PMID- 31695620
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 10
DP  - 2019
TI  - Activation and Biological Properties of Human beta Defensin 4 in Stem Cells Derived 
      From Human Exfoliated Deciduous Teeth.
PG  - 1304
LID - 10.3389/fphys.2019.01304 [doi]
LID - 1304
AB  - Pulpitis in primary teeth, a condition caused by presence of bacteria, is highly 
      prevalent worldwide. The use of biocompatibility materials with 
      anti-inflammatory, anti-bacterial, and regenerative properties is critical for 
      prognosis of this endodontic disease. This study aimed to identify expression of 
      human beta defensin 4 (HBD4) in stem cells derived from human exfoliated deciduous 
      teeth (SHED) and characterize the effects of HBD4 on SHED. Quantitative 
      polymerase chain reaction (qPCR) was used to detect HBD4 expression in SHED and 
      the effect of HBD4 on inflammatory factors in lipopolysaccharide (LPS)-stimulated 
      SHED. Affinity measurement was made by the Fortebio Octet System to explore the 
      potential interaction between LPS and HBD4. Western blot analysis was used to 
      explore the effect of HBD4 on mitogen-activated protein kinase (MAPK) pathway. 
      Colony-forming unit methods and scanning electron microscopy were applied to 
      study antimicrobial effect of HBD4 on Fusobacterium nucleatum and Porphyromonas 
      gingivalis. Alkaline phosphatase staining, alizarin red staining, qPCR and 
      western blot were taken to detect effects of HBD4 on osteoblast/odontoblast 
      differentiation of SHED. RT(2) Profiler PCR Array was used to explore the 
      potential signaling pathways involved in the osteogenic/odontogenic 
      differentiation. HBD4 was highly expressed in SHED stimulated by TNF-alpha and IL-1alpha. 
      HBD4 could bind to LPS directly and down-regulate IL-1alpha, IL-1beta, IL-6, TNF-alpha in 
      LPS-stimulated SHED, thus the activation of MAPK pathway decreased. HBD4 was 
      sensitive to P. gingivalis and enhanced osteoblast/odontoblast differentiation 
      potential of SHED by modulating Notch pathway. HBD4 was highly expressed in SHED 
      stimulated by proinflammatory cytokines, and possessed anti-inflammatory, 
      anti-bacterial activity. HBD4 promoted osteogenic/odontogenic differentiation of 
      SHED. HBD4 may thus represent a suitable agent for vital pulp therapy in future 
      clinic application.
CI  - Copyright (c) 2019 Zhai, Wang, Rao, Li, Li, Fang, Zhao and Ge.
FAU - Zhai, Yue
AU  - Zhai Y
AD  - Department of Pediatric Dentistry, Peking University School and Hospital of 
      Stomatology, Beijing, China.
FAU - Wang, Yuanyuan
AU  - Wang Y
AD  - Department of Pediatric Dentistry, Peking University School and Hospital of 
      Stomatology, Beijing, China.
FAU - Rao, Nanquan
AU  - Rao N
AD  - Department of Pediatric Dentistry, Peking University School and Hospital of 
      Stomatology, Beijing, China.
FAU - Li, Jingzhi
AU  - Li J
AD  - Department of Pediatric Dentistry, Peking University School and Hospital of 
      Stomatology, Beijing, China.
FAU - Li, Xiaoxia
AU  - Li X
AD  - Department of Pediatric Dentistry, Peking University School and Hospital of 
      Stomatology, Beijing, China.
FAU - Fang, Tengjiaozi
AU  - Fang T
AD  - Department of Pediatric Dentistry, Peking University School and Hospital of 
      Stomatology, Beijing, China.
FAU - Zhao, Yuming
AU  - Zhao Y
AD  - Department of Pediatric Dentistry, Peking University School and Hospital of 
      Stomatology, Beijing, China.
FAU - Ge, Lihong
AU  - Ge L
AD  - Department of Pediatric Dentistry, Peking University School and Hospital of 
      Stomatology, Beijing, China.
LA  - eng
PT  - Journal Article
DEP - 20191022
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC6817489
OTO - NOTNLM
OT  - SHED
OT  - anti-inflammatory
OT  - human beta defensin 4
OT  - pulp regeneration
OT  - stem cell differentiation
EDAT- 2019/11/07 06:00
MHDA- 2019/11/07 06:01
PMCR- 2019/10/22
CRDT- 2019/11/08 06:00
PHST- 2019/06/13 00:00 [received]
PHST- 2019/09/30 00:00 [accepted]
PHST- 2019/11/08 06:00 [entrez]
PHST- 2019/11/07 06:00 [pubmed]
PHST- 2019/11/07 06:01 [medline]
PHST- 2019/10/22 00:00 [pmc-release]
AID - 10.3389/fphys.2019.01304 [doi]
PST - epublish
SO  - Front Physiol. 2019 Oct 22;10:1304. doi: 10.3389/fphys.2019.01304. eCollection 
      2019.