2017 Jun;1863(6):1264-1272. doi: 
      10.1016/j.bbadis.2017.04.002. Epub 2017 Apr 5.