Related Experiment Video

Updated: Oct 1, 2026

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
06:14

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function

Published on: June 11, 2017

[Role of pp60c-src in mitogen-activated protein kinase activation of vascular smooth muscle cells]

D Liu1, J S Lu, X L Yin

  • 1Department of Cardiology, The Second Affiliated Hospital to Zhejiang University Medical School, Hangzhou 310006. liuding99cn@yahoo.com.cn

Sheng Li Xue Bao : [Acta Physiologica Sinica]
|April 10, 2002
PubMed

Insights

Vascular smooth muscle cell proliferation involves signaling pathways. This study shows pp60c-src is crucial for angiotensin II-induced mitogen-activated protein kinase activation in these cells.

Area of Science:

  • Cellular signaling
  • Molecular biology
  • Vascular biology

Context:

  • Angiotensin II (Ang II) stimulates vascular smooth muscle cells (VSMCs) proliferation.
  • Understanding the signal transduction pathways involved in VSMC proliferation is critical for cardiovascular research.

Purpose:

  • To investigate the role of pp60c-src in mitogen-activated protein kinase (MAPK) activation induced by Ang II in VSMCs.
  • To elucidate the signaling mechanism underlying Ang II-mediated VSMC proliferation.

Summary:

  • Transfection of VSMCs with antisense c-src oligodeoxynucleotides significantly reduced pp60c-src content and kinase activity.
  • Ang II stimulation of these transfected VSMCs resulted in a marked inhibition of MAPK activation.
  • These findings indicate that pp60c-src is essential for Ang II-induced MAPK activation in VSMCs.

Impact:

  • pp60c-src acts as a key signaling molecule in the Ang II-mediated activation of MAPK.
  • This research highlights pp60c-src as a potential therapeutic target for abnormal VSMC proliferation and related cardiovascular diseases.

More Related Videos

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro08:28

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Published on: February 15, 2022

Human Saphenous Vein Endothelial Cell Isolation and Exposure to Controlled Levels of Shear Stress and Stretch09:10

Human Saphenous Vein Endothelial Cell Isolation and Exposure to Controlled Levels of Shear Stress and Stretch

Published on: April 21, 2023

Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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 rapamycin-insensitive companion...
Amplifying Signals via Second Messengers01:15

Amplifying Signals via Second Messengers

Many receptor binding ligands are hydrophilic; they do not cross the cell membrane but bind to cell-surface receptors. Thus, their message must be relayed by second messengers present in the cell cytoplasm. There are several second messenger pathways, each with its own way of relaying information. For example, the G protein-coupled receptors can activate both phosphoinositol and cyclic AMP (cAMP) second messenger pathways. The phosphoinositol pathway is active when the receptor induces...
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
Regulation of Angiogenesis and Blood Supply01:24

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...