PMID- 23739770
OWN - NLM
STAT- MEDLINE
DCOM- 20140609
LR  - 20161125
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Linking)
VI  - 32
IP  - 2
DP  - 2013 Aug
TI  - Effects of a Rho kinase inhibitor on the sequential expression of ICAM-1, HIF-1alpha, 
      Bcl-2 and caspase-3 in the retina of rats with oxygen-induced retinopathy.
PG  - 457-63
LID - 10.3892/ijmm.2013.1410 [doi]
AB  - The aim of the present study was to evaluate the effects of blocking the Rho 
      kinase pathway on non-perfused regions and angiogenesis in the retina of rats 
      using a rat model of oxygen-induced retinopathy (OIR) by observing the sequential 
      expression of intercellular adhesion molecule-1 (ICAM-1), hypoxia-inducible 
      factor-1 (HIF-1), B-cell lymphoma/leukemia-2 gene (Bcl-2) and caspase-3 mRNA 
      following the administration of the Rho kinase inhibitor, fasudil (FSD). A total 
      of 240 newborn rats were randomly divided into a normoxia control (N) group, a 
      hyperoxia (H) group and a H + FSD (HF) group. The rats were sacrificed, and the 
      eyes were enucleated from postnatal day (P)12 to P21. Samples were prepared for 
      retinal flat mounts, mRNA and protein quantification. On P14, a higher number of 
      circuitous retinal veins was observed in the H group compared with the HF group. 
      In the HF group, the avascular area was significantly reduced compared with the H 
      group on P18 (P<0.01). In the HF group, the mRNA expression of Bcl-2 was 
      significantly increased on P15 compared with the N and H group (P<0.01). On P15 
      and P17 in the H group and on P13 in the HF group, the mRNA expression of ICAM‑1 
      was significantly increased compared with the other groups (P<0.05). In the H and 
      HF group, the expression of HIF-1alpha was significantly increased on P12 compared 
      with the N group (P<0.05). On P19 and P21, HIF-1alpha expression was significantly 
      increased to a maximum level in the HF group compared with the H and N group 
      (P<0.01). In conclusion, these results suggest that FSD inhibits the expression 
      of ICAM-1, assisting in the release of Bcl-2, suppressing caspase-3. In the HF 
      group, the retinal flat mounts revealed that FSD had a vasorelaxant effect. On 
      P18, a double-layered retinal vascular network was formed, and the number of 
      non-perfused regions was significantly reduced. However, the late-phase peak 
      expression of HIF-1alpha resulted in an inevitable increase in vascular endothelial 
      growth factor expression and further accelerated neovascularization and vascular 
      reconstruction in the immature retinal model.
FAU - Wang, Haiying
AU  - Wang H
AD  - Department of Ophthalmology, The Fourth People's Hospital of Shenyang, Shenyang, 
      Liaoning 110031, P.R. China.
FAU - Chen, Xiaolong
AU  - Chen X
LA  - eng
PT  - Journal Article
DEP - 20130605
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 84477-87-2 (1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine)
RN  - EC 2.7.11.1 (rho-Associated Kinases)
RN  - EC 3.4.22.- (Caspase 3)
RN  - Q0CH43PGXS (fasudil)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/analogs & derivatives/pharmacology
MH  - Animals
MH  - Caspase 3/*genetics/metabolism
MH  - Disease Models, Animal
MH  - Gene Expression Regulation/*drug effects
MH  - Hyperoxia
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/*genetics/metabolism
MH  - Intercellular Adhesion Molecule-1/*genetics/metabolism
MH  - Oxygen/adverse effects
MH  - Protein Kinase Inhibitors/*pharmacology
MH  - Proto-Oncogene Proteins c-bcl-2/*genetics/metabolism
MH  - Rats
MH  - Retinal Diseases/chemically induced/*genetics/metabolism
MH  - rho-Associated Kinases/antagonists & inhibitors
EDAT- 2013/06/07 06:00
MHDA- 2014/06/10 06:00
CRDT- 2013/06/07 06:00
PHST- 2013/02/28 00:00 [received]
PHST- 2013/05/03 00:00 [accepted]
PHST- 2013/06/07 06:00 [entrez]
PHST- 2013/06/07 06:00 [pubmed]
PHST- 2014/06/10 06:00 [medline]
AID - 10.3892/ijmm.2013.1410 [doi]
PST - ppublish
SO  - Int J Mol Med. 2013 Aug;32(2):457-63. doi: 10.3892/ijmm.2013.1410. Epub 2013 Jun 
      5.