PMID- 30206961
OWN - NLM
STAT- MEDLINE
DCOM- 20191231
LR  - 20210721
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Linking)
VI  - 120
IP  - 1
DP  - 2019 Jan
TI  - Effects of RNA interference-mediated E-selectin gene silencing on cell adhesion 
      molecule expression and cell-cell adhesion in vascular endothelial cells in mice 
      with immunologic contact urticaria.
PG  - 115-125
LID - 10.1002/jcb.27150 [doi]
AB  - Contact urticaria is recognized as the wheal and flare reaction at a site from 
      direct contact with a chemical or protein agent. Ongoing studies have proposed 
      that gene silencing may have a promising future in finding optimal treatment of a 
      variety of disease; hence, the aim of the study was to investigate the effect of 
      RNA interference-mediated E-selectin ( SELE) gene silencing on cell adhesion 
      molecule expression and on cell-cell adhesion in vascular endothelial cells 
      (VECs) in a mouse model of immunologic contact urticaria (ICU). Following the 
      successful establishment of mouse models of ICU induced by antidinitrophenol 
      immunoglobulin E (IgE) combining 2,4-dinitrofluorobenzene challenge, 
      enzyme-linked immunosorbent assay and immunohistochemistry were used to measure 
      the levels of IgE, interleukin 4 (IL-4), interferon-gamma (IFN-gamma), and histamine as 
      well as the positive expression rate of SELE, respectively. The siRNA- SELE 
      vector was constructed and transfection efficiency was estimated prior to 
      performing quantitative reverse-transcription polymerase chain reaction and 
      Western blot assay to determine the relative expression of SELE, eosinophil 
      cationic protein (ECP), intercellular adhesion molecule 1 (ICAM-1), 
      L-selectin (CD62L), and the alpha chain of leukocyte function-associated 
      antigen-1 (CD11a). Adhesion assay was then performed to assess the cell adhesion 
      ability in VECs. Elevated levels of IgE, IL-4, IFN-gamma, and histamine and increased 
      positive expression rate of SELE were indicative of successful establishment of 
      mouse models of ICU. Furthermore, the relative expression levels of SELE, ECP, 
      ICAM-1, CD62L, and CD11a were highest in the OE- SELE group. Besides, cell 
      adhesion ability of VECs was notably promoted. Collectively, the current study 
      define the potential role of SELE silencing as an inhibitor to ICU development by 
      inhibiting cell adhesion ability of VECs.
CI  - (c) 2018 Wiley Periodicals, Inc.
FAU - Meng, Zu-Dong
AU  - Meng ZD
AD  - The First Department of Dermatology, Renmin Hospital, Hubei University of 
      Medicine, Shiyan, China.
FAU - Wang, Xiao-Lan
AU  - Wang XL
AD  - The First Department of Dermatology, Renmin Hospital, Hubei University of 
      Medicine, Shiyan, China.
FAU - Du, Tian-Ping
AU  - Du TP
AD  - Department of Neurosurgery, Renmin Hospital, Hubei University of Medicine, 
      Shiyan, China.
FAU - Wang, Yu
AU  - Wang Y
AD  - The First Department of Dermatology, Renmin Hospital, Hubei University of 
      Medicine, Shiyan, China.
FAU - Qin, Gui-Fang
AU  - Qin GF
AD  - The Second Department of Dermatology, Renmin Hospital, Hubei University of 
      Medicine, Shiyan, China.
FAU - Zhao, Hong-Bo
AU  - Zhao HB
AD  - The Second Department of Dermatology, Renmin Hospital, Hubei University of 
      Medicine, Shiyan, China.
FAU - Chen, Yu-Jie
AU  - Chen YJ
AD  - The First Department of Dermatology, Renmin Hospital, Hubei University of 
      Medicine, Shiyan, China.
FAU - Tian, Bo
AU  - Tian B
AUID- ORCID: 0000-0003-2364-7117
AD  - The Second Department of Dermatology, Renmin Hospital, Hubei University of 
      Medicine, Shiyan, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Retracted Publication
DEP - 20180911
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (E-Selectin)
RN  - 0 (IFNG protein, mouse)
RN  - 0 (Icam1 protein, mouse)
RN  - 0 (Il4 protein, mouse)
RN  - 0 (RNA, Small Interfering)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 207137-56-2 (Interleukin-4)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 820484N8I3 (Histamine)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
RIN - J Cell Biochem. 2021 Nov;122 Suppl 1:S112. PMID: 34288054
MH  - Animals
MH  - Cell Adhesion/*drug effects
MH  - Cell Line, Tumor
MH  - Disease Models, Animal
MH  - E-Selectin/*genetics/metabolism
MH  - Endothelial Cells/*metabolism
MH  - Endothelium, Vascular/pathology
MH  - Female
MH  - Genetic Therapy/*methods
MH  - Histamine/metabolism
MH  - Humans
MH  - Immunoglobulin E/metabolism
MH  - Intercellular Adhesion Molecule-1/*metabolism
MH  - Interferon-gamma/metabolism
MH  - Interleukin-4/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - *RNA Interference
MH  - RNA, Small Interfering/genetics
MH  - Urticaria/chemically induced/*therapy
OTO - NOTNLM
OT  - E-selectin
OT  - RNA interference
OT  - cell adhesion molecule
OT  - cell-cell adhesion
OT  - gene silencing
OT  - immunologic contact urticaria
OT  - vascular endothelial cells
EDAT- 2018/09/13 06:00
MHDA- 2020/01/01 06:00
CRDT- 2018/09/13 06:00
PHST- 2017/12/18 00:00 [received]
PHST- 2018/05/18 00:00 [accepted]
PHST- 2018/09/13 06:00 [pubmed]
PHST- 2020/01/01 06:00 [medline]
PHST- 2018/09/13 06:00 [entrez]
AID - 10.1002/jcb.27150 [doi]
PST - ppublish
SO  - J Cell Biochem. 2019 Jan;120(1):115-125. doi: 10.1002/jcb.27150. Epub 2018 Sep 
      11.