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The Production of Biologically Active Peptides in Brain Tissues
Published in Gerard O’Cuinn, Metabolism of Brain Peptides, 2020
With the exception of carnosine, all other neuropeptides are thought to be synthesized ribosomally as protein precursors from which active neuropeptides may be subsequently excised by specific enzymatic mechanisms. These protein precursors may contain sequences for quite closely related, but not identical, peptides as well as sequences for quite unrelated neuropeptides. To ensure the integrity of a particular peptide could require the segregation of the nascent precursor away from non-specific degradation mechanisms and towards organelles and/or vesicles containing the enzymes appropriate for specific excision, thereby increasing the diversity of molecules that are to be used for chemical signalling between cells. Thus, the production of neuropeptides from multipotential precursors could be dependent on the enzyme complement of the secretory vesicles or other subcellular compartments in various brain regions. Delaying the production of an active peptide until it reaches a secretory vesicle has the potential advantage of preventing it from acting inside the cell that synthesizes it. Our current perspectives on all of these events are reviewed here.
Neuroendocrine Morphology
Published in Paul V. Malven, Mammalian Neuroendocrinology, 2019
Cytological Features of Adenohypophysial Secretion. Hormones are synthesized, packaged into secretory vesicles, and secreted from adenohypophysial cells in ways that appear to be similar to those of other hormone-secreting cells. Gene transcription and RNA processing occurs in the nucleus followed by transport of the mRNA to the RER where synthesis of the prohormone occurs. The prohormone is cleaved into the products for secretion, and occasionally subunits produced from different gene transcripts are covalently linked. The secretory products are packaged into dense-core secretory vesicles in the Golgi apparatus from which they migrate to a position near the plasma membrane to await release. Release into the extracellular space occurs by exocytosis wherein (1) the membrane of the secretory vesicle fuses with the inner surface of the plasma membrane, (2) the double layer of fused membrane breaks down, and (3) the contents of the secretory vesicle enter the extracellular space. The speed of the entire process of synthesis, packaging, and exocytosis probably depends upon the intensity of stimulation of the adenohypophysial cell. Studies with strongly stimulated mammotrophs from rats suggest that the entire process can occur in as little as 50 min, but this may represent a lower limit.
Enzymes
Published in Stephen W. Carmichael, Susan L. Stoddard, The Adrenal Medulla 1986 - 1988, 2017
Stephen W. Carmichael, Susan L. Stoddard
Using monoclonal antibodies specific for the p60c-src, Parsons and Creutz (1986) detected high levels of this kinase in adrenal medullary tissue and in highly purified chromaffin vesicle membranes. An immune complex kinase assay was applied to fractions of adrenal medulla resolved on sucrose-density gradients. Thirty-seven percent of the total tissue p60c-src activity was found in association with chromaffin vesicles. Localization of a significant fraction of total cellular kinase activity to this secretory vesicle membrane suggests that the kinase may function in the regulation of neurotransmitter release.
Inhibitory evaluation of Curculigo latifolia on α-glucosidase, DPP (IV) and in vitro studies in antidiabetic with molecular docking relevance to type 2 diabetes mellitus
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Nur Athirah Zabidi, Nur Akmal Ishak, Muhajir Hamid, Siti Efliza Ashari, Muhammad Alif Mohammad Latif
Apparently, the active compounds regulated in the extracts also contribute to promoting the effects by improving the secretion of insulin. Relatively, the observation made on the in vitro effect of the extracts on insulin secretion seen in BRIN-BD11 cell line, clearly establishes that root extracts appear to display a better activity in the secretion of insulin as compared with fruit extracts. The presence of phytochemicals in the extracts that facilitate the insulin release on pancreatic cell substantiates our observed effectiveness. With the presence of cinnamic acid derivatives, this active compounds capable in inducing Ca2+ in pancreatic β-cell and this indicates that the stimulating insulin secretion process by cinnamic acid is due to an increase in Ca2+ flow through the L-type Ca2+ channels without causing membrane depolarisation by closing the KATP channels34. The consequent depolarisation leading to the opening of Ca2+ channels and Ca2+ intracellular elevation mediating insulin secretory vesicle exocytosis36. These findings were in well correlate with other studies that reporting the enhancement in promoting insulin release that being stimulated with the presence of cinnamic acid37.
Recent advances in the understanding of enterovirus A71 infection: a focus on neuropathogenesis
Published in Expert Review of Anti-infective Therapy, 2021
Han Kang Tee, Mohd Izwan Zainol, I-Ching Sam, Yoke Fun Chan
In recent years, HS has gained importance in EV-A71 entry and pathogenesis [46]. It is a negatively charged linear polysaccharide that consists of repeating units of uronic acid and D-glucosamine [62]. HS is attached to a core protein and is therefore known as heparan sulfate proteoglycan (HSPGs). HSPGs can be divided into three main groups depending on their locations: membrane, secreted extracellular matrix, and secretory vesicle proteoglycan [63]. HS-receptor interaction was reported to be mediated by electrostatic interaction between amino acid clusters on the ligand and concentrated negatively charged regions on the sulfated polysaccharide chains [64]. Tan and colleagues (2013) discovered that EV-A71 utilizes HS as an attachment receptor to facilitate infection in cell culture [46]. They further showed that multiple VP1 residues, specifically VP1-98 and VP1-145 residues at the five-fold axis of EV-A71 possess high plasticity and are responsible for HS interaction [65]. Due to this HS interaction, EV-A71 tends to mutate and acquire positively charged residues at the five-fold axis when propagated in cell culture, leading to HS-associated adaptation [65,66]. Tee et al. (2019) analyzed multiple EV-A71 clinical isolate sequences available from GenBank and found that HS-binding viruses were more likely selected through cell culture adaptation [66]. In contrast, HS-binding viruses are disadvantaged in vivo, as previously demonstrated in suckling mice [66]. We have previously hypothesized that weak heparin-binding viruses are associated with virulence in humans, as evidenced by the detection of VP1-145E in the sequences of a fatal encephalitis autopsy specimen [34].
Assessing the role of Porphyromonas gingivalis in periodontitis to determine a causative relationship with Alzheimer’s disease
Published in Journal of Oral Microbiology, 2019
Ding et al. [62] investigated periodontal disease effects on the brain in C57BL/6J wild-type mice in four (young) and 52-week (middle-aged) groups (Table 1). Induction of experimental periodontitis was by an oral dose of live P. gingivalis (ATCC 33277T) mono-infection using 1 × 109 CFU, which was repeated every 48 h over six weeks in each group. Evidence of intracerebral inflammation was obtained by inflammatory cytokine gene expression (using molecular biology methodologies), and protein release (using ELISA assay). Cytokine levels (IL-1β, IL-6 and TNF-α) by both methods were significantly higher in the P. gingivalis mono-infected older age group. Ding et al. [62] also performed behavioural tests and demonstrated statistically significant outcomes for impaired spatial learning and memory in the older age (middle-aged, 52 week) group infected with P. gingivalis compared to the younger (4-week old) and middle-aged uninfected mice. Increased intracerebral inflammation accounted for the impaired spatial learning and memory following experimental periodontitis. The lack of demonstration of P. gingivalis or its LPS entry into the mouse brain alongside omission of observations towards Aβ protein in the neuronal cell body is a weakness of the study. This may imply that any sequestered Aβ in the regulated secretory vesicle pathway generated by cathepsin B processing was below detection limits, provided the bacterium and or its LPS entered the brain. However, functional tests provide useful causal links with AD phenotype according to advancing age, but imply that this is an inflammation-mediated event secondary to infection.