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

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

2.5K
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...
2.5K
Notch Signaling Pathway03:14

Notch Signaling Pathway

4.2K
The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
4.2K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

2.0K
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.0K
Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

5.2K
Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
5.2K
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

2.5K
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...
2.5K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

3.3K
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...
3.3K

You might also read

Related Articles

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

Sort by
Same author

Targeting S100A8/A9 Ameliorates Heart Failure with Preserved Ejection Fraction by Modulating TLR4/NF-κB-Mediated Inflammation.

Clinical and experimental pharmacology & physiology·2026
Same author

Association of urinary thallium with hypertension in children and adolescents aged 8-17 years: NHANES 2005-2018.

Environmental science and pollution research international·2023
Same author

Klotho improves cardiac fibrosis, inflammatory cytokines, ferroptosis, and oxidative stress in mice with myocardial infarction.

Journal of physiology and biochemistry·2023
Same author

Dapagliflozin modulates the faecal microbiota after myocardial infarction in non-diabetic mice.

Clinical and experimental pharmacology & physiology·2022
Same author

Dapagliflozin Improves Cardiac Function, Remodeling, Myocardial Apoptosis, and Inflammatory Cytokines in Mice with Myocardial Infarction.

Journal of cardiovascular translational research·2021
Same author

Speckle Tracking Echocardiography Verified the Efficacy of Qianyangyuyin Granules in Alleviating Left Ventricular Remodeling in a Hypertensive Rat Model.

Evidence-based complementary and alternative medicine : eCAM·2021

Related Experiment Video

Updated: May 21, 2025

Efficient Production and Purification of Recombinant Murine Kindlin-3 from Insect Cells for Biophysical Studies
13:52

Efficient Production and Purification of Recombinant Murine Kindlin-3 from Insect Cells for Biophysical Studies

Published on: March 19, 2014

23.3K

Kindlin-3 Promotes Angiogenesis via Notch Signalling and Is Crucial for Functional Recovery Postmyocardial

Yan Sun1, Wei Zheng1, Xianling Liu1

  • 1Department of Cardiology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China.

Journal of Cellular and Molecular Medicine
|March 18, 2025
PubMed
Summary

Kindlin-3 enhances blood vessel formation (angiogenesis) after heart attack (myocardial infarction). This protein improves heart function and reduces damage, offering a potential new therapy for cardiac repair.

Keywords:
CMECsKindlin‐3Notchangiogenesismyocardial infraction

More Related Videos

A Modified Surgical Model of Hind Limb Ischemia in ApoE-/- Mice using a Miniature Incision
05:47

A Modified Surgical Model of Hind Limb Ischemia in ApoE-/- Mice using a Miniature Incision

Published on: May 13, 2021

3.8K
An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice
09:29

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice

Published on: July 14, 2023

719

Related Experiment Videos

Last Updated: May 21, 2025

Efficient Production and Purification of Recombinant Murine Kindlin-3 from Insect Cells for Biophysical Studies
13:52

Efficient Production and Purification of Recombinant Murine Kindlin-3 from Insect Cells for Biophysical Studies

Published on: March 19, 2014

23.3K
A Modified Surgical Model of Hind Limb Ischemia in ApoE-/- Mice using a Miniature Incision
05:47

A Modified Surgical Model of Hind Limb Ischemia in ApoE-/- Mice using a Miniature Incision

Published on: May 13, 2021

3.8K
An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice
09:29

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice

Published on: July 14, 2023

719

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Regenerative Medicine

Background:

  • Angiogenesis is vital for recovery after myocardial infarction (MI).
  • The role of Kindlin-3 in cardiac angiogenesis post-MI is not well understood.
  • Kindlin-3 is known to influence angiogenesis in other contexts, like breast cancer.

Purpose of the Study:

  • To investigate the function of Kindlin-3 in promoting angiogenesis for cardiac repair post-MI.
  • To explore the therapeutic potential of Kindlin-3 in myocardial infarction.

Main Methods:

  • Studied Kindlin-3 expression in cardiac microvascular endothelial cells (CMECs) in mice post-MI.
  • Utilized adeno-associated virus serotype 9 (AAV9) for Kindlin-3 overexpression in vivo.
  • Performed in vitro assays to assess CMEC proliferation, migration, and tube formation.
  • Investigated the involvement of the Notch signaling pathway and β1 integrin.

Main Results:

  • Kindlin-3 was upregulated in CMECs post-MI.
  • Kindlin-3 overexpression enhanced angiogenesis, improved cardiac function, reduced cardiomyocyte apoptosis, and decreased fibrosis.
  • In vitro, Kindlin-3 promoted CMEC proliferation, migration, tube formation, and angiogenesis-related gene expression.
  • Kindlin-3 activated the Notch signaling pathway.

Conclusions:

  • Kindlin-3 is a novel enhancer of angiogenesis in the context of myocardial infarction.
  • Kindlin-3 plays a significant role in cardiac repair post-MI.
  • Kindlin-3 represents a potential therapeutic target for myocardial regeneration.