Cardiomyocyte apoptosis is closely related to cardiovascular diseases such as arrhythmia, hypertension, atherosclerosis, acute coronary syndrome, myocardial ischemia-reperfusion injury, cardiomyopathy, myocarditis, congenital heart disease, heart failure and so on. Endoplasmic reticulum stress (ERS) plays an important role in cardiomyocyte apoptosis caused by cardiovascular disease, and has become a hot spot of recent research. Endoplasmic reticulum (ER) is an important organelle in eukaryotic cells, which is mainly involved in the modification and folding of membrane proteins and secretory proteins.

Fig. 1 Cardiomyocyte ER Stress Model (Blackwood et al., 2020)

Endoplasmic reticulum is sensitive to the external environment. Metabolic abnormalities, inhibition of protein glycosylation and disorder of disulfide bond formation caused by various stress can cause misfolded and unfolded proteins to accumulate in the endoplasmic reticulum cavity, destroy the homeostasis of endoplasmic reticulum and cause endoplasmic reticulum stress (ERS). Creative Bioarray induced neonatal rat cardiomyocytes with tunicamycin to construct human ERS model. The model is expected to provide a research basis for further exploring the mechanism of endoplasmic reticulum stress-induced cardiomyocyte apoptosis and related diseases.

Technology Principle

Tunicamycin is a commonly used inducer of ERS, which can inhibit the production of long terpenol tetradecose diphosphate in protein glycosylation pathway, make the sugar chain process hands and feet, form deglycoprotein, hinder the glycosylation modification of new proteins in endoplasmic reticulum, damage the function of endoplasmic reticulum, and finally cause ERS.

Through the gradient experimental model, we determined the optimal amount and treatment time of tunicamycin for the establishment of cardiomyocyte cell endoplasmic reticulum stress model.

After ERS, on the one hand, cells restore the function of endoplasmic reticulum through unfolded protein reaction (UPR).On the other hand, ERS is too strong or lasts too long, resulting in the balance and function of endoplasmic reticulum can not be reconstructed, and UPR reaction will induce apoptosis of damaged cells. Glucose regulatory protein 78 (GRP78) and CCAAT / hadron binding protein (CHOP) are marker proteins in ERS.

Service Content

We provide cell model construction and sales services.

In addition, we can also adjust the modeling process according to the specific needs of customers, provide administration experiment, pharmacology, efficacy evaluation and pharmacokinetic analysis, and assist customers to study the physiological and / or pathological significance of cardiomyocyte ers, which has important theoretical significance for clarifying digestive related diseases (cardiomyocyte apoptosis, etc.). We will determine the modeling by detecting Er markers by WB, proliferation and survival by MTT, and apoptosis caused by tunicamycin by TUNEL.

Model Application

Objective to study the ERS and signaling pathway of cardiomyocyte under the action of tunicamycin
To study the molecular mechanism of ERS mediated cardiomyocyte apoptosis related diseases
To investigate the physiological and / or pathological significance of cardiomyocyte ERS
To study the etiology of cardiomyocyte related diseases
The discovery and screening of antioxidants and the development of cardiomyocyte protective drugs

Creative Bioarray is dedicated to providing high-quality products, comprehensive services, and tailored solutions to support and facilitate life sciences and pharmaceutical research and development. If you have any questions or needs, please contact us, and our customer service staff will help you at the first time.

Reference

1. Blackwood, E., Thuerauf, D., Stastna, M., Stephens, H., Sand, Z., & Pentoney, A. et al. (2020). Proteomic analysis of the cardiac myocyte secretome reveals extracellular protective functions for the ER stress response. Journal Of Molecular And Cellular Cardiology, 143, 132-144.

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