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

Intracellular Signaling Cascades01:24

Intracellular Signaling Cascades

53.8K
Once a ligand binds to a receptor, the signal is transmitted through the membrane and into the cytoplasm. The continuation of a signal in this manner is called signal transduction. Signal transduction only occurs with cell-surface receptors, which cannot interact with most components of the cell, such as DNA. Only internal receptors can interact directly with DNA in the nucleus to initiate protein synthesis. When a ligand binds to its receptor, conformational changes occur that affect the...
53.8K
Rab Cascades01:25

Rab Cascades

3.6K
Rab GTPases act in a regulated cascade during membrane fusion, helping the lipid bilayers mix. The Rab family of proteins are active when bound to GTP, and inactive when bound to GDP. Hence, they act as guanine nucleotide-dependent molecular switches. Rab-GTP recognizes and binds to long or short-range tethering proteins to capture the target vesicle. These tethers coordinate with SNAREs on the vesicle and the target membrane to assemble the trans SNARE complex that locks the mixing bilayers.
3.6K
Complement System01:27

Complement System

11.0K
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...
11.0K
Complementation Tests00:49

Complementation Tests

6.3K
A complementation test is a simple cross to identify whether the two mutations are located on the same gene or different genes. It was first performed by Edward Lewis in the 1940s while working on fruit flies. He developed the test to identify the location and arrangement of different mutations on chromosomes.
Organisms heterozygous for different mutations are crossed pairwise in all combinations. If present on different genes, the mutations can complement each other by providing the missing...
6.3K
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

18.7K
When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
18.7K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

8.6K
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...
8.6K

You might also read

Related Articles

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

Sort by
Same author

Tet-ON and Tet-OFF regulation in hypervirulent <i>Klebsiella pneumoniae</i>.

Microbiology spectrum·2026
Same author

Pharmacokinetic robustness of direct oral anticoagulants vs. phenprocoumon in the emergency setting: impact of renal and hepatic impairment.

European journal of internal medicine·2026
Same author

Letter to the editor: 'Advances in biomarker discovery for peripartum cardiomyopathy: current status and future directions'.

Expert review of cardiovascular therapy·2026
Same author

Novel bioactive glass CAR12N versus BG1393: CAR12N enhances chondrogenic marker expression in chondrocytes and human mesenchymal stem cells.

Biomaterials advances·2026
Same author

Special Issue "Ligament/Tendon and Cartilage Tissue Engineering and Reconstruction".

International journal of molecular sciences·2026
Same author

D-dimer levels and outcomes in heart failure with mildly reduced ejection fraction.

International journal of cardiology. Heart & vasculature·2026

Related Experiment Video

Updated: Feb 14, 2026

Depletion of Specific Cell Populations by Complement Depletion
06:17

Depletion of Specific Cell Populations by Complement Depletion

Published on: February 5, 2010

22.7K

Osteoarthritis and the Complement Cascade.

Sandeep Silawal1,2, Jakob Triebel3, Thomas Bertsch3

  • 1Department of Anatomy, Paracelsus Medical University, Nuremberg, Germany.

Clinical Medicine Insights. Arthritis and Musculoskeletal Disorders
|February 14, 2018
PubMed
Summary

Complement activation contributes to osteoarthritis (OA) pathogenesis by influencing cartilage degradation and inflammation. Balancing complement activity may offer a future therapeutic strategy for OA treatment and progression prevention.

Keywords:
Osteoarthritischondrocytecomplementexercise

More Related Videos

Ameliorating Osteoarthritis in Mice Using Silver Nanoparticles
05:50

Ameliorating Osteoarthritis in Mice Using Silver Nanoparticles

Published on: June 2, 2023

1.9K
Author Spotlight: Fu's Subcutaneous Needling for Knee Osteoarthritis Pain
07:19

Author Spotlight: Fu's Subcutaneous Needling for Knee Osteoarthritis Pain

Published on: March 24, 2023

6.1K

Related Experiment Videos

Last Updated: Feb 14, 2026

Depletion of Specific Cell Populations by Complement Depletion
06:17

Depletion of Specific Cell Populations by Complement Depletion

Published on: February 5, 2010

22.7K
Ameliorating Osteoarthritis in Mice Using Silver Nanoparticles
05:50

Ameliorating Osteoarthritis in Mice Using Silver Nanoparticles

Published on: June 2, 2023

1.9K
Author Spotlight: Fu's Subcutaneous Needling for Knee Osteoarthritis Pain
07:19

Author Spotlight: Fu's Subcutaneous Needling for Knee Osteoarthritis Pain

Published on: March 24, 2023

6.1K

Area of Science:

  • Immunology
  • Rheumatology
  • Biochemistry

Background:

  • Osteoarthritis (OA) pathogenesis involves complement activation, but its regulation and interactions with other pathways in joint tissues are not fully understood.
  • Complement system mediators play a crucial role in OA, influencing catabolic and inflammatory processes.
  • Understanding complement's role is key to developing effective OA treatments.

Purpose of the Study:

  • To summarize and discuss recent insights into complement activation in osteoarthritis (OA) pathogenesis.
  • To provide a comprehensive picture of complement's involvement in OA development and progression.
  • To explore the potential of complement modulation as a therapeutic strategy for OA.

Main Methods:

  • Review and synthesis of current scientific literature on complement activation and osteoarthritis.
  • Analysis of the interplay between complement mediators, extracellular matrix (ECM) components, and mechanical stress in OA.
  • Discussion of evidence linking complement to OA-associated cellular and tissue changes.

Main Results:

  • Complement activation is implicated in OA pathogenesis, affecting ECM degradation, inflammatory responses of chondrocytes and synoviocytes, cell lysis, synovitis, bone remodeling, osteophyte formation, stem cell recruitment, and cartilage angiogenesis.
  • Various ECM components and their degradation products, released during cartilage breakdown, can activate the complement system.
  • Some ECM components can inhibit complement activation, indicating complex regulatory interactions.

Conclusions:

  • Complement activation is a significant factor in osteoarthritis pathogenesis, influencing multiple disease processes.
  • The complement system interacts dynamically with ECM components and may be activated by mechanical stress.
  • Modulating complement activation presents a potential therapeutic avenue for managing OA and preventing its progression.