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Related Concept Videos

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Mesenchymal stem cells (MSCs) are adult stem cells that can differentiate into most connective tissue cell types, except for hematopoietic cells, depending upon the source of MSCs. For example, bone-marrow-derived MSCs (BM-MSCs) can differentiate into osteocytes, hepatocytes, and pancreatic and neuronal cells. MSCs can be isolated from various sources such as bone marrow, placenta, adipose tissue, teeth, and Wharton’s jelly, a gelatinous substance in the umbilical cord. The ease of their...
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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Mesenchymal stem cells decrease lung inflammation during sepsis, acting through inhibition of the MAPK pathway.

Leonardo Pedrazza1, Monica Cubillos-Rojas2, Fernanda Cristina de Mesquita3

  • 1Laboratório de Pesquisa em Biofísica Celular e Inflamação, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Rio Grande do Sul, CEP 90619-900, Brazil. leopedrazza@gmail.com.

Stem Cell Research & Therapy
|December 24, 2017
PubMed
Summary

Mesenchymal stem cells (MSCs) modulate the immune response in sepsis by inhibiting the mitogen-activated protein kinase (MAPK) pathway. This finding is crucial for developing new sepsis treatments by remodeling host cell responses.

Keywords:
MacrophagesMesenchymal stem cellsMitogen-activated protein kinasesSepsis

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Area of Science:

  • Immunology
  • Cell Biology
  • Pharmacology

Background:

  • Sepsis is a leading cause of global mortality with persistently high incidence.
  • Mesenchymal stem cells (MSCs) are known immune modulators with therapeutic potential in preclinical sepsis models.
  • The precise mechanisms by which MSCs alter host immune effector cells in sepsis are not fully understood.

Purpose of the Study:

  • To investigate the effects of MSCs on immune cell responses in a preclinical model of sepsis.
  • To elucidate the molecular pathways targeted by MSCs during sepsis treatment.

Main Methods:

  • Experiments utilized a mouse model of polymicrobial sepsis and in vitro co-cultures of macrophages with MSCs.
  • Key molecular markers including cyclooxygenase-2 (COX-2), nuclear factor kappa B (NF-κB), and mitogen-activated protein kinases (MAPKs) were analyzed.

Main Results:

  • In vivo, MSC treatment reduced COX-2 and NF-κB expression, leading to decreased inflammatory cytokine production.
  • In vitro, MSCs inhibited macrophage COX-2 and NF-κB expression by suppressing ERK, RSK, and p38 MAPK phosphorylation.
  • These results indicate MSCs directly impact inflammatory signaling pathways in immune cells.

Conclusions:

  • MSCs effectively inhibit MAPK pathway activation, thereby modulating the inflammatory response in sepsis.
  • Understanding MSCs' ability to remodel host immune cell responses is vital for advancing sepsis therapeutics.
  • This study provides a mechanistic basis for MSC-based therapies in sepsis management.