BIOS 251 Week 4 Case Study: Tissue

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Chamberlain University

BIOS-251 Anatomy & Physiology I

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BIOS 251 Week 4 Case Study: Tissue

The five layers of the skin, referred to as the epidermis, include the stratum corneum, stratum lucidum, stratum spinosum, stratum granulosum, and stratum basale. These layers have distinct characteristics and roles. The stratum corneum, being the most superficial, is the layer that people can visibly see. It consists of dead skin cells filled with keratin, a tough protein that makes the skin waterproof (Lawton, 2021). The stratum lucidum is the next layer, which also contains dead keratinocytes, making it more prevalent in thick skin areas like the palms of the hands and soles of the feet (Lawton, 2021). The stratum spinosum and granulosum layers, located beneath, contribute to skin strength and flexibility due to their spiny-shaped cells (Saladin, 2019). The stratum basale, the deepest layer, is close to the blood supply in the dermis and is responsible for producing keratinocytes. This layer undergoes continuous mitosis, pushing older cells upward to the stratum corneum, where they eventually die and form the skin’s outermost layer.

Cell junctions play a vital role in cellular communication and structure. There are four primary types: tight junctions, adherens junctions, desmosomes, and gap junctions. Tight junctions connect nearby cells, sealing off the intercellular gap and forcing substances to move through cells rather than between them. Adherens junctions connect cells by linking microfilaments, while desmosomes, which are patches that hold cells together, provide mechanical strength and prevent stress-induced damage (Saladin, 2019). Gap junctions consist of connexons that allow material and signals to pass between cells.

The plakophilin gene produces a protein known as plakophilin 2, which plays a significant role in the structural integrity of desmosomes, essential for cell-to-cell adhesion. According to Cerrone et al. (2017), plakophilin 2 helps maintain the structure and function of cellular junctions, particularly in cardiac cells. Mutations in the plakophilin gene can lead to disruptions in these cell junctions. Plakophilin 2 is involved in coupling intercellular signals and interacting with sodium channel complexes, which are crucial for maintaining the heart’s rhythm (Cerrone et al., 2017). When the plakophilin gene is mutated, desmosomes weaken, leading to issues such as sudden cardiac arrest. The mutation could also contribute to hyperhidrosis, a condition characterized by excessive sweating. Since desmosomes join epithelial cells, a mutation in the plakophilin gene may lead to defective cellular communication, increasing the likelihood of sweat passing through the skin (Mayo Clinic, 2020).

References

Cerrone, M., Montnach, J., Lin, X., Zhao, Y.-T., Zhang, M., Agullo-Pascual, E., Leo-Macias, A., Alvarado, F. J., Dolgalev, I., Karathanos, T. V., Malkani, K., Van Opbergen, C. J. M., van Bavel, J. J. A., Yang, H.-Q., Vasquez, C., Tester, D., Fowler, S., Liang, F., Rothenberg, E., … Delmar, M. (2017, July 24). Plakophilin-2 is required for transcription of genes that control calcium cycling and cardiac rhythm. Nature News. Retrieved September 22, 2021, from https://www.nature.com/articles/s41467-017-00127-0

BIOS 251 Week 4 Case Study: Tissue

Mayo Foundation for Medical Education and Research. (2020, August 18). Hyperhidrosis. Mayo Clinic. Retrieved September 22, 2021, from https://www.mayoclinic.org/diseases-conditions/hyperhidrosis/symptoms-causes/syc-20367152

Saladin, K. (2019). Anatomy and Physiology: The Unity of Form and Function (9th ed.). McGraw-Hill.