The Role of Contractility in Coordinating Morphogenesis and Cell Fate in Hair Follicles – Insights from Nature Cell Biology

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Identification of BRD4 as a Key Regulator of Cardiomyocyte Differentiation through Genome-wide CRISPR Screen – Insights from Nature Cardiovascular Research...

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How Truncated Vitronectin with E-cadherin Facilitates Xeno-Free Generation of Human Embryonic Stem Cells

How Truncated Vitronectin with E-cadherin Facilitates Xeno-Free Generation of Human Embryonic Stem Cells

Human embryonic stem cells (hESCs) hold great promise for regenerative medicine and the treatment of various diseases. However, their clinical applications have been hindered by the use of animal-derived components in the culture medium, which can introduce potential risks such as contamination and immune rejection. To overcome these challenges, scientists have been working on developing xeno-free culture systems that eliminate the need for animal-derived components. One such advancement is the use of truncated vitronectin with E-cadherin, which has shown promising results in facilitating the xeno-free generation of hESCs.

Vitronectin is a glycoprotein found in the extracellular matrix and plays a crucial role in cell adhesion and migration. It has been widely used as a coating material for hESC culture due to its ability to support cell attachment and maintain pluripotency. However, the full-length form of vitronectin is derived from human plasma or recombinant sources, which raises concerns about potential contamination with pathogens or animal-derived components.

To address these concerns, researchers have developed a truncated form of vitronectin that retains its cell adhesion properties while eliminating potential risks associated with animal-derived components. This truncated vitronectin is generated by removing the heparin-binding domain, which is responsible for binding to heparan sulfate proteoglycans found in the extracellular matrix. By removing this domain, the truncated vitronectin can be produced using recombinant DNA technology, ensuring its purity and eliminating the risk of contamination.

In addition to truncated vitronectin, the inclusion of E-cadherin in the culture system further enhances the generation of hESCs in a xeno-free environment. E-cadherin is a calcium-dependent cell adhesion molecule that plays a crucial role in maintaining the pluripotency and self-renewal of hESCs. Its presence in the culture medium promotes cell-cell adhesion and signaling, which are essential for the formation and maintenance of hESC colonies.

The combination of truncated vitronectin and E-cadherin provides a robust and xeno-free culture system for the generation of hESCs. Studies have shown that hESCs cultured on truncated vitronectin with E-cadherin exhibit enhanced attachment, survival, and proliferation compared to traditional culture systems. Moreover, these cells maintain their pluripotency and can differentiate into various cell types, making them suitable for regenerative medicine applications.

The use of truncated vitronectin with E-cadherin not only eliminates the risks associated with animal-derived components but also offers several advantages over other xeno-free culture systems. The truncated vitronectin provides a stable and defined surface for cell attachment, while E-cadherin promotes cell-cell interactions, mimicking the natural microenvironment of hESCs. This combination ensures optimal conditions for hESC growth and differentiation, leading to improved efficiency and reproducibility in generating high-quality hESC lines.

In conclusion, the development of truncated vitronectin with E-cadherin has revolutionized the field of hESC culture by providing a xeno-free and efficient system for their generation. This advancement not only addresses the concerns associated with animal-derived components but also offers improved cell attachment, survival, and proliferation. With further research and optimization, this culture system holds great potential for the clinical translation of hESCs in regenerative medicine and disease treatment.

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