PMID- 25031298
OWN - NLM
STAT- MEDLINE
DCOM- 20150520
LR  - 20211203
IS  - 1752-8976 (Electronic)
IS  - 1470-3203 (Linking)
VI  - 15
IP  - 3
DP  - 2014 Sep
TI  - Effect of all-trans retinoic acid treatment on prohibitin and 
      renin-angiotensin-aldosterone system expression in hypoxia-induced renal tubular 
      epithelial cell injury.
PG  - 243-9
LID - 10.1177/1470320314542727 [doi]
AB  - BACKGROUND AND OBJECTIVE: All-trans retinoic acid (ATRA) exerts various effects 
      on physiological processes such as cell growth, differentiation, apoptosis and 
      inflammation. Prohibitins (PHB), including prohibitin 1 (PHB1) and prohibitin 2 
      (PHB2), are evolutionary conserved and pleiotropic proteins implicated in various 
      cellular functions, including proliferation, tumor suppression, apoptosis, 
      transcription, and mitochondrial protein folding. The 
      renin-angiotensin-aldosterone system plays a pivotal role in the regulation of 
      blood pressure and volume homeostasis. All these factors and systems have been 
      implicated in renal interstitial fibrosis. Therefore, the objective of this study 
      was to investigate the effect of ATRA treatment on the 
      renin-angiotensin-aldosterone system and expression of prohibitins to further 
      understand its role in the processes leading to renal interstitial fibrosis. 
      METHODS: The hypoxic and oxidative stress conditions in obstructive renal disease 
      were simulated in a hypoxia/reoxygenation model with renal tubular epithelial 
      cells (RTEC) as a model system. Subsequently, the effect of ATRA on mRNA and 
      protein expression levels was determined and correlations were established 
      between factors involved in the renin-angiotensin-aldosterone system, the 
      prohibitins, cellular redox status, renal interstitial fibrosis and ATRA 
      treatment. RESULTS: Correlation analysis showed that both PHB1 and PHB2 protein 
      levels were negatively correlated with angiotensin I, ACE1, angiotensin II, 
      TGF-beta1, Col-IV, FN, ROS, and MDA (PHB1: r = -0.792, -0.834, -0.805, -0.795, 
      -0.778, -0.798, -0.751, -0.682; PHB2: r = -0.872, -0.799, -0.838, -0.773, -0.769, 
      -0.841, -0.794, -0.826; each p < 0.05), but positively correlated with ACE2, SOD, 
      and GSH (PHB1: r = 0.796, 0.879, 0.824; PHB2: r = 0.785, 0.914, 0.849; each p < 
      0.05). ACE1 was positively correlated with angiotensin I, angiotensin II, TGF-beta1, 
      Col-IV, FN, ROS, and MDA, and negatively correlated with ACE2, SOD, and GSH (each 
      p < 0.05). ACE2 was negatively correlated with ACE1, angiotensin I, angiotensin 
      II, TGF-beta1, Col-IV, FN, ROS, and MDA, and positively correlated with SOD and GSH 
      (each p < 0.05). CONCLUSION: The results suggest that ATRA acts as a positive 
      regulator of PHB1, PHB2 and ACE2, and as a negative regulator of ACE1, 
      angiotensin I, and angiotensin II in a RTEC model system under 
      hypoxia/reoxygenation conditions.
CI  - (c) The Author(s) 2014.
FAU - Zhou, Tian-Biao
AU  - Zhou TB
AD  - Department of Nephrology, the Sixth Affiliated Hospital, Sun Yat-Sen University, 
      Guangzhou, China a126tianbiao@126.com.
FAU - Ou, Chao
AU  - Ou C
AD  - Department of Experimental Pathology, The Affiliated Tumor Hospital of Guangxi 
      Medical University, NanNing China.
FAU - Rong, Liang
AU  - Rong L
AD  - Department of Pediatric-neonatology, Baylor College of Medicine, Houston, Texas, 
      USA.
FAU - Drummen, Gregor P C
AU  - Drummen GP
AD  - Cellular Stress and Ageing Program, Bionanoscience and Bio-Imaging Program, Bio & 
      Nano-Solutions, Dusseldorf, Germany.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140716
PL  - England
TA  - J Renin Angiotensin Aldosterone Syst
JT  - Journal of the renin-angiotensin-aldosterone system : JRAAS
JID - 100971636
RN  - 0 (Collagen Type IV)
RN  - 0 (Fibronectins)
RN  - 0 (Phb protein, rat)
RN  - 0 (Prohibitins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Repressor Proteins)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 11128-99-7 (Angiotensin II)
RN  - 5688UTC01R (Tretinoin)
RN  - 9041-90-1 (Angiotensin I)
RN  - EC 3.4.15.1 (Peptidyl-Dipeptidase A)
SB  - IM
MH  - Angiotensin I/genetics/metabolism
MH  - Angiotensin II/genetics/metabolism
MH  - Animals
MH  - Cell Hypoxia/drug effects
MH  - Collagen Type IV/metabolism
MH  - Epithelial Cells/*metabolism/*pathology
MH  - Fibronectins/metabolism
MH  - Kidney Tubules/*pathology
MH  - Oxidation-Reduction/drug effects
MH  - Oxidative Stress/drug effects
MH  - Peptidyl-Dipeptidase A/genetics/metabolism
MH  - Prohibitins
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Renin-Angiotensin System/*drug effects
MH  - Repressor Proteins/genetics/*metabolism
MH  - Transforming Growth Factor beta1/genetics/metabolism
MH  - Tretinoin/*pharmacology
OTO - NOTNLM
OT  - All-trans retinoic acid
OT  - angiotensin-converting enzyme 1
OT  - angiotensin-converting enzyme 2
OT  - extracellular matrix
OT  - fibrosis
OT  - oxidative stress
OT  - prohibitin 1
OT  - prohibitin 2
OT  - renal tubular epithelial cell
OT  - transforming growth factor-beta1
EDAT- 2014/07/18 06:00
MHDA- 2015/05/21 06:00
CRDT- 2014/07/18 06:00
PHST- 2014/07/18 06:00 [entrez]
PHST- 2014/07/18 06:00 [pubmed]
PHST- 2015/05/21 06:00 [medline]
AID - 1470320314542727 [pii]
AID - 10.1177/1470320314542727 [doi]
PST - ppublish
SO  - J Renin Angiotensin Aldosterone Syst. 2014 Sep;15(3):243-9. doi: 
      10.1177/1470320314542727. Epub 2014 Jul 16.