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

Phosphoinositides and PIPs01:42

Phosphoinositides and PIPs

9.9K
Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
Different phosphoinositides are synthesized and recruited on the cytosolic face of the plasma membrane. The localization of specific phosphoinositides concentrated in separate membrane...
9.9K
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

5.9K
Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
5.9K
IP3/DAG Signaling Pathway01:11

IP3/DAG Signaling Pathway

14.0K
Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
14.0K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

5.1K
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...
5.1K
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

7.0K
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
7.0K
Mechanism of Lamellipodia Formation01:31

Mechanism of Lamellipodia Formation

3.4K
Cells migrating in response to external stimuli form lamellipodia, which are thin membrane protrusions supported by a mesh of linked, branched, or unbranched actin filaments. These actin filaments interact with myosin motor proteins, creating the dynamic actomyosin complex within the cytoskeleton. Contractility, or the ability to generate contractile stress, is inherent to the actomyosin complex. It helps cells detect the stiffness of the surrounding ECM and exert contractile force for...
3.4K

You might also read

Related Articles

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

Sort by
Same author

Is the future of cardiac repair cell-free?

European heart journal·2026
Same author

Correction: Marchetti et al. MicroRNA-24-3p Targets Notch and Other Vascular Morphogens to Regulate Post-ischemic Microvascular Responses in Limb Muscles. <i>Int. J. Mol. Sci</i>. 2020, <i>21</i>, 1733.

International journal of molecular sciences·2026
Same author

A comprehensive pharmacological survey across heterogeneous patient-derived glioblastoma stem cell models.

iScience·2026
Same author

Identification of drug candidates against glioblastoma with machine learning and high-throughput screening of heterogeneous cellular models.

Digital discovery·2026
Same author

Intercellular transport of miR-146a from macrophages to vascular smooth muscle cells: a novel mechanism and therapeutic target for atherosclerosis.

Cardiovascular research·2026
Same author

Discovery of a Highly Potent and Selective mTOR Inhibitor that Strongly Suppresses Glioblastoma Multiforme Cell Growth.

Journal of medicinal chemistry·2026

Related Experiment Video

Updated: Dec 23, 2025

Expression and Purification of the Human Lipid-sensitive Cation Channel TRPC3 for Structural Determination by Single-particle Cryo-electron Microscopy
08:27

Expression and Purification of the Human Lipid-sensitive Cation Channel TRPC3 for Structural Determination by Single-particle Cryo-electron Microscopy

Published on: January 7, 2019

9.8K

Trichoplein binds PCM1 and controls endothelial cell function by regulating autophagy.

Andrea Martello1, Angela Lauriola2, David Mellis1

  • 1University/BHF Centre for Cardiovascular Science, QMRI, University of Edinburgh, Edinburgh, UK.

EMBO Reports
|April 28, 2020
PubMed
Summary

Trichoplein (TCHP) is crucial for endothelial cell function by regulating autophagy. Loss of TCHP impairs autophagy, leading to vascular problems, but this can be reversed by inhibiting NF-κB.

Keywords:
GABARAPSQSTM1/p62autophagycentriolar satellitesendothelial cells

More Related Videos

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

7.6K
Stimulation of Vascular Endothelial Cells Using Neutrophil Extracellular Traps in the Presence of Low-Density Lipoprotein
07:26

Stimulation of Vascular Endothelial Cells Using Neutrophil Extracellular Traps in the Presence of Low-Density Lipoprotein

Published on: August 12, 2025

623

Related Experiment Videos

Last Updated: Dec 23, 2025

Expression and Purification of the Human Lipid-sensitive Cation Channel TRPC3 for Structural Determination by Single-particle Cryo-electron Microscopy
08:27

Expression and Purification of the Human Lipid-sensitive Cation Channel TRPC3 for Structural Determination by Single-particle Cryo-electron Microscopy

Published on: January 7, 2019

9.8K
siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

7.6K
Stimulation of Vascular Endothelial Cells Using Neutrophil Extracellular Traps in the Presence of Low-Density Lipoprotein
07:26

Stimulation of Vascular Endothelial Cells Using Neutrophil Extracellular Traps in the Presence of Low-Density Lipoprotein

Published on: August 12, 2025

623

Area of Science:

  • Cellular Biology
  • Vascular Biology
  • Autophagy Research

Background:

  • Autophagy is a vital cellular process for maintaining vascular homeostasis.
  • Endothelial cell (EC) function is critical for vascular health.
  • The molecular mechanisms linking autophagy to EC function require further elucidation.

Purpose of the Study:

  • To investigate the role of trichoplein (TCHP) in regulating autophagy in endothelial cells.
  • To determine the impact of TCHP on endothelial cell function and vascular homeostasis.
  • To explore the therapeutic potential of targeting TCHP or related pathways.

Main Methods:

  • Investigated TCHP localization and its interaction with PCM1 in ECs.
  • Assessed autophagic flux, SQSTM1/p62 (p62) levels, and autophagosome maturation in TCHP-depleted cells.
  • Analyzed TCHP and p62 levels in patient-derived ECs and Tchp knockout mouse models.

Main Results:

  • TCHP stabilizes PCM1 at centriolar satellites; TCHP loss causes PCM1 and GABARAP degradation.
  • TCHP depletion impairs basal autophagic flux and leads to p62 accumulation in ECs.
  • Reduced TCHP and elevated p62 correlate with impaired EC function in coronary artery disease patients and Tchp knockout mice, affecting cardiac vascularization.

Conclusions:

  • Trichoplein (TCHP) is a key regulator of endothelial cell function through an autophagy-dependent mechanism.
  • TCHP deficiency impairs autophagosome maturation and clearance, contributing to vascular dysfunction.
  • Targeting TCHP or NF-κB pathway may offer therapeutic strategies for vascular diseases.