Actions of steroid hormones

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There are five main classes of natural steroid hormones and these are; glucocorticoids, mineralocorticoids, androgens, estrogens and progestagens. They are made from cholesterol and they are able to carry out their actions by moving through the membrane and attaching themselves to steroid hormone receptors. Once a steroid hormone has attached itself to a ligand of a particular receptor; this results in the receptor undergoing an alteration in conformation. Thus causing the steroid hormone receptor to come apart from proteins; enabling attached ligand to bind to steroid hormone response elements hence control expression. So, therefore steroid hormone receptors have always been thought to exert their actions by controlling procedures of transcription, although more recently, non genomic actions of steroid hormones have been distinguished. Non genomic actions are for example, dependant upon proteins and do not rely on protein synthesis or even transcription [1]. Steroid hormone receptors directly affect gene expression whereas non genomic actions of steroid hormones do not, but instead function via signalling cascades.

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A non genomic action of a steroid hormone occurs when the steroid hormone is not able to move into a cell or it is not able to communicate with the receptors inside. These non genomic actions of steroid hormones usually tend to last a very short time scale; so from the time the steroid is administered to the start of the response takes somewhere between seconds to minutes. In contradiction, the genomic actions of steroid hormones lasts for several hours; this suggests that non genomic mechanisms may be reversed straight away. Non genomic actions are not affected by transcription or even the inhibitors of translation but they do utilise second messengers [2]. Moreover, further evidence of non genomic actions can be seen with the use of receptor antagonists which cannot function because they are unable to inhibit the non genomic effects of steroid hormones. I shall now go into depth on the evidence obtained for the non genomic actions of various steroid hormones.

Vitamin D is a lipophilic, steroid hormone derivative. 1 alpha, 25-dihydroxyvitamin D3 is an example of vitamin D and there is evidence that it carries out non genomic actions in osteoblasts [3] which inevitably influence the functioning of phospholipase C and additionally, the activation of 1 alpha, 25-dihydroxyvitamin D3 results in elevated levels of calcium in the heart in a time scale of seconds to minutes. Osteoblasts do not consist of a vitamin D receptor so it is assumed that the non genomic actions indicate a connection with a signalling cascade and there has been evidence of a receptor located in the osteoblasts when the vitamin D receptor is not present. It is this receptor which then identifies 1 alpha, 25-dihydroxyvitamin D3 and these non genomic mechanisms regulate the hormone's actions. This in turn could suggest evidence that these non genomic actions have a role in regulating the actions influenced by 1 alpha, 25-dihydroxyvitamin D3.

Furthermore, non genomic actions of the steroid hormones; progesterone and androstenedione for example, on the reproductive cells; granulosa cells and oocytes [4] affect the generation of second messengers in an accelerated fashion, which includes calcium. These non genomic actions are initiated by the attachment of the aforementioned steroid hormones to their steroid hormone receptor. Additionally, the non genomic effects of progesterone on male reproductive cells of humans have been studied [5]. The non genomic effects of progesterone stimulate sperm throughout fertilisation. Progesterone initiates a fast entry of calcium ions in the sperm which initiates a reaction in the acrosome. This entry of calcium ions is not blocked by antagonists and studies have shown that antagonists of receptors are unable to inhibit a rise in calcium. Only recently, proteins have been identified as progesterone's membrane receptor but more work is yet to be done. Also, another study has shown that incubating the sperm of humans with 17ß estradiol activates the movement of sperm [4]. Actions of estrogens are regulated by non genomic effects as sperm is tightly packed with DNA and the chances of protein synthesis occurring is highly unlikely therefore, genomic effects of steroid hormones is beyond the bounds of possibility. I shall go into more depth on further non genomic actions of estrogens later.

In mammals, progesterone regulates pregnancy by maintaining the uterus and it is able to do this by reducing the effects of oxytocin on the reproductive organ [6]. The non genomic actions of progesterone which involve progesterone binding to the oxytocin receptor prevent oxytocin attaching itself to its receptor in the reproductive organ hence causing the prevention of signalling. This binding causes an alteration in the conformation of the oxytocin receptor which results in oxytocin being unable to form a complex with its receptor. This example is evidence that steroid hormones need not always have to bring about modifications in expression. Similarly, when progesterone binds to oxytocin receptors in rats; this prevents the generation of calcium for example. This occurs because progesterone binds to the oxytocin receptor; resulting in an alteration to the receptor's structure hence oxytocin is unable to bind to its specific receptor. This is evidence of a non genomic mechanism of progesterone and it can be reversed straight away.

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Additionally, in rodents it is known that sexual receptivity is regulated by androgens and progestins [7]. The presence of progesterone in the ventral tegmental area and ventromedial hypothalamus is crucial for aiding lordosis but the effects of progesterone in both these locations are not the same. Investigations into female rodents have suggested that the effects of progesterone at the ventral tegmental area do not need progestin receptors whereas at the ventromedial hypothalamus, they do need progestin receptors [7]. When progestins are administered to the ventral tegmental area, they assist with the progress of lordosis. The control of GABAa benzodiazepine receptor complexes within the ventral tegmental area leads to a change in lordosis [7]. This alteration implies that progestins could engage with GABAa benzodiazepine receptor complexes in order to assist with the behaviour. In the ventral tegmental area, for example if the metabolism of progesterone to 3a,5a-tetrahydroprogesterone is affected then this causes sexual receptivity to weaken [7]. There is a possibility that progesterone could assist with the progress of lordosis after this metabolism of progesterone. This may result in actions at these receptor complexes to regulate sexual receptivity. Furthermore, when there are no androgen receptors present, 3a-androstanediol is able to put a stop to this behaviour. 3a-androstanediol is able to prevent lordosis when the actions of these complexes have changed [7]. This evidence implies that 3a,5a-tetrahydroprogesterone and 3a-androstanediol undergo actions non genomically in order to affect lordosis.

Moreover, it has been shown in an investigation that glucocorticoids behave in a non genomic fashion and the investigation was carried out in the B103 cells of a rat [8]. These cells were incubated with corticosterone which prevented an increase in calcium concentration however, it was reported that 5-hydroxytyptamine caused an increase in calcium straight away but stimulation of protein kinase C decreased calcium concentration and effects of glucocorticoids are regulated by protein kinase C [8]. Antagonists to the glucocorticoid receptor were unable to affect the effects. This study gives evidence that in these cells; glucocorticoids are able to regulate the 5-hydroxytyptamine which brings about calcium increase non genomically.

Aldosterone originates from mineralocorticoids and investigations into the actions of aldosterone in lymphocytes show that aldosterone undergoes non genomic actions [9]. The non genomic actions of aldosterone cause the activation of protein kinase C in the kidney and these non genomic actions lead to second messengers increasing [9]. Studies have shown that within the kidney, aldosterone activates the hydrogen ion ATPase [9] through movement to the tip of the membrane which is linked to a rise in calcium ion and protein kinase C stimulation. It was proved that an antagonist to a mineralocorticoid receptor was unable to influence the actions of aldosterone [9]. This is expected because non genomic actions cannot be inhibited by receptor antagonists.

Not to mention, the actions of estrogens are controlled via the estrogen receptors a and ß. Non genomic actions of estrogen mean that the estrogen receptors control gene expression where there are no response elements of estrogen. For example, as I have previously mentioned, studies have shown that 17ß-estradiol acts in a non genomic manner and it is able to increase the influx of calcium but also generates cyclic adenosine monophosphate by stimulating the protein kinase network [10]. It has been reported that in varied cells such as endothelial cells; estrogens are able to stimulate the generation of endothelial nitric oxide synthase which results in blood vessels dilating very fast [11]. In addition, some estrogen receptors become stimulated by binding to caveolin-1 [10] and associating with tyrosine kinase which enables signals to be released. They can also associate with striatin which causes the estrogen receptor to increase calcium concentration and inevitably increase stimulation of endothelial nitric oxide synthase. Also the estrogen receptor is able to associate with the Insulin-like growth factor 1 receptor because it is stimulated by 17ß-estradiol. This results in the Insulin-like growth factor 1 receptor becoming activated hence the protein kinase signalling network becomes stimulated. It's been suggested that estrogen receptor antagonists could prevent endothelial nitric oxide synthase release [11] but more research is yet to be done.

In conclusion, I have explained the non genomic responses of various steroid hormones and only recently has the idea that steroid hormones are able to initiate a response from cells without having to rely on transcription been identified. The non genomic effects of steroid hormones are dependant upon the constituents utilised and this means the steroid used. In addition, the signalling cascades of individual steroid hormones seem to be alike however, the procedures carried out are not the same. Second messengers are able to affect non genomic aswel as genomic actions and this cross communication seems to be vital in the actions of steroid hormones. Non genomic actions of steroid hormones have been evident for longer than a few decades but the mechanisms of the receptors bringing about these increased actions are yet to be fully understood. Physiological but also clinical purpose of steroid hormone effects is a crucial objective that should eventually be achieved. Much research into the non genomic actions of steroid hormones is still necessary, such as there are still no precise proteins known to be assuming the role of a membrane receptor which causes steroid hormone action. Lastly, a clone of this receptor would be a great progress in development although, not all important research yet to be done requires a clone of the receptor.

References

  1. Wehling, M. and Losel, R (2006). Non-genomic steroid hormone effects: Membrane of intracellular receptors? The Journal of Steroid Biochemistry and Molecular Biology. 102 (1-5), pp. 180-183
  2. Falkenstein, E., Tillmann, H.-C., Christ, M., Feuring, M., Wehling, M (2000). Multiple actions of steroid hormones-a focus of rapid, nongenomic effects. Pharmacological Reviews. 52 (4), pp. 513-556
  3. Baran, D (1994). Nongenomic actions of the steroid hormone 1 alpha, 25-dihydroxyvitamin D3. J. Cell. Biochem. 56, pp. 303-306
  4. Revelli, A., Massobrio, M., Tesarik, J (1998). Nongenomic actions of steroid hormones in reproductive tissues. Endocrine Reviews. 19 (1), pp. 3-17
  5. Baldi, E., Krausz, C., Luconi, M., Bonaccorsi, L., Maggi, M., Forti, G (1995). Actions of progesterone on human sperm: A model of non-genomic effects of steroids. The Journal of Steroid Biochemistry and Molecular Biology. 53 (1-6), pp. 199-203
  6. Dunlap, K. and Stormshak, F (2004). Nongenomic inhibition of oxytocin binding by progesterone in the ovine uterus. Biology of Reproduction. 70 (1), pp. 65-69
  7. Frye, C (2001). The role of neurosteroids and non-genomic effects of progestins and androgens in mediating sexual receptivity of rodents. Brain Research Reviews. 37 (1-3), pp. 201-222
  8. Han, J.-Z., Lin, W., Lou, S.-J., Qiu, J., Chen, Y.-Z (2002). A rapid, nongenomic action of glucocorticoids in rat B103 neuroblastoma cells. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 1591 (1-3), pp. 21-27
  9. Chun, T.-Y. and Pratt, J.-H (2004). Non-genomic effects of aldosterone: new actions and questions. Trends in Endocrinology and Metabolism. 15 (8), pp. 353-354
  10. Bjornstrom, L. and Sjoberg, M (2005). Mechanisms of estrogen receptor signalling: convergence of genomic and nongenomic actions on target genes. Molecular Endocrinology. 19 (4), pp. 833-842
  11. Mendelsohn, M.-E (2002). Genomic and nongenomic effects of estrogen in the vasculature. The American Journal of Cardiology. 90 (1), pp. F3-F4
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