Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0031099 (
periodontitis
)
12,489
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Periodontitis
is a chronic inflammatory disease that can lead to the loss of periodontal bone tissue. The osteogenic potential of periodontal ligament stem cells (PDLSCs) is significantly decreased in
periodontitis
microenvironment. However, the mechanism is still unclear. We used Porphyromonas gingivalis lipopolysaccharide (LPS) as a stimulator of PDLSCs to mimic the periodontal inflammatory environment. The mineralization capability was restrained in LPS-stimulated PDLSCs, and the level of miR-148a increased, while the level of
Neuropilin 1
(
NRP1
) decreased. Downregulation of miR-148a could reverse the osteogenesis deficiency of PDLSCs under LPS treatment. In addition, the expression of miR-148a in PDLSCs was negatively correlated with the expression of
NRP1
. Furthermore, overexpression of
NRP1
upregulated the osteogenesis ability of LPS-stimulated PDLSCs, while inhibition of
NRP1
eliminated the stimulative effect of miR-148a inhibitor on osteogenic differentiation. These data illustrated that the inflammatory environment mimicked by LPS inhibits osteogenesis by upregulation of miR-148a and subsequent downregulation of
NRP1
. We also found, compared to healthy periodontal tissues, miR-148a level increased, while
NRP1
level decreased in
periodontitis
tissues. These two phenomena also exist in PDLSCs that come from the upper two types of tissues. To summarize, the decline of osteogenic potential of PDLSCs under inflammatory condition of
periodontitis
is related to miR-148a/
NRP1
functional axis. This study may provide a novel strategy in the molecular aspect for the therapy of
periodontitis
.
...
PMID:Dysfunction of MiR-148a-NRP1 Functional Axis Suppresses Osteogenic Differentiation of Periodontal Ligament Stem Cells Under Inflammatory Microenvironment. 3180 9