PMID- 26012521
OWN - NLM
STAT- MEDLINE
DCOM- 20160809
LR  - 20151009
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Linking)
VI  - 116
IP  - 12
DP  - 2015 Dec
TI  - MicroRNA-155 Regulates ROS Production, NO Generation, Apoptosis and Multiple 
      Functions of Human Brain Microvessel Endothelial Cells Under Physiological and 
      Pathological Conditions.
PG  - 2870-81
LID - 10.1002/jcb.25234 [doi]
AB  - The microRNA-155 (miR155) regulates various functions of cells. Dysfunction or 
      injury of endothelial cells (ECs) plays an important role in the pathogenesis of 
      various vascular diseases. In this study, we investigated the role and potential 
      mechanisms of miR155 in human brain microvessel endothelial cells (HBMECs) under 
      physiological and pathological conditions. We detected the effects of miR155 
      silencing on ROS production, NO generation, apoptosis and functions of HBMECs at 
      basal and in response to oxidized low density lipoprotein (ox-LDL). Western blot 
      and q-PCR were used for analyzing the gene expression of epidermal growth factor 
      receptor (EGFR)/extracellular regulated protein kinases (ERK)/p38 
      mitogen-activated protein kinase (p38 MAPK), phosphatidylinositol-3-kinase (PI3K) 
      and serine/threonine kinase(Akt), activated caspase-3, and intercellular adhesion 
      molecule-1 (ICAM-1). Results showed that under both basal and challenge 
      situations: (1) Silencing of miR155 decreased apoptosis and reactive oxygen 
      species (ROS) production of HBMECs, whereas, promoted nitric oxide (NO) 
      generation. (2) Silencing of miR155 increased the proliferation, migration, and 
      tube formation ability of HBMECs, while decreased cell adhesion ability. (3) Gene 
      expression analyses showed that EGFR/ERK/p38 MAPK and PI3K/Akt were increased and 
      that activated caspase-3 and ICAM-1 mRNA were decreased after knockdown of 
      miR155. In conclusion, knockdown of miR155 could modulate ROS production, NO 
      generation, apoptosis and function of HBMECs via regulating diverse gene 
      expression, such as caspase-3, ICAM-1 and EGFR/ERK/p38 MAPK and PI3K/Akt 
      pathways.
CI  - (c) 2015 Wiley Periodicals, Inc.
FAU - Liu, Yajing
AU  - Liu Y
AD  - Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Institute 
      of Neurology, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 
      524001, China.
FAU - Pan, Qunwen
AU  - Pan Q
AD  - Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Institute 
      of Neurology, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 
      524001, China.
FAU - Zhao, Yuhui
AU  - Zhao Y
AD  - Department of Pharmacology and Toxicology, Boonshoft School of Medicine, Wright 
      State University, Dayton, Ohio, 45435.
FAU - He, Caixia
AU  - He C
AD  - Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Institute 
      of Neurology, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 
      524001, China.
FAU - Bi, Kexia
AU  - Bi K
AD  - Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Institute 
      of Neurology, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 
      524001, China.
FAU - Chen, Yusen
AU  - Chen Y
AD  - Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Institute 
      of Neurology, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 
      524001, China.
FAU - Zhao, Bin
AU  - Zhao B
AD  - Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Institute 
      of Neurology, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 
      524001, China.
FAU - Chen, Yanfang
AU  - Chen Y
AD  - Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Institute 
      of Neurology, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 
      524001, China.
AD  - Department of Pharmacology and Toxicology, Boonshoft School of Medicine, Wright 
      State University, Dayton, Ohio, 45435.
FAU - Ma, Xiaotang
AU  - Ma X
AD  - Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Institute 
      of Neurology, Affiliated Hospital of Guangdong Medical College, Zhanjiang, 
      524001, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (MIRN155 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (oxidized low density lipoprotein)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Apoptosis/genetics
MH  - Brain/*metabolism/pathology
MH  - Caspase 3/biosynthesis
MH  - Endothelial Cells/metabolism/pathology
MH  - Gene Expression Regulation
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/biosynthesis
MH  - Lipoproteins, LDL/metabolism
MH  - MicroRNAs/antagonists & inhibitors/*genetics/metabolism
MH  - Microvessels/metabolism/pathology
MH  - Nitric Oxide/biosynthesis/*metabolism
MH  - Proto-Oncogene Proteins c-akt/biosynthesis
MH  - Reactive Oxygen Species/*metabolism
MH  - Signal Transduction/genetics
MH  - p38 Mitogen-Activated Protein Kinases/biosynthesis
OTO - NOTNLM
OT  - CELL FUNCTION
OT  - HUMAN BRAIN MICROVESSEL ENDOTHELIAL CELLS
OT  - ISCHEMIC STROKE
OT  - OXIDATIVE STRESS
OT  - REGULATORY MECHANISM
OT  - miR155
EDAT- 2015/05/28 06:00
MHDA- 2016/08/10 06:00
CRDT- 2015/05/28 06:00
PHST- 2015/01/09 00:00 [received]
PHST- 2015/05/14 00:00 [accepted]
PHST- 2015/05/28 06:00 [entrez]
PHST- 2015/05/28 06:00 [pubmed]
PHST- 2016/08/10 06:00 [medline]
AID - 10.1002/jcb.25234 [doi]
PST - ppublish
SO  - J Cell Biochem. 2015 Dec;116(12):2870-81. doi: 10.1002/jcb.25234.