Related Experiment Video
Updated: Aug 17, 2026

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
Published on: April 1, 2022
alphaB-crystallin is phosphorylated during myocardial infarction: involvement of platelet-derived growth factor-BB
En Shu1, Hiroyuki Matsuno, Shigeru Akamastu
1Department of Pharmacology, Gifu University Graduate School of Medicine, Japan.
Insights
Platelet-derived growth factor (PDGF-BB) triggers alphaB-crystallin phosphorylation via p38 MAP kinase during heart attacks. This finding offers new insights into myocardial infarction treatment strategies.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Heat Shock Proteins
Background:
- AlphaB-crystallin is a key heat shock protein in the heart, known for its cardioprotective effects during myocardial infarction.
- Platelet-derived growth factor (PDGF) has shown promise in improving cardiac function post-myocardial infarction.
Purpose of the Study:
- To investigate the phosphorylation of alphaB-crystallin during myocardial infarction.
- To determine the role of Platelet-Derived Growth Factor-BB (PDGF-BB) in this process.
Main Methods:
- Utilized a mouse model of myocardial infarction.
- Measured alphaB-crystallin phosphorylation at Ser-59.
- Assessed plasma PDGF-BB levels.
- Employed SB203580, a p38 MAP kinase inhibitor, in cultured cardiac myocytes.
Main Results:
- Phosphorylation of alphaB-crystallin at Ser-59 increased over time following myocardial infarction.
- Plasma PDGF-BB levels were elevated concurrently with alphaB-crystallin phosphorylation.
- PDGF-BB-induced phosphorylation was inhibited by SB203580, implicating p38 MAP kinase.
Conclusions:
- PDGF-BB signaling pathway, mediated by p38 MAP kinase, is involved in alphaB-crystallin phosphorylation during myocardial infarction.
- This mechanism may contribute to the cardioprotective roles of both alphaB-crystallin and PDGF-BB.
Abstract:
alphaB-crystallin is the most abundant low-molecular-weight heat shock protein in heart and recent studies have demonstrated that it plays a cardioprotective role during myocardial infarction both in vivo and in vitro. On the other hand, platelet-derived growth factor (PDGF), a potent serum mitogen, has been reported to improve cardiac function after myocardial infarction. In the present study, using a mouse myocardial infarction model, we investigated whether alphaB-crystallin is phosphorylated during myocardial infarction and the implication of PDGF-BB. Phosphorylation of alphaB-crystallin at Ser-59 was time dependently induced and plasma PDGF-BB levels were concomitantly increased. Moreover, PDGF-BB-stimulated phosphorylation of alphaB-crystallin was suppressed by SB203580, a specific inhibitor of p38 mitogen-activated protein (MAP) kinase, in primary cultured cardiac myocytes. Our results indicate that PDGF-BB induces phosphorylation of alphaB-crystallin via p38 MAP kinase during myocardial infarction.
Related Concept Videos
TGF - β Signaling Pathway
Intracellular Signaling Affects Focal Adhesions
Some...
Clot Retraction and Fibrinolysis
Coronary Artery Disease II: Pathophysiology
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
cAMP-dependent Protein Kinase Pathways

