UVB Activates Hypothalamic–Pituitary–Adrenal Axis in C57BL/6 Mice

Abstract

To test the hypothesis that ultraviolet B (UVB) can activate the hypothalamic-pituitary-adrenal (HPA) axis, the shaved back skin of C57BL/6 mice was exposed to 400 mJ/cm2 of UVB or was shame irradiated. After 12 and 24 h of exposure, plasma, skin, brain, and adrenals were collected and processed to measure corticotropin-releasing hormone (CRH), urocortin (Ucn), β-endorphin (β-END), ACTH and corticosterone (CORT) or brain was fixed for immunohistochemical detection of CRH. UVB stimulated plasma levels of CRH, Ucn, β-END, ACTH and CORT, and increased skin expression of Ucn, β-END and CORT at the gene and protein/peptide levels. UVB stimulated CRH gene and protein expression in the brain that was localized to the paraventricular nucleus of the hypothalamus. In adrenal glands it increased mRNAs of melanocortin receptor type 2, StAR and CYP11B1. Hypophysectomy abolished UVB stimulation of plasma but not of skin CORT levels, and had no effect on UVB stimulation of CRH and Ucn levels in the plasma, demonstrating the requirement of an intact pituitary for the systemic effect. In conclusion, we identify mechanism of the regulation of body homeostasis by UVB through activation of the HPA axis that originates in the skin and requires pituitary for the systemic effect.

The Expression of the Endogenous mTORC1 Inhibitor Sestrin 2 Is Induced by UVB and Balanced with the Expression Level of Sestrin 1

“…To restore skin homeostasis in response to UVB induced harm, several signalling cascades such as the cutaneous neuroendocrine hypothalamic-pituitary-adrenal axis and pathways resulting in the stabilisation of p53 are activated [27, 37–40]. The tumor suppressor p53 has an important cellular gatekeeper function maintaining genomic stability in response to cellular stress, such as UVB induced DNA-damage, by inducing DNA-repair or apoptosis [38].…”

“…The former acts not only locally by regulating e.g. the skin barrier function and increasing the pigment production, but contributes also to systemic effects such as the immunosuppressive activity and the attenuation of autoimmune processes [22–27]. …”

Sun Exposure and Its Effects on Human Health: Mechanisms through Which Sun Exposure Could Reduce the Risk of Developing Obesity and Cardiometabolic Dysfunction

“…α-MSH may help prevent obesity by suppressing appetite and enhancing catabolic signals to promote energy consumption through melanocortin receptors 3 and 4 [122,123]. Exposure to UVR is also followed by an increase in other products of POMC such as β-endorphin [115,121,124,125] and adrenocorticotrophin [124] in the skin, serum and hypothalamus. While α-MSH suppresses appetite, β-endorphin has the opposing effect [126].…”

Giant Basal Cell Carcinomas Express Neuroactive Mediators and Show a High Growth Rate: A Case–Control Study and Meta-Analysis of Etiopathogenic and Prognostic Factors

“…20–23 It has been shown that UVR stimulates β-endorphin expression in the skin and serum, 24,25 which may lead to increased pain thresholds and generates addiction to UVR in rodents. 26 Moreover, both β-endorphin and ACTH are expressed more prominently in skin tumors including BCC than in normal skin.…”