PMID- 28348463
OWN - NLM
STAT- MEDLINE
DCOM- 20170710
LR  - 20220311
IS  - 1466-1861 (Electronic)
IS  - 0962-9351 (Print)
IS  - 0962-9351 (Linking)
VI  - 2017
DP  - 2017
TI  - Human beta-Defensin 3 Reduces TNF-alpha-Induced Inflammation and Monocyte Adhesion in 
      Human Umbilical Vein Endothelial Cells.
PG  - 8529542
LID - 10.1155/2017/8529542 [doi]
LID - 8529542
AB  - The aim of this study was to investigate the role of human beta-defensin 3 (hBD3) in 
      the initiation stage of atherosclerosis with human umbilical vein endothelial 
      cells (HUVECs) triggered by tumor necrosis factor- (TNF-) alpha. The effects of hBD3 
      on TNF-alpha-induced endothelial injury and inflammatory response were evaluated. Our 
      data revealed that first, hBD3 reduced the production of interleukin-6 (IL-6), 
      IL-8, monocyte chemoattractant protein-1 (MCP-1), and macrophage migration 
      inhibitory factor (MIF) in HUVECs in a dose-dependent manner. In addition, hBD3 
      significantly prevented intracellular reactive oxygen species (ROS) production by 
      HUVECs. Second, western blot analysis demonstrated that hBD3 dose-dependently 
      suppressed the protein levels of intracellular adhesion molecule-1 (ICAM-1) and 
      vascular cell adhesion molecule-1 (VCAM-1) in TNF-alpha-induced HUVECs. As a result, 
      hBD3 inhibited monocyte adhesion to TNF-alpha-treated endothelial cells. 
      Additionally, hBD3 suppressed TNF-alpha-induced F-actin reorganization in HUVECs. 
      Third, hBD3 markedly inhibited NF-kappaB activation by decreasing the phosphorylation 
      of IKK-alpha/beta, IkappaB, and p65 subunit within 30 min. Moreover, the phosphorylation of 
      p38 and c-Jun N-terminal protein kinase (JNK) in the mitogen-activated protein 
      kinase (MAPK) pathway were also inhibited by hBD3 in HUVECs. In conclusion, hBD3 
      exerts anti-inflammatory and antioxidative effects in endothelial cells in 
      response to TNF-alpha by inhibiting NF-kappaB and MAPK signaling.
FAU - Bian, Tianying
AU  - Bian T
AD  - Department of Periodontology, Nanjing Stomatological Hospital, Medical School of 
      Nanjing University, Nanjing, Jiangsu, China; Central Laboratory of Stomatology, 
      Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 
      Jiangsu, China.
FAU - Li, Houxuan
AU  - Li H
AD  - Department of Periodontology, Nanjing Stomatological Hospital, Medical School of 
      Nanjing University, Nanjing, Jiangsu, China; Central Laboratory of Stomatology, 
      Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 
      Jiangsu, China.
FAU - Zhou, Qian
AU  - Zhou Q
AD  - Central Laboratory of Stomatology, Nanjing Stomatological Hospital, Medical 
      School of Nanjing University, Nanjing, Jiangsu, China; Department of Endodontics, 
      Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 
      Jiangsu, China.
FAU - Ni, Can
AU  - Ni C
AD  - Department of Periodontology, Nanjing Stomatological Hospital, Medical School of 
      Nanjing University, Nanjing, Jiangsu, China; Central Laboratory of Stomatology, 
      Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 
      Jiangsu, China.
FAU - Zhang, Yangheng
AU  - Zhang Y
AD  - Department of Periodontology, Nanjing Stomatological Hospital, Medical School of 
      Nanjing University, Nanjing, Jiangsu, China; Central Laboratory of Stomatology, 
      Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 
      Jiangsu, China.
FAU - Yan, Fuhua
AU  - Yan F
AUID- ORCID: 0000-0001-5632-9487
AD  - Department of Periodontology, Nanjing Stomatological Hospital, Medical School of 
      Nanjing University, Nanjing, Jiangsu, China; Central Laboratory of Stomatology, 
      Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 
      Jiangsu, China.
LA  - eng
PT  - Journal Article
DEP - 20170228
PL  - United States
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
RN  - 0 (DEFB103A protein, human)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (beta-Defensins)
SB  - IM
MH  - Blotting, Western
MH  - Cell Adhesion/drug effects
MH  - Cell Survival/drug effects
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Fluorescent Antibody Technique
MH  - Human Umbilical Vein Endothelial Cells/*drug effects/*metabolism
MH  - Humans
MH  - Inflammation/*chemically induced/*metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - beta-Defensins/*pharmacology
PMC - PMC5350351
COIS- The authors have no conflict of interests to declare.
EDAT- 2017/03/30 06:00
MHDA- 2017/07/14 06:00
PMCR- 2017/02/28
CRDT- 2017/03/29 06:00
PHST- 2016/11/27 00:00 [received]
PHST- 2017/01/27 00:00 [revised]
PHST- 2017/02/14 00:00 [accepted]
PHST- 2017/03/29 06:00 [entrez]
PHST- 2017/03/30 06:00 [pubmed]
PHST- 2017/07/14 06:00 [medline]
PHST- 2017/02/28 00:00 [pmc-release]
AID - 10.1155/2017/8529542 [doi]
PST - ppublish
SO  - Mediators Inflamm. 2017;2017:8529542. doi: 10.1155/2017/8529542. Epub 2017 Feb 
      28.