PMID- 26830289
OWN - NLM
STAT- MEDLINE
DCOM- 20161213
LR  - 20200325
IS  - 1573-6903 (Electronic)
IS  - 0364-3190 (Linking)
VI  - 41
IP  - 5
DP  - 2016 May
TI  - Inhibiting Matrix Metalloproteinase 3 Ameliorates Neuronal Loss in the Ganglion 
      Cell Layer of Rats in Retinal Ischemia/Reperfusion.
PG  - 1107-18
LID - 10.1007/s11064-015-1800-1 [doi]
AB  - It has been demonstrated that matrix metalloproteinase 3 (MMP3) is integrally 
      involved in the neuronal degeneration of the central nervous system by promoting 
      glial activation, neuronal apoptosis and damage to the brain-blood barrier. 
      However, whether MMP3 also contributes to the neuronal degeneration induced by 
      retinal ischemia/reperfusion is still uncertain. In the present study, we 
      detected the cellular localization of MMP3 in adult rat retinae and explored the 
      relationship of its expression with neuronal loss in the ganglion cell layer 
      (GCL) in retinal ischemia/reperfusion. We found that MMP3 was widely expressed in 
      many cells throughout the layers of the rat retinae, including Vertebrate 
      neuron-specific nuclear protein (NeuN)-, parvalbumin-, calbindin-, protein kinase 
      C-alpha-, glial fibrillary acidic protein-, glutamine synthetase- and CD11b-positive 
      cells. Furthermore, all rats were treated with high intraocular pressure (HIOP) 
      for 1 h (h) and sacrificed at 6 h, 1 day (d), 3 d, and 7 d after HIOP. Compared 
      to the normal control, the expression of both proenzyme MMP3 and active MMP3 were 
      significantly up-regulated after HIOP treatment without alteration of the laminar 
      distribution pattern. Moreover, inhibiting MMP3 ameliorated the loss of 
      NeuN-positive cells in the GCL following HIOP. In summary, our data demonstrates 
      that MMP3 is expressed in multiple types of neurons and glial cells in normal rat 
      retinae. Simultaneously, the up-regulation of its expression and activity are 
      closely involved in neuronal loss in the GCL in retinal ischemia/reperfusion.
FAU - Hu, Tu
AU  - Hu T
AD  - Department of Anatomy and Neurobiology, School of Basic Medical Science, Central 
      South University, Changsha, 410013, Hunan Province, People's Republic of China.
FAU - You, Qiuting
AU  - You Q
AD  - Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan 
      Province, People's Republic of China.
FAU - Chen, Dan
AU  - Chen D
AD  - Department of Anatomy and Neurobiology, School of Basic Medical Science, Central 
      South University, Changsha, 410013, Hunan Province, People's Republic of China.
FAU - Tong, Jianbin
AU  - Tong J
AD  - Department of Anesthesia, The Third Xiangya Hospital of Central South University, 
      Changsha, 410013, Hunan Province, People's Republic of China.
FAU - Shang, Lei
AU  - Shang L
AD  - Department of Anatomy and Neurobiology, School of Basic Medical Science, Central 
      South University, Changsha, 410013, Hunan Province, People's Republic of China.
FAU - Luo, Jia
AU  - Luo J
AD  - Department of Anatomy and Neurobiology, School of Basic Medical Science, Central 
      South University, Changsha, 410013, Hunan Province, People's Republic of China.
FAU - Qiu, Yi
AU  - Qiu Y
AD  - Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan 
      Province, People's Republic of China.
FAU - Yu, Huimin
AU  - Yu H
AD  - Department of Ophthalmology, The Third Xiangya Hospital of Central South 
      University, Changsha, 410013, Hunan Province, People's Republic of China.
FAU - Zeng, Leping
AU  - Zeng L
AD  - Department of Anatomy and Neurobiology, School of Basic Medical Science, Central 
      South University, Changsha, 410013, Hunan Province, People's Republic of China. 
      zenglp0205@csu.edu.cn.
FAU - Huang, Jufang
AU  - Huang J
AD  - Department of Anatomy and Neurobiology, School of Basic Medical Science, Central 
      South University, Changsha, 410013, Hunan Province, People's Republic of China. 
      huangjufang@csu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160130
PL  - United States
TA  - Neurochem Res
JT  - Neurochemical research
JID - 7613461
RN  - 0 (Acetamides)
RN  - 0 (Antigens, Nuclear)
RN  - 0 (Matrix Metalloproteinase Inhibitors)
RN  - 0 (NNGH compound)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Protein Precursors)
RN  - 0 (Rbfox3 protein, rat)
RN  - 0 (Sulfonamides)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
SB  - IM
MH  - Acetamides/*pharmacology
MH  - Animals
MH  - Antigens, Nuclear/metabolism
MH  - Intraocular Pressure
MH  - Ischemia/enzymology/pathology/physiopathology
MH  - Matrix Metalloproteinase 3/*metabolism
MH  - Matrix Metalloproteinase Inhibitors/*pharmacology
MH  - Nerve Tissue Proteins/metabolism
MH  - Neuroglia/enzymology
MH  - Protein Precursors/antagonists & inhibitors/metabolism
MH  - Rats, Sprague-Dawley
MH  - Reperfusion
MH  - Retina/*drug effects/enzymology/pathology
MH  - Retinal Ganglion Cells/*drug effects/pathology
MH  - Sulfonamides/*pharmacology
OTO - NOTNLM
OT  - High intraocular pressure
OT  - Matrix metalloproteinase 3
OT  - N-Isobutyl-N-(4-methoxyphenylsulfonyl)glycyl-hydroxamic acid
OT  - Retinal ischemia/reperfusion
EDAT- 2016/02/03 06:00
MHDA- 2016/12/15 06:00
CRDT- 2016/02/03 06:00
PHST- 2015/09/21 00:00 [received]
PHST- 2015/12/09 00:00 [accepted]
PHST- 2015/12/08 00:00 [revised]
PHST- 2016/02/03 06:00 [entrez]
PHST- 2016/02/03 06:00 [pubmed]
PHST- 2016/12/15 06:00 [medline]
AID - 10.1007/s11064-015-1800-1 [pii]
AID - 10.1007/s11064-015-1800-1 [doi]
PST - ppublish
SO  - Neurochem Res. 2016 May;41(5):1107-18. doi: 10.1007/s11064-015-1800-1. Epub 2016 
      Jan 30.