Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Caspases

Caspases

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 cells.

The Intrinsic Apoptotic Pathway

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...

The Extrinsic Apoptotic Pathway

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...

Apoptosis

Apoptosis

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 reduction of the tissue.

Regulation of Angiogenesis and Blood Supply

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...

Cellular Injury V: Apoptosis and Autophagy

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...

You might also read

Related Articles

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

Sort by

Same author

Sublingual immunotherapy in mite-sensitized patients with atopic dermatitis: a randomized controlled study.

Postepy dermatologii i alergologii·2021

Same author

Performance of Two Novel Obesity Indicators for the Management of Metabolic Syndrome in Young Adults.

Frontiers in endocrinology·2021

Same author

Has the incidence of total joint arthroplasty in rheumatoid arthritis decreased in the era of biologics use? A population-based cohort study.

Rheumatology (Oxford, England)·2021

Same author

Altered properties of human adipose-derived mesenchymal stromal cell during continuous in vitro cultivation.

Cytotechnology·2021

Same author

Baricitinib Rapidly Improves Skin Pain Resulting in Improved Quality of Life for Patients with Atopic Dermatitis: Analyses from BREEZE-AD1, 2, and 7.

Dermatology and therapy·2021

Same author

Inferring single cell expression profiles from overlapped pooling sequencing data with compressed sensing strategy.

Nucleic acids research·2021

Search research articles

Related Experiment Video

Updated: Jun 24, 2026

Detecting Anastasis In Vivo by CaspaseTracker Biosensor

Detecting Anastasis In Vivo by CaspaseTracker Biosensor

Published on: February 1, 2018

Endostar induces apoptotic effects in HUVECs through activation of caspase-3 and decrease of Bcl-2.

Yun Ling¹, Na Lu, Ying Gao

¹Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, Nanjing 210009 People's Republic of China.

Anticancer Research

|April 1, 2009

Summary

Endostar triggers apoptosis in human umbilical vein endothelial cells (HUVECs) by activating caspase-3 and reducing the Bcl-2 to Bax ratio, revealing its anti-angiogenesis mechanism.

More Related Videos

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Related Experiment Videos

Last Updated: Jun 24, 2026

Detecting Anastasis In Vivo by CaspaseTracker Biosensor

Detecting Anastasis In Vivo by CaspaseTracker Biosensor

Published on: February 1, 2018

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Area of Science:

Biochemistry
Molecular Biology
Cell Biology

Background:

Endostar, a modified recombinant human endostatin, exhibits anti-angiogenesis effects by inhibiting endothelial cell proliferation.
The precise molecular mechanisms underlying Endostar's anti-angiogenesis activity were previously unclear.

Purpose of the Study:

To elucidate the molecular mechanism by which Endostar induces apoptosis in human umbilical vein endothelial cells (HUVECs).

Main Methods:

Apoptosis was assessed using DAPI staining and Annexin V-FITC assay.
Western blotting was employed to investigate the expression of apoptosis-related proteins.

Main Results:

Endostar treatment led to significant apoptosis in HUVECs.
Caspase-3 activation was observed, while caspase-8 remained unchanged, indicating involvement of the mitochondria-mediated pathway.
Endostar treatment decreased Bcl-2 expression with minimal impact on Bax levels, altering the Bcl-2/Bax ratio.

Conclusions:

Endostar induces apoptosis in HUVECs via caspase-3 activation.
The observed decrease in the Bcl-2 to Bax ratio contributes to Endostar-induced apoptosis.