Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Role of Hematopoietic Growth Factors01:28

Role of Hematopoietic Growth Factors

Hematopoietic growth factors are molecules that regulate the differentiation rate of hematopoietic stem cells (HSCs). Erythropoietin (EPO), primarily produced by the kidneys, plays a crucial role in erythrocyte production. When oxygen levels in the blood are low, EPO is released into the bloodstream, reaching the bone marrow, where it stimulates HSCs to differentiate and mature into erythrocytes, which are vital for oxygen transport.
Thrombopoietin (TPO), mainly released by the liver,...
Factors Affecting Erythropoiesis01:24

Factors Affecting Erythropoiesis

The cardiovascular system regulates the number of erythrocytes in the bloodstream to ensure optimal oxygen transport. It also prevents over-proliferation of these cells, which helps to maintain blood viscosity and flow rate.
Several factors influence the erythrocyte production rate, with tissue oxygen level being among the most critical. Intense exercise or high altitudes can cause tissue hypoxia, which triggers the kidneys to release more erythropoietin (EPO) into the bloodstream.
EPO then...
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...
Erythropoiesis01:14

Erythropoiesis

Red blood cells  (RBCs) transport oxygen to all body tissues. These cells survive only for 120 days and then need to be replenished. Erythropoiesis is the process of RBC production. In healthy individuals, erythropoiesis ensures all tissues are amply supplied with oxygen. In addition, blood loss due to injury leads to a drop in the physiological oxygen level that will cause erythropoiesis. Any defect in erythropoiesis leads to several physiological disorders, including thalassemia, anemia, and...
Regulation of Hematopoietic Stem Cells01:01

Regulation of Hematopoietic Stem Cells

All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Is There More than One Erythropoietin Receptor? Can the Hematopoietic Effects of EPO Be Dissociated from the Organ-Protective Effects by Carbamylated Erythropoietin?: Derivatives of erythropoietin that are tissue protective but not erythropoietic. Science 305: 239-242, 2004.

Journal of the American Society of Nephrology : JASN·2023
Same author

Corrigendum to "European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)" [Redox Biol. 13 (2017) 94-162].

Redox biology·2017
Same author

It could suddenly happen: delayed rupture of the trachea after total thyroidectomy. A case report.

Il Giornale di chirurgia·2014
Same author

The erythropoietin-derived peptide ARA290 reverses mechanical allodynia in the neuritis model.

Neuroscience·2012
Same author

Beneficial effects of PKF275-055, a novel, selective, orally bioavailable, long-acting dipeptidyl peptidase IV inhibitor in streptozotocin-induced diabetic peripheral neuropathy.

The Journal of pharmacology and experimental therapeutics·2011
Same author

Targeting Toll-like receptors in autoimmunity.

Current drug targets·2009

Related Experiment Video

Updated: May 13, 2026

Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method
16:07

Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method

Published on: September 16, 2017

Erythropoietin does not affect TNF and IL-6 production directly.

I Cervellini1, S Sacre, P Ghezzi

  • 1Brighton and Sussex Medical School, Falmer, UK

Journal of Biological Regulators and Homeostatic Agents
|March 16, 2013
PubMed
Summary

Erythropoietin (EPO) does not directly inhibit inflammatory cytokines induced by cell death signals. Its anti-inflammatory effects are likely indirect, stemming from tissue protection or requiring prior injury.

More Related Videos

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro
07:51

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro

Published on: March 18, 2019

Related Experiment Videos

Last Updated: May 13, 2026

Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method
16:07

Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method

Published on: September 16, 2017

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro
07:51

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro

Published on: March 18, 2019

Area of Science:

  • Immunology
  • Cell Biology
  • Pharmacology

Background:

  • Erythropoietin (EPO) exhibits tissue-protective effects, often linked to reduced inflammation in animal models.
  • In vitro studies show conflicting results regarding EPO's impact on inflammatory cytokine production induced by lipopolysaccharide (LPS).
  • Publication bias may lead to underreporting of negative findings concerning EPO's inflammatory effects.

Purpose of the Study:

  • To investigate the hypothesis that EPO specifically inhibits inflammatory cytokine induction by danger signals associated with cell death.
  • To examine EPO's effect on interleukin-6 (IL-6) and tumor necrosis factor (TNF) induction by high-mobility group-box 1 protein (HMGB1) or necrotic cells.
  • To assess EPO's influence on responses to toll-like receptor (TLR) agonists and inflammasome activation.

Main Methods:

  • In vitro experiments using cell culture models.
  • Stimulation of cells with danger signals like HMGB1 and necrotic cells.
  • Assessment of IL-6 and TNF production.
  • Evaluation of responses to LPS, other TLR agonists, and extracellular ATP-induced inflammasome activation.

Main Results:

  • EPO did not significantly inhibit IL-6 or TNF induction by HMGB1 or necrotic cells.
  • EPO did not affect cellular responses to TLR agonists other than LPS.
  • EPO did not modulate inflammasome activation mediated by extracellular ATP.

Conclusions:

  • Direct inhibition of inflammatory cytokine induction by danger signals is not a mechanism of EPO's anti-inflammatory action.
  • EPO's anti-inflammatory effects may be indirect, secondary to its tissue-protective properties.
  • EPO's anti-inflammatory activity might necessitate prior tissue injury or priming.