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Postulated Physiological and Pathophysiological Roles on Motility
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
Hans-Dieter Allescher, Sultan Ahmad
Proenkephalin B, which is also termed prodynorphin and is expressed in the CNS and in the digestive tract, contains a variety of opioid peptides (α-neoendorphin, β-neoendorphin, dynorphin A [1—17, 1—13, 1—9, 1—8], dynorphin B [1—29, 1—12], and rimorphin).
Selective Post-Translational Processing of Opioid Peptides in Cardioregulatory Mechanisms of the Dorsal Medulla
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
William R. Millington, Michael D. Hirsch
Prodynorphin processing is relatively uncomplicated compared to POMC and proenkephalin.27,28 The prohormone contains three copies of leu-enkephalin clustered near its C-terminal, each of which forms the N-terminal of a different set of dynorphin peptides; α-neo-endorphin, dynorphin A (dynorphin-1-17), and dynorphin B-29 (leumorphin). These, in turn, serve as precursors to yet smaller forms. Hence, α-neo-endorphin is converted to β-neo-endorphin through removal of its C-terminal arginine residue, and dynorphin-1-17 undergoes endoproteolytic cleavage at a single arginine residue, forming dynorphin-1-8. Dynorphin B-29 is similarly processed at a single arginine, forming a 13-amino-acid peptide, dynorphin B (rimorphin). Leu-enkephalin may also be a product of prodynorphin processing, at least in certain brain regions.60 Like other opioids, the ratio of dynorphin peptides varies regionally, although dynorphin-18, dynorphin B, and α-neo-endorphin predominate in many brain areas.25,26,28,61
Neuropeptide Alterations in Depression and Anxiety Disorders
Published in Siegfried Kasper, Johan A. den Boer, J. M. Ad Sitsen, Handbook of Depression and Anxiety, 2003
David A. Gutman, Dominique L. Musselman, Charles B. Nemeroff
At the genomic level, there are three genes responsible for the precursors of opioid peptides: pro-opiomelanocortin (POMC), proenkephalin, and prodynorphin. Consequently, there are at least three classes of opioid peptides with different biosynthetic and neuronal pathways: the endorphins, enkephalins, and dynorphins. In the adenohypophysis [133], POMC is processed to yield only ACTH and β-lipotropin. β-lipotropin is then processed to yield at least three compounds, including β-γ, and β-endorphin. The second endogenous opioid system is composed of met- and leuenkephalin, whose precursor is proenkephalin. Derivatives of prodynorphin are the third group of endogenous opioid peptides, including dynorphin A, dynorphin B, and neoendorphin, which are located almost exclusively in the posterior pituitary.
The impact of smoking and the influence of other factors on lung cancer
Published in Expert Review of Respiratory Medicine, 2019
The catecholamine neurotransmitters Epi and Nor are also called stress neurotransmitters because they are released from the adrenal gland and from the sympathicus branch of the autonomic nervous system in response to psychological stress. Psychological stress, therefore, enhances beta-adrenergic receptor signaling throughout the mammalian body. In accord with the preclinical studies that identified β-ARs as important regulators of PAC cell proliferation and migration in vitro, studies in mice have shown that experimentally induced chronic social stress significantly promoted the growth of xenografts from human PAC cell lines with Clara cell phenotype [76]. This effect was associated with increased systemic corticosterone levels and increased levels of Epi, Nor, cAMP, and VEGF in the tumors and blood, while GABA levels were decreased. Moreover, the expression of multiple activated signaling proteins associated with cell proliferation and migration was increased in the tumor tissue. All of these cancer-promoting effects of social stress were completely abrogated by treatment of the animals with GABA [76]. The observed stress-induced promotion of PAC xenograft growth was further supported by findings that Epi stimulated the self-renewal of PAC cancer stem cells in vitro via beta-adrenergic cAMP-mediated signaling that enhanced the expression of the stem cell markers sonic hedgehog (SHH), aldehyde dehydrogenase-1 (ALDH-1) and Gli1 [77]. These effects were inhibited by GABA and dynorphin B, both of which blocked the formation of cAMP via Gi-coupled GABAB-Rs and opioid peptide receptors, respectively [77]. These findings suggest that positive emotions that increase the levels of endogenous GABA and opioids may inhibit the development of PAC. In support of this hypothesis, stress reduction by environmental enrichment had strong growth-inhibiting effects on PAC xenografts in mice [77]. This effect was accompanied by decreases in stress neurotransmitters cAMP, VEGF and by reductions in activated tumor stimulating signaling proteins, whereas the levels of GABA and the endogenous opioid peptides dynorphin B and methenkephalin were significantly elevated [77]. Collectively, these preclinical findings indicate that psychological factors can strongly influence the development and progression of PAC. Since stressful situations are among the factors that prompt smokers to crave a cigarette [78], stress in smokers may increase their risk for the development of PAC and promote the progression of this cancer. However, while epidemiological and clinical observations have reported that psychological stress increases lung cancer mortality [79] and lung cancer risk [80], these studies did not distinguish between individual histological lung cancer types.