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 JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

9.3K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
9.3K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

7.7K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.7K
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

2.8K
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
2.8K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

7.9K
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...
7.9K
Fibril-associated Collagen01:11

Fibril-associated Collagen

2.7K
Fibril-associated collagens are a type of collagens present in the extracellular matrix with interrupted triple helices or FACIT (Fibril-associated collagens interrupted triple-helices). FACIT help connect and attach the collagen fibrils with each other as well as with other proteins of the extracellular matrix.
For example, the type II collagen fibrils in cartilage have covalently bound type IX fibril-associated collagens at regular intervals. Other types of fibril-associated collagens are...
2.7K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

4.0K
The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
4.0K

You might also read

Related Articles

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

Sort by
Same author

Pixel-scale broadband absorption enhancement in PbSe thin films via a multimode-coupled metasurface.

Optics express·2026
Same author

Temporal Profile of Stroke-Associated Pneumonia and Deep Vein Thrombosis after Stroke.

Cerebrovascular diseases extra·2026
Same author

Room-Temperature Aldol Condensation for n-Type Elastic-Plastic Organic Mixed Ionic-Electronic Conductors.

ACS macro letters·2026
Same author

Discovery of actinators, actin-derived bioactive peptides that modulate cytoskeleton and actin-related cellular activities.

Science advances·2026
Same author

Model Based on Ultrasound Radiomics and Machine Learning for Differentiating Uterine Fibroids and Adenomyomas.

Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine·2026
Same author

The Yin-Yang balance of SIRT1 and SIRT2 in cancer metabolic remodeling.

International journal of biological sciences·2026

Related Experiment Video

Updated: Sep 19, 2025

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
09:12

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

16.2K

Fibrinogen regulates microglial function through the JAK2/STAT3 signaling pathway.

Xiaohui Li1, Xiujuan Song1, Fei Yi1

  • 1Department of Neurology, The Second Hospital of Hebei Medical University, Shi Jiazhuang 050000, China.

Cellular Immunology
|June 5, 2025
PubMed
Summary

Fibrinogen triggers neuroinflammation by activating the JAK2/STAT3 pathway in microglia, increasing pro-inflammatory cytokines. Cryptotanshinone, a STAT3 inhibitor, reverses this effect, offering therapeutic potential for neurological diseases.

Keywords:
CytokinesFibrinogenJAK2/STAT3MicrogliaNeuroinflammation

More Related Videos

Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model
08:15

Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model

Published on: June 6, 2025

193
Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain
10:40

Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain

Published on: October 27, 2019

33.0K

Related Experiment Videos

Last Updated: Sep 19, 2025

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
09:12

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

16.2K
Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model
08:15

Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model

Published on: June 6, 2025

193
Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain
10:40

Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain

Published on: October 27, 2019

33.0K

Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Neuroinflammation is central to neurological disorders, involving microglia activation.
  • Microglia have dual roles, mediating both protective and harmful effects.
  • Fibrinogen is a pro-inflammatory mediator linked to neurological disease progression.

Purpose of the Study:

  • To investigate fibrinogen's effects on primary microglial function.
  • To examine the role of the JAK2/STAT3 signaling pathway in fibrinogen-induced microglial activation.
  • To assess the impact of the STAT3 inhibitor cryptotanshinone on microglial responses to fibrinogen.

Main Methods:

  • Primary microglial cells were isolated from neonatal mice.
  • Cells were treated with fibrinogen and cryptotanshinone.
  • Quantitative PCR, immunofluorescence, and Western blot were used to analyze inflammatory markers and signaling proteins.

Main Results:

  • Fibrinogen upregulated JAK2 and STAT3 phosphorylation in microglia.
  • Cryptotanshinone inhibited STAT3 phosphorylation and JAK2 activation.
  • Fibrinogen increased pro-inflammatory cytokine release (IL-6, IL-1β).

Conclusions:

  • Fibrinogen activates the JAK2/STAT3 pathway, driving pro-inflammatory cytokine production in microglia.
  • This mechanism contributes to fibrinogen-induced neuroinflammation.
  • Targeting the JAK2/STAT3 pathway may offer therapeutic strategies for neurological diseases.