Complement C5aR/LPS-induced BDNF and NGF modulation in human dental pulp stem cells

Stem cells with the ability to differentiate into a variety of cells and secrete nerve regeneration factors have become an emerging option in nerve regeneration. Dental pulp stem cells (DPSCs) appear to be a good candidate for nerve regeneration given their accessibility, neural crest origin, and ne...

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Published inScientific reports Vol. 12; no. 1; pp. 2042 - 11
Main Authors Irfan, Muhammad, Kim, Ji Hyun, Druzinsky, Robert E., Ravindran, Sriram, Chung, Seung
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 07.02.2022
Nature Publishing Group
Nature Portfolio
Subjects
631/532
631/532/2074
631/61/2320
Axonogenesis
Bone marrow
Brain-derived neurotrophic factor
Brain-Derived Neurotrophic Factor - metabolism
Cell differentiation
Complement component C5a
Dental pulp
Dental Pulp - cytology
Enzyme-linked immunosorbent assay
Fibroblasts
Humanities and Social Sciences
Humans
Inflammation
Lipopolysaccharides
Lipoteichoic acid
Mesenchymal Stem Cells - metabolism
Mesenchyme
multidisciplinary
Nerve growth factor
Nerve Growth Factor - metabolism
Nerve Regeneration - genetics
Neural crest
Receptor, Anaphylatoxin C5a - physiology
Regeneration
Science
Science (multidisciplinary)
Stem cells
Stem Cells - metabolism
Stem Cells - physiology
Online AccessGet full text
ISSN2045-2322
2045-2322
DOI10.1038/s41598-022-06110-0

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Abstract Stem cells with the ability to differentiate into a variety of cells and secrete nerve regeneration factors have become an emerging option in nerve regeneration. Dental pulp stem cells (DPSCs) appear to be a good candidate for nerve regeneration given their accessibility, neural crest origin, and neural repair qualities. We have recently demonstrated that the complement C5a system, which is an important mediator of inflammation and tissue regeneration, is activated by lipoteichoic acid-treated pulp fibroblasts, and governs the production of brain-derived nerve growth factor (BDNF). This BDNF secretion promotes neurite outgrowth towards the injury site. Here, we extend our observation to DPSCs and compare their neurogenic ability to bone marrow-derived mesenchymal stem cells (BM-MSCs) under inflammatory stimulation. Our ELISA and immunostaining data demonstrate that blocking the C5a receptor (C5aR) reduced BDNF production in DPSCs, while treatment with C5aR agonist increased the BDNF expression, which suggests that C5aR has a positive regulatory role in the BDNF modulation of DPSCs. Inflammation induced by lipopolysaccharide (LPS) treatment potentiated this effect and is C5aR dependent. Most important, DPSCs produced significantly higher levels of C5aR-mediated BDNF compared to BM-MSCs. Taken together, our data reveal novel roles for C5aR and inflammation in modulation of BDNF and NGF in DPSCs.
AbstractList Stem cells with the ability to differentiate into a variety of cells and secrete nerve regeneration factors have become an emerging option in nerve regeneration. Dental pulp stem cells (DPSCs) appear to be a good candidate for nerve regeneration given their accessibility, neural crest origin, and neural repair qualities. We have recently demonstrated that the complement C5a system, which is an important mediator of inflammation and tissue regeneration, is activated by lipoteichoic acid-treated pulp fibroblasts, and governs the production of brain-derived nerve growth factor (BDNF). This BDNF secretion promotes neurite outgrowth towards the injury site. Here, we extend our observation to DPSCs and compare their neurogenic ability to bone marrow-derived mesenchymal stem cells (BM-MSCs) under inflammatory stimulation. Our ELISA and immunostaining data demonstrate that blocking the C5a receptor (C5aR) reduced BDNF production in DPSCs, while treatment with C5aR agonist increased the BDNF expression, which suggests that C5aR has a positive regulatory role in the BDNF modulation of DPSCs. Inflammation induced by lipopolysaccharide (LPS) treatment potentiated this effect and is C5aR dependent. Most important, DPSCs produced significantly higher levels of C5aR-mediated BDNF compared to BM-MSCs. Taken together, our data reveal novel roles for C5aR and inflammation in modulation of BDNF and NGF in DPSCs.
Stem cells with the ability to differentiate into a variety of cells and secrete nerve regeneration factors have become an emerging option in nerve regeneration. Dental pulp stem cells (DPSCs) appear to be a good candidate for nerve regeneration given their accessibility, neural crest origin, and neural repair qualities. We have recently demonstrated that the complement C5a system, which is an important mediator of inflammation and tissue regeneration, is activated by lipoteichoic acid-treated pulp fibroblasts, and governs the production of brain-derived nerve growth factor (BDNF). This BDNF secretion promotes neurite outgrowth towards the injury site. Here, we extend our observation to DPSCs and compare their neurogenic ability to bone marrow-derived mesenchymal stem cells (BM-MSCs) under inflammatory stimulation. Our ELISA and immunostaining data demonstrate that blocking the C5a receptor (C5aR) reduced BDNF production in DPSCs, while treatment with C5aR agonist increased the BDNF expression, which suggests that C5aR has a positive regulatory role in the BDNF modulation of DPSCs. Inflammation induced by lipopolysaccharide (LPS) treatment potentiated this effect and is C5aR dependent. Most important, DPSCs produced significantly higher levels of C5aR-mediated BDNF compared to BM-MSCs. Taken together, our data reveal novel roles for C5aR and inflammation in modulation of BDNF and NGF in DPSCs.Stem cells with the ability to differentiate into a variety of cells and secrete nerve regeneration factors have become an emerging option in nerve regeneration. Dental pulp stem cells (DPSCs) appear to be a good candidate for nerve regeneration given their accessibility, neural crest origin, and neural repair qualities. We have recently demonstrated that the complement C5a system, which is an important mediator of inflammation and tissue regeneration, is activated by lipoteichoic acid-treated pulp fibroblasts, and governs the production of brain-derived nerve growth factor (BDNF). This BDNF secretion promotes neurite outgrowth towards the injury site. Here, we extend our observation to DPSCs and compare their neurogenic ability to bone marrow-derived mesenchymal stem cells (BM-MSCs) under inflammatory stimulation. Our ELISA and immunostaining data demonstrate that blocking the C5a receptor (C5aR) reduced BDNF production in DPSCs, while treatment with C5aR agonist increased the BDNF expression, which suggests that C5aR has a positive regulatory role in the BDNF modulation of DPSCs. Inflammation induced by lipopolysaccharide (LPS) treatment potentiated this effect and is C5aR dependent. Most important, DPSCs produced significantly higher levels of C5aR-mediated BDNF compared to BM-MSCs. Taken together, our data reveal novel roles for C5aR and inflammation in modulation of BDNF and NGF in DPSCs.
Abstract Stem cells with the ability to differentiate into a variety of cells and secrete nerve regeneration factors have become an emerging option in nerve regeneration. Dental pulp stem cells (DPSCs) appear to be a good candidate for nerve regeneration given their accessibility, neural crest origin, and neural repair qualities. We have recently demonstrated that the complement C5a system, which is an important mediator of inflammation and tissue regeneration, is activated by lipoteichoic acid-treated pulp fibroblasts, and governs the production of brain-derived nerve growth factor (BDNF). This BDNF secretion promotes neurite outgrowth towards the injury site. Here, we extend our observation to DPSCs and compare their neurogenic ability to bone marrow-derived mesenchymal stem cells (BM-MSCs) under inflammatory stimulation. Our ELISA and immunostaining data demonstrate that blocking the C5a receptor (C5aR) reduced BDNF production in DPSCs, while treatment with C5aR agonist increased the BDNF expression, which suggests that C5aR has a positive regulatory role in the BDNF modulation of DPSCs. Inflammation induced by lipopolysaccharide (LPS) treatment potentiated this effect and is C5aR dependent. Most important, DPSCs produced significantly higher levels of C5aR-mediated BDNF compared to BM-MSCs. Taken together, our data reveal novel roles for C5aR and inflammation in modulation of BDNF and NGF in DPSCs.
ArticleNumber 2042
Author Chung, Seung
Irfan, Muhammad
Druzinsky, Robert E.
Ravindran, Sriram
Kim, Ji Hyun
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  surname: Irfan
  fullname: Irfan, Muhammad
  organization: Department of Oral Biology, College of Dentistry, University of Illinois Chicago
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  givenname: Ji Hyun
  surname: Kim
  fullname: Kim, Ji Hyun
  organization: Department of Oral Biology, College of Dentistry, University of Illinois Chicago
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  surname: Druzinsky
  fullname: Druzinsky, Robert E.
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  surname: Chung
  fullname: Chung, Seung
  email: chungsh@uic.edu
  organization: Department of Oral Biology, College of Dentistry, University of Illinois Chicago
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  publication-title: Stem Cells Transl. Med.
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  publication-title: Stem cells
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Snippet Stem cells with the ability to differentiate into a variety of cells and secrete nerve regeneration factors have become an emerging option in nerve...
Abstract Stem cells with the ability to differentiate into a variety of cells and secrete nerve regeneration factors have become an emerging option in nerve...
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Axonogenesis
Bone marrow
Brain-derived neurotrophic factor
Brain-Derived Neurotrophic Factor - metabolism
Cell differentiation
Complement component C5a
Dental pulp
Dental Pulp - cytology
Enzyme-linked immunosorbent assay
Fibroblasts
Humanities and Social Sciences
Humans
Inflammation
Lipopolysaccharides
Lipoteichoic acid
Mesenchymal Stem Cells - metabolism
Mesenchyme
multidisciplinary
Nerve growth factor
Nerve Growth Factor - metabolism
Nerve Regeneration - genetics
Neural crest
Receptor, Anaphylatoxin C5a - physiology
Regeneration
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Science (multidisciplinary)
Stem cells
Stem Cells - metabolism
Stem Cells - physiology
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Title Complement C5aR/LPS-induced BDNF and NGF modulation in human dental pulp stem cells
URI https://link.springer.com/article/10.1038/s41598-022-06110-0
https://www.ncbi.nlm.nih.gov/pubmed/35132159
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Volume 12
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