Related Experiment Video

Updated: Jun 25, 2026

Isolation and In vitro Culture of Bone Marrow-Derived Macrophages for the Study of NO-Redox Biology
06:34

Isolation and In vitro Culture of Bone Marrow-Derived Macrophages for the Study of NO-Redox Biology

Published on: May 31, 2022

p38 MAPK signaling mediates IL-17-induced nitric oxide synthase expression in bone marrow cells

Aleksandra Krstić1, Vesna Ilić, Slavko Mojsilović

  • 1Institute for Medical Research, University of Belgrade, Belgrade, Serbia.

Growth Factors (Chur, Switzerland)
|February 11, 2009
PubMed

Insights

Interleukin-17 (IL-17) influences bone marrow cells by increasing nitric oxide synthase (NOS) expression and impacting red blood cell production via p38 MAPK signaling. This highlights a novel link between IL-17, NO, and hematopoiesis.

Area of Science:

  • Immunology
  • Hematopoiesis
  • Molecular Biology

Background:

  • Interleukin-17 (IL-17) is a cytokine with diverse biological functions.
  • The role of IL-17 in regulating hematopoiesis, particularly in bone marrow, requires further elucidation.
  • Mitogen-activated protein kinases (MAPKs) are key signaling pathways involved in cellular responses.

Purpose of the Study:

  • To investigate the effects of IL-17 on nitric oxide synthase (NOS) expression in murine bone marrow cells.
  • To determine the involvement of MAPKs, specifically p38 MAPK, in IL-17-mediated signaling.
  • To explore the impact of IL-17 on erythroid progenitor cell growth (CFU-E) and its underlying mechanisms.

Main Methods:

  • Murine bone marrow cells were treated with IL-17.
  • Expression of NOS isoforms (mRNA) and phosphorylation of p38 MAPK were analyzed.
  • In vitro and in vivo assays were used to assess CFU-E growth inhibition and the effects of NOS inhibition (L-NAME).

Main Results:

  • IL-17 upregulated mRNA expression for both inducible NOS (iNOS) and endothelial NOS (eNOS).
  • IL-17 enhanced p38 MAPK phosphorylation, and this pathway was crucial for IL-17's NOS-inducing and inhibitory effects on CFU-E growth in vitro.
  • In vivo, IL-17's inhibitory effect on bone marrow CFU-E was abolished by L-NAME, indicating mediation via NOS activation.

Conclusions:

  • IL-17 modulates bone marrow cell function through the p38 MAPK pathway, influencing NOS expression.
  • The observed effects of IL-17 on erythroid progenitor cells are mediated by nitric oxide.
  • This study reveals a significant connection between IL-17, nitric oxide, and the regulation of hematopoiesis.

More Related Videos

Bone Marrow-derived Macrophage Production07:06

Bone Marrow-derived Macrophage Production

Published on: November 22, 2013

Related Concept Videos

Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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...
NF-kB-dependent Signaling Pathway02:26

NF-kB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...