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

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

6.6K
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...
6.6K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

6.4K
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...
6.4K
Complement System01:27

Complement System

2.4K
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
2.4K
Caspases01:24

Caspases

12.6K
Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
12.6K
Apoptosis01:30

Apoptosis

11.6K
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
11.6K
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

3.9K
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...
3.9K

You might also read

Related Articles

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

Sort by
Same author

Genome-wide identification, evolutionary dynamics, and abiotic stress response networks of the magnesium transporter gene family in foxtail millet (<i>Setaria italica</i> L.).

Frontiers in plant science·2026
Same author

The effects of flavonoids on female animal reproductive performance.

Reproductive biology·2026
Same author

K-SALT Equation for Urinary Sodium Estimation in CKD.

Kidney international reports·2026
Same author

6-Methoxyluteolin from the Invasive Plant <i>Tithonia diversifolia</i> Suppresses Melanization and Impairs Epidermal Integrity in <i>Spodoptera litura</i> Larvae.

Insects·2026
Same author

Efficacy and safety analysis of double plasma molecular adsorption system plus plasma exchange for treating acute-on-chronic liver failure.

American journal of translational research·2026
Same author

Clinicopathological and prognostic significance of immune-related PD-L1 expression in locally advanced gastric cancer with HER2-low expression.

Pathology, research and practice·2026

Related Experiment Video

Updated: Jul 15, 2025

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

2.6K

Complement C3 Reduces Apoptosis via Interaction with the Intrinsic Apoptotic Pathway.

Zhou Fang1, Haekyung Lee1, Junying Liu1

  • 1Departments of Anesthesiology, SUNY Downstate Health Science University, 450 Clarkson Avenue, Brooklyn, NY 11203, USA.

Cells
|September 28, 2023
PubMed
Summary

Complement C3 significantly reduces heart cell apoptosis after ischemia/reperfusion injury. This protein interacts with the intrinsic apoptosis pathway, offering a potential therapeutic target for heart attack recovery.

Keywords:
apoptosiscomplement C3cytochrome cischemia/reperfusion injury (IRI)pro-caspase 3

More Related Videos

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

17.5K
Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

8.7K

Related Experiment Videos

Last Updated: Jul 15, 2025

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

2.6K
Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

17.5K
Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

8.7K

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Cellular Apoptosis

Background:

  • Myocardial ischemia/reperfusion (I/R) injury triggers inflammation involving complement factors.
  • Previous studies indicated reduced necrosis in complement C3-deficient mice post-I/R.
  • The role of C3 in myocardial apoptosis remained to be elucidated.

Purpose of the Study:

  • To investigate the effect of complement C3 on myocardial apoptosis following I/R injury.
  • To determine if C3 regulates apoptosis in human cardiomyocytes.
  • To explore the molecular mechanisms underlying C3's action on apoptosis.

Main Methods:

  • Utilized a mouse model of heart I/R.
  • Employed comparative proteomics to identify proteins within the myocardial C3 complex.
  • Conducted cell culture experiments with human cardiomyocytes and a cell-free apoptosis system.

Main Results:

  • Cytochrome c was identified within the myocardial C3 complex in wild-type mice post-I/R.
  • Exogenous human C3 reduced apoptosis in human cardiomyocytes lacking endogenous C3.
  • Human C3 inhibited the intrinsic apoptosis pathway in a cell-free system and bound pro-caspase 3.

Conclusions:

  • Complement C3 plays a protective role by reducing myocardial apoptosis after I/R injury.
  • C3 directly interacts with the intrinsic apoptosis pathway, involving pro-caspase 3.
  • These findings highlight C3 as a potential therapeutic target for mitigating I/R-induced cardiac damage.