PMID- 22717542
OWN - NLM
STAT- MEDLINE
DCOM- 20130103
LR  - 20220701
IS  - 1941-7225 (Electronic)
IS  - 0895-7061 (Linking)
VI  - 25
IP  - 9
DP  - 2012 Sep
TI  - Carboxyl terminus of heat shock protein 70-interacting protein inhibits 
      angiotensin II-induced cardiac remodeling.
PG  - 994-1001
LID - 10.1038/ajh.2012.74 [doi]
AB  - BACKGROUND: The carboxyl terminus of heat shock protein 70-interacting protein 
      (CHIP), an E3 ligase/chaperone, was found to protect cardiomyocytes against 
      apoptosis induced by ischemic injury; however, the functional role of CHIP in 
      remodeling induced by angiotensin II (Ang II) remains unclear. METHODS: We 
      generated CHIP-overexpressed transgenic (TG) mice infused with Ang II (1,500 
      ng/kg/min) or saline for days or small interfering RNA (siRNA) knockdown of 
      neonatal rat cardiomyocytes. Heart sections were stained with hematoxylin and 
      eosin, Masson trichrome, TdT-mediated dUTP nick-end labeling (TUNEL) staining, 
      and immunohistochemistry, and the levels of nuclear factor-kappaB (NF-kappaB) and 
      mitogen-activated protein kinases (MAPK) were measured by western blot analysis. 
      RESULTS: Seven days after Ang II infusion, cardiac-specific overexpression of 
      CHIP significantly enhanced cardiac contractile performance in mice and 
      attenuated cardiac apoptosis, fibrosis, and inflammation: the number of 
      TUNEL-positive cells, fibrotic areas, macrophage infiltration, and the expression 
      of interleukin-1beta (IL-1beta), IL-6, monocyte chemoattractant protein-1 (MCP-1) and 
      intercellular adhesion molecule-1 (ICAM-1) in heart tissues were decreased as 
      compared with wild-type (WT) mice (all P < 0.05). In contrast, CHIP siRNA 
      knockdown markedly increased Ang II-induced apoptosis and the expression of 
      proinflammatory cytokines, as compared with siRNA control. The mechanisms 
      underlying these beneficial actions were associated with CHIP-mediated inhibition 
      of NF-kappaB and MAPK (p38 and JNK) pathways. CONCLUSIONS: CHIP plays an important 
      role in regulating Ang II-triggered hypertensive cardiac apoptosis, inflammation, 
      and fibrosis.
FAU - Yang, Kun
AU  - Yang K
AD  - Department of Pathology, Institute of Basic Medical Sciences, Chinese Academy of 
      Medical Sciences and Peking Union Medical College, Beijing, China.
FAU - Zhang, Tian-Peng
AU  - Zhang TP
FAU - Tian, Cui
AU  - Tian C
FAU - Jia, Li-Xin
AU  - Jia LX
FAU - Du, Jie
AU  - Du J
FAU - Li, Hui-Hua
AU  - Li HH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120621
PL  - United States
TA  - Am J Hypertens
JT  - American journal of hypertension
JID - 8803676
RN  - 0 (Angiotensins)
RN  - 0 (NF-kappa B)
RN  - 11128-99-7 (Angiotensin II)
RN  - EC 2.3.2.27 (Stub1 protein, mouse)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
EIN - Am J Hypertens. 2022 Jul 1;35(7):677-678. PMID: 35776550
MH  - Angiotensin II/*drug effects
MH  - Angiotensins/*antagonists & inhibitors
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Fibrosis
MH  - Heart/*drug effects
MH  - Mice
MH  - Mice, Transgenic
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - Myocardium/pathology
MH  - Myocytes, Cardiac
MH  - NF-kappa B/antagonists & inhibitors
MH  - Rats
MH  - Ubiquitin-Protein Ligases/biosynthesis/*physiology
MH  - Ventricular Remodeling/physiology
EDAT- 2012/06/22 06:00
MHDA- 2013/01/04 06:00
CRDT- 2012/06/22 06:00
PHST- 2012/06/22 06:00 [entrez]
PHST- 2012/06/22 06:00 [pubmed]
PHST- 2013/01/04 06:00 [medline]
AID - ajh201274 [pii]
AID - 10.1038/ajh.2012.74 [doi]
PST - ppublish
SO  - Am J Hypertens. 2012 Sep;25(9):994-1001. doi: 10.1038/ajh.2012.74. Epub 2012 Jun 
      21.