Introduction
Human skin can withstand visible light radiation; however, it is sensitive to ultraviolet radiation (UV radiation). As an adaptive measure, the human body produces biological pigment, which helps to screen the skin against UV radiations. Scientists refer to the organic pigment as melanin. By definition, melanin is a dark pigment, which occurs on human skin, hair, and eye iris. The tanning of human skin when it gets into contact with UV radiation is as a result of the melanin. Epidermal units of the epidermis produce melanin through a process called melanogenesis. According to Brenner and Hearing, (2008), melanin determines the skin, eye, and hair color in humans. However, the most critical role of melanin is protecting the skin against UV radiation, Photoprotection, as it is capable of absorbing UV radiations. This essay will evaluate the role of melanin in protecting human skin against UV radiation and explore the initiation signals that result in the proliferation of melanogenesis after exposure of the skin to UV radiation.
Production of melanin takes place in the Melanocyte cell, which is located in the epidermis. These cells lie in the lower part of the skin called the Stratum Basale (Brenner & Hearing, 2008). After production, melanocyte cells package melanin in granules and distribute them to keratinocytes, which carry the pellets to the skin surface. Thus, the melanocytes and the keratinocytes play a critical role in determining human skin color (Brenner & Hearing, 2008). Once on the skin surface, the melanin acts as UV radiation screen as it scatters UV radiation. When exposed to UV radiation, the human skin responds first by building up its shield to minimize the amount of the damaging radiation getting into the skin. The second response is mobilizing repair of the damage caused by the UV radiation. In this case, melanin acts as the first line of defense by diverting or absorbing the UV radiations.
The mechanisms of melanogenesis: The process of melanogenesis takes place in the melanocyte cells. Melanin synthesis takes through different complex stages from melanocytes embryogenesis to melanosome distribution to the neighboring keratinocytes. These stages are of great importance since if one fails to take place completely, it can result in genetic defects. Several factors regulate the process of melanogenesis. However, the main extrinsic factor is ultraviolet radiation, while alpha-melanocyte-stimulating hormone is the primary intrinsic factor (Brenner & Hearing, 2008). Further study of the interactions of melanocytes and keratinocytes reveals that the skin is a neuroendocrine organ. According to Fajuyigbe and Young (2016), melanocytes produce two types of melanin, the pheomelanin, and the eumelanin. The ratio of these two particular types of melanin results in the differences in human skin color. Individuals who have a higher amount of pheomelanin than eumelanin tend to have light skin, while those who have a higher amount of eumelanin concentration as compare to pheomelanin concentration have darker skin.
Signals influencing the increase in melanin production: D'Mello, Finlay, Baguley, and Askarian-Amiri (2016) opine that there are several signaling systems and transcription factors initiate and regulate the process of melanogenesis. Some of these factors and signals include tyrosine kinase receptor KIT, SCF (Stem Cell Factor), and the Melanocyte Inducing Transcription Factor (MITF). The Melanocortin 1 Receptor (MC1R) agonists', Alpha-Melanocyte-Stimulating Hormone (a-MSH), and Adrenocorticotropic Hormone (ACTH) stimulate the production of eumelanin while Agouti-Signaling Protein (ASP) simulates pheomelanin synthesis. The pituitary gland and in the keratinocytes produce the a-MSH, which is a part of the precursor protein pro-opiomelanocortin (POMC). UV radiation acts as stimulating factors to the production of the POMC gene manifestation. In addition, UVR-triggers oxidative stress which leads to the creation of POMC peptide (Videira, Moura, & Magina, 2013). It is widely accepted that this signaling pathway is essential in the physiological adaptations of the human skin to ultraviolet radiations exposure. The SCF-KIT receptor tyrosine kinase, combine with the a-MSH-MCR1 signaling pathway, to aid in melanocyte pigmentation and development by initiating the Microphthalmia-associated transcription factor (MITF) transcription (D'Mello, Finlay, Baguley, & Askarian-Amiri, 2016). The MIFT genes control the melanocyte pigmentation.
Even though scientists have done several pieces of research, the mechanisms of transcriptional and post-transcriptional which govern the melanogenic molecular pathways are yet to be fully understood. However, transcriptional stimulation is accomplished through the Cyclic Adenosine Monophosphate (CAMP) pathway-dependent initiation by MITF genes. MITF also targets the Tyrosinase (TYR) gene resulting in an increase in TYR production. According to D'Mello, Finlay, Baguley, and Askarian-Amiri, (2016), the rise of tyrosinase in melanocytes is as a response to a-Melanocyte-stimulating hormone stimulation. Elevating of intracellular cAMP agents such as forskolin increases the MITF protein levels without a connected introduction of messenger RNA, an indication of how the post-transcriptional regulation mechanisms of MITF protein induction function. Although a-MSH regulates the pigment type produced in melanocytes, it is possible that the presence of other elements, for example, thiol compounds pigment type. Tyrosinase defines the pigmentation of human hair and skin. An increase of the tyrosinase enzyme may result in skin diseases such as melisma, actinic damage, and age spots (D'Mello, Finlay, Baguley, & Askarian-Amiri, 2016). Melanin production is lowered by avoiding ultraviolet radiations, or inhibition of melanocyte metabolism and proliferation.
Conclusion
In conclusion, the skin is a vital organ to humans as it has a critical role in protecting the body against UV radiations. Investing in further studies on the process of melanogenesis could as a result of a better understanding of dermatological diseases and skin cancer. Thus, it might help people get a cure for these disorders.
References
Brenner, M., & Hearing, V. J. (2008). The protective role of melanin against UV damage in human skin. Photochemistry and photobiology, 84(3), 539-549.
D'Mello, S., Finlay, G., Baguley, B., & Askarian-Amiri, M. (2016). Signaling pathways in melanogenesis. International journal of molecular sciences, 17(7), 1144.
Fajuyigbe, D., & Young, A. R. (2016). The impact of skin color on human photobiological responses. Pigment cell & melanoma research, 29(6), 607-618.
Videira, I. F. D. S., Moura, D. F. L., & Magina, S. (2013). Mechanisms regulating melanogenesis. Anais brasileiros de dermatologia, 88(1), 76-83.
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