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

Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...

You might also read

Related Articles

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

Sort by
Same author

Randomised trial of Aureobasidium pullulans-produced beta 1,3-1,6-glucans in patients with Duchenne muscular dystrophy: favourable changes in gut microbiota and clinical outcomes indicating their potential in epigenetic manipulation.

BMJ nutrition, prevention & health·2026
Same author

Improving the therapeutic efficacy of gene therapy for duchenne muscular dystrophy (DMD) by evaluating and managing inflammation.

Frontiers in genetics·2025
Same author

Effects of Nichi BRITE β-glucans as an onco-nutrition adjuvant in patients undergoing subtotal stomach-preserving pancreaticoduodenectomy (SSPPD) for pancreatic, bile duct and duodenal malignancies: A clinical study.

Nutrition (Burbank, Los Angeles County, Calif.)·2025
Same author

Modulation of neutrophil-to-lymphocyte ratio and gut microbiome balance in astronauts: potential benefits of novel beta-glucans during space missions.

Frontiers in immunology·2025
Same author

Efficient Control of IL-6, CRP and Ferritin in COVID-19 Patients With Two Variants of Beta-1,3-1,6 Glucans in Combination: An Open-Label, Prospective, Randomised Clinical Trial.

Global advances in integrative medicine and health·2025
Same author

Enhanced expression of dystrophin, IGF-1, CD44 and MYH3 in plasma and skeletal muscles including diaphragm of mdx mice after oral administration of Neu REFIX beta 1,3-1,6 glucan.

Scientific reports·2025

Related Experiment Video

Updated: Jul 9, 2026

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries
08:49

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

Decrease in CD93 (C1qRp) expression in a human monocyte-like cell line (U937) treated with various apoptosis-inducing

Nobunao Ikewaki1, Hidekazu Tamauchi, Hidetoshi Inoko

  • 1Kyushu University of Health, Welfare School of Health Science, Takahashi Educational Institute, Nobeoka, Miyazaki, Japan. immuneni@phoenix.ac.jp

Microbiology and Immunology
|December 21, 2007
PubMed
Summary

Human CD93 expression significantly decreases on apoptotic myeloid cells, offering a new model to study immune cell regulation during apoptosis. This research explores CD93 modulation in U937 cells undergoing apoptosis induced by chemical agents.

More Related Videos

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex
07:17

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex

Published on: August 2, 2021

Related Experiment Videos

Last Updated: Jul 9, 2026

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries
08:49

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex
07:17

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex

Published on: August 2, 2021

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Human CD93 (C1qRp) is a myeloid lineage receptor involved in phagocytosis and immune responses.
  • Previous studies showed protein kinase C (PKC) activators up-regulate CD93 expression.
  • The regulation of CD93 in apoptotic myeloid cells remains poorly understood.

Purpose of the Study:

  • To investigate the modulation of CD93 expression on human monocyte-like U937 cells during chemically induced apoptosis.
  • To analyze the secretion of soluble CD93 (sCD93) in apoptotic U937 cells.

Main Methods:

  • U937 cells were treated with apoptosis-inducing agents (ActD, CPT, CHX, EPS, MMC).
  • Apoptosis was assessed using Annexin V and 7-amino actinomycin D (7AAD) via flow cytometry.
  • CD93 expression was analyzed using flow cytometry and immunoblotting; sCD93 secretion was measured by EIA.

Main Results:

  • Apoptosis-inducing agents significantly decreased CD93 expression on U937 cells in early apoptosis.
  • Expressions of HLA-class I, HLA-class II, CD18, and CD54 were also decreased on apoptotic U937 cells.
  • Apoptotic U937 cells rapidly secreted sCD93 in the presence of PMA, but not otherwise.

Conclusions:

  • CD93 expression is dramatically decreased on U937 cells with apoptotic properties.
  • The decrease in CD93 expression on apoptotic myeloid cells provides a model for studying CD93 regulation.
  • This finding contributes to understanding immune responses during apoptosis.