Fibroblasts/Dermis - Medicine Essay Example

The dermis is the layer forming an animal's true skin and is situated below the epidermis, and is made up of living tissues. It is constituted of structures such as blood capillaries, hair follicles and sweat glands among others. Fibroblasts are cells found within the dermis of the skin whose role in the animal's body is to produce extracellular matrix (ECM) and collagen that form the structural framework of tissues (Cole et al., 2018). The components synthesized play a significant part in repairing any worn out tissues in the body. Moreover, fibroblasts are the primary connective tissues in the body. They are associated with various aspects that are part of an animal's daily existence such as scars, aging, cellulite, and ECM hyper and hypo diseases among others. The cells produce collagens that enable a wounded skin to heal and in the process a scar is formed as the tissues enlarge (Shi et al., 2013). The interaction between the fibroblasts and ECM is interrupted during aging and this leads to an imbalance between the matrix-degrading metalloproteinase and ECM proteins of which facilitates the aging process (Tobin, 2017). Cellulite can be identified as disorder where the connective tissues are damaged by matrix metalloproteinase (MMP) generated when there is an estrogen on the fibroblasts. ECM hyper and hypo diseases such as the Hypo-plastic Left Heart Syndrome (HLHS) are caused by malfunctioning of the fibroblasts' components such as fibroins the ability of the cells to interact with the ECM is interrupted.

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At a young age, the fibroblasts are able to generate and integrate with the ECM where protein molecules such as collagen type 1 and fibril are found. The interaction helps in effective structuring and composition of the dermal ECM of which enables effective maintenance of the connective tissues as there is a balanced production of building proteins and damaging MMPs (Tigges et al., 2014). However, with aging the damaging MMPs are more than the proteins and the fibroblasts have reduced contact with the collagen fibril essential for skin maintenance (Yu et al., 2013). Thus, the tissues' binding capacity is reduced leading to aging of the animal's skin. Further, when the skin is exposed to ultraviolet radiation (UV), oxygen components are produced and they have the ability to damage and reduction of the ECM elements including the laminin and fibronectin (Philips et al., 2007). The antioxidant defenses such as Vitamin E and C responsible for repairing any damages on the skin are overwhelmed by these oxygen elements due to the repeated exposure and they are unable to protect it from aging of which is premature in some instances. Hence, this can be prevented by ensuring less exposure to UV to avoid excessive generation of the harmful oxygen species (Gilchrest, 1989). However, in instances where the damage has occurred, absorption of adequate amounts of Vitamin E and C will help in developing an ample defense to prevent these species from destroying the dermal ECM elements maintaining the skin (Pullar et al, 2017).

Scars change the appearance and histopathology of an animal's skin as they are enlarged tissues or elements found within the dermis. Fibroblasts play a significant role in skin scarring since they have a responsibility in wound healing (Chan & Longaker, 2017). Upon an injury, there is a cleaning process including clotting after which the fibroblasts cells become prominent in which they form connective tissues to counter the damage. As these cells migrate around the collapsed collagens, they lead to granulation of the tissues within the dermis resulting to scar hyperplasia. The scar acts as a closing component to prevent harmful aspects associating with the true skin (Grierson et al. 1988). It is recommended to avoid exposure of scars to UV especially during the early stages of healing. The exposure facilitates to an increased risk of the formation of scars and this can lead to harmful consequences such as hyper or hypo-pigmentation. Also, the UV can lead to extreme sunburns that can lead to the change of the skin color and appearance. Therefore, immature scars can be prevented from becoming pigmented by avoiding a direct exposure with the UV of which is essential in protecting the skin's appearance and histopathology.

References

Chan, C. K., & Longaker, M. T. (2017). Fibroblasts become fat to reduce scarring. Science, 355(6326), 693-694.

Cole, M. A., Quan, T., Voorhees, J. J., & Fisher, G. J. (2018). Extracellular matrix regulation of fibroblast function: redefining our perspective on skin aging. Journal of cell communication and signaling, 1-9.

Gilchrest, B. A. (1989). Skin aging and photoaging: an overview. Journal of the American Academy of Dermatology, 21(3), 610-613.

Grierson, I., Joseph, J., Miller, M., & Day, J. E. (1988). Wound repair: the fibroblast and the inhibition of scar formation. Eye, 2(2), 135.

Philips, N., Auler, S., Hugo, R., & Gonzalez, S. (2011). Beneficial regulation of matrix metalloproteinases for skin health. Enzyme research, 2011.

Philips, N., Keller, T., Hendrix, C., Hamilton, S., Arena, R., Tuason, M., & Gonzalez, S. (2007). Regulation of the extracellular matrix remodeling by lutein in dermal fibroblasts, melanoma cells, and ultraviolet radiation exposed fibroblasts. Archives of dermatological research, 299(8), 373-379.

Pullar, J. M., Carr, A. C., & Vissers, M. (2017). The roles of vitamin C in skin health. Nutrients, 9(8), 866.

Shi, H. X., Lin, C., Lin, B. B., Wang, Z. G., Zhang, H. Y., Wu, F. Z., ... & Zhang, G. Y. (2013). The anti-scar effects of basic fibroblast growth factor on the wound repair in vitro and in vivo. PloS one, 8(4), e59966.

Tigges, J., Krutmann, J., Fritsche, E., Haendeler, J., Schaal, H., Fischer, J. W., ... & Ventura, N. (2014). The hallmarks of fibroblast ageing. Mechanisms of ageing and development, 138, 26-44.

Tobin, D. J. (2017). Introduction to skin aging. Journal of tissue viability, 26(1), 37-46.

Yu, T. Y., Pang, J. H. S., Wu, K. P. H., Chen, M. J., Chen, C. H., & Tsai, W. C. (2013). Aging is associated with increased activities of matrix metalloproteinase-2 and-9 in tenocytes. BMC musculoskeletal disorders, 14(1), 2.