Cardiac Myocyte Medium-serum free

Name: Cardiac Myocyte Medium-serum free
Brand: Sciencell Research Laboratories
SKU: 6101
Price: 155 USD
Availability: InStock

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Catalog No.

6101

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$155.00

Cardiac Myocyte Medium-serum free (CMM-sf) consists of 500 ml of basal medium, 5 ml of Cardiac Myocyte Growth Supplement-serum free (CMGS-sf, Cat. #6152) and 5 ml of penicillin/streptomycin solution (P/S, Cat. #0503).

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Cardiac Myocyte Medium-serum free (CMM-sf), when used with Cardiac Myocyte Growth Supplement-serum free (CMGS-sf, Cat #6152) is a complete medium designed for the culture of normal cardiac myocytes in serum-free conditions. It is a sterile, liquid medium which contains essential and non-essential amino acids, vitamins, organic and inorganic compounds, hormones, growth factors and trace minerals. The medium is HEPES and bicarbonate buffered and has a pH of 7.4 when equilibrated in an incubator with an atmosphere of 5% CO2/95% air. The medium is formulated (quantitatively and qualitatively) to provide an optimally balanced nutritional environment that selectively supports the culture of normal cardiac myocytes in vitro under serum free conditions.

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Catalog No.	6101
Country of Manufacture	United States
Product Code	CMM-sf
Size/Quantity	500 ml
Product use	This product is for research use only. It is not approved for use in humans, animals, or in vitro diagnostic procedures.
Storage	Store the basal medium at 4°C, the ECGS, the FBS and the P/S solution at -20°C. Protect from light.
Shipping	Basal medium: room temperature. Supplements: dry ice.

1. Wu, P., Kong, L., & Li, J. (2019). MicroRNA 494 3p protects rat cardiomyocytes against septic shock via PTEN. Experimental and Therapeutic Medicine, 17, 1706-1716. https://doi.org/10.3892/etm.2018.7116

The aim of the present study was to investigate the role of microRNA (miR)‑494‑3p in myocardial injury in patients with septic shock and the underlying mechanism. A t... More

The aim of the present study was to investigate the role of microRNA (miR)‑494‑3p in myocardial injury in patients with septic shock and the underlying mechanism. A total of 22 patients with sepsis and 17 patients with septic shock were included in the present study. In addition, 20 healthy subjects were recruited as the control group. Peripheral blood was collected from all subjects and a rat cardiomyocyte model of myocardial injury was constructed. Reverse transcription‑quantitative polymerase chain reaction was used to measure miR‑494‑3p expression, while cell counting kit‑8 assays were performed to assess cell proliferation. Flow cytometry was performed to investigate cell cycle distribution and apoptosis. Lactate dehydrogenase (LDH) assays were performed to measure LDH levels. ELISA was also performed to measure LDH, tumor necrosis factor (TNF)‑α and interleukin (IL)‑6 levels in cell culture supernatants. Western blotting was employed to detect phosphatase and tensin homolog (PTEN) protein expression and dual luciferase reporter assays were performed to identify the interaction between miR‑494‑3p and PTEN mRNA. Reduced miR‑494‑3p expression was correlated with myocardial damage in patients with septic shock. Sera from patients with septic shock downregulated miR‑494‑3p expression in rat cardiomyocytes. miR‑494‑3p overexpression inhibited rat cardiomyocyte injury induced by treatment with sera from patients with septic shock. Furthermore, miR‑494‑3p overexpression reduced the synthesis and release of TNF‑α and IL‑6 from rat cardiomyocytes. PTEN knockdown alleviated rat cardiomyocyte injury following treatment with serum from patients with septic shock. PTEN was demonstrated to induce the release of TNF‑α and IL‑6 from rat cardiomyocytes treated with septic shock serum, while miR‑494‑3p was demonstrated to bind to the 3'‑untranslated seed region of PTEN mRNA to regulate its expression. The results of the present study suggest that miR‑494‑3p is downregulated in the peripheral blood of patients with septic shock and is negatively correlated with myocardial injury. The present study also indicates that miR‑494‑3p regulates PTEN expression, inhibits sepsis‑induced myocardial injury and protects the function of cardiomyocytes. The protective effect and mechanism of action of miR‑494‑3p indicate that it has potential for use in the clinical diagnosis and therapy of myocardial damage. Less

ScienCell Research Laboratories (SRL) takes pride in being a resource for researchers all over the world. The publications listed here are not meant as an endorsement or confirmation of the reliability of the products.