Melanocortins: Anti-Inflammatory and Neuroprotective Peptides

Caruso, Carla Mariana; Carniglia, Lila; Durand, Daniela Elizabeth; Scimonelli, Teresa Nieves; Lasaga, Mercedes

doi:10.5772/32672

Cited by 6 publications

(9 citation statements)

References 180 publications

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“…These are G protein-coupled receptors (GPCRs) with seven transmembrane domains, all positively coupled with adenylate cyclase (AC) [33]. Nonetheless, cAMP-independent pathways have also been shown to mediate MCR signaling (reviewed in [34]). In the brain, the most abundant MCR subtypes are MC3R and MC4R [35, 36].…”

Section: Pomc-derived Peptidesmentioning

confidence: 99%

Neuropeptides and Microglial Activation in Inflammation, Pain, and Neurodegenerative Diseases

Carniglia

Ramírez

Durand

et al. 2017

Mediators of Inflammation

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Microglial cells are responsible for immune surveillance within the CNS. They respond to noxious stimuli by releasing inflammatory mediators and mounting an effective inflammatory response. This is followed by release of anti-inflammatory mediators and resolution of the inflammatory response. Alterations to this delicate process may lead to tissue damage, neuroinflammation, and neurodegeneration. Chronic pain, such as inflammatory or neuropathic pain, is accompanied by neuroimmune activation, and the role of glial cells in the initiation and maintenance of chronic pain has been the subject of increasing research over the last two decades. Neuropeptides are small amino acidic molecules with the ability to regulate neuronal activity and thereby affect various functions such as thermoregulation, reproductive behavior, food and water intake, and circadian rhythms. Neuropeptides can also affect inflammatory responses and pain sensitivity by modulating the activity of glial cells. The last decade has witnessed growing interest in the study of microglial activation and its modulation by neuropeptides in the hope of developing new therapeutics for treating neurodegenerative diseases and chronic pain. This review summarizes the current literature on the way in which several neuropeptides modulate microglial activity and response to tissue damage and how this modulation may affect pain sensitivity.

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Section: Pomc-derived Peptidesmentioning

confidence: 99%

Neuropeptides and Microglial Activation in Inflammation, Pain, and Neurodegenerative Diseases

Carniglia

Ramírez

Durand

et al. 2017

Mediators of Inflammation

Self Cite

176

131

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“…It is important to emphasize that NEP activity is implicated not only in ending ACTH signalling, but is also critical to catabolize the amyloid fibrils; the two different systems share the same enzyme to regulate their presence. More provocative is that the ACTH/α‐MSH loop regulates immune and inflammatory reactions, but these factors are also linked to pathologies such as Alzheimer's disease, characterized by an important inflammatory component . Apart from these immunomodulators, the dialogue between the immune and neuroendocrine systems is also mediated by numerous cytokines, as demonstrated in lymphocytes .…”

Section: Discussionmentioning

confidence: 99%

“…It is now recognized that in both invertebrates and vertebrates the non‐self presence is perceived and managed by the two systems, able to influence each other mutually. ACTH and α‐MSH are released by the immunocompetent cells to control immune reactivity . These factors regulate the cellular functions of the immune system locally, in an autocrine and paracrine manner, influencing the proliferation of immune mediator production and immunocyte trafficking .…”

Section: Introductionmentioning

confidence: 99%

NET amyloidogenic backbone in human activated neutrophils

Pulze

Bassani

Gini

et al. 2015

Clinical and Experimental Immunology

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SummaryActivated human neutrophils produce a fibrillar DNA network [neutrophil extracellular traps (NETs)] for entrapping and killing bacteria, fungi, protozoa and viruses. Our results suggest that the neutrophil extracellular traps show a resistant amyloidogenic backbone utilized for addressing reputed proteins and DNA against the non-self. The formation of amyloid fibrils in neutrophils is regulated by the imbalance of reactive oxygen species (ROS) in the cytoplasm. The intensity and source of the ROS signal is determinant for promoting stress-associated responses such as amyloidogenesis and closely related events: autophagy, exosome release, activation of the adrenocorticotrophin hormone/ a-melanocyte-stimulating hormone (ACTH/a-MSH) loop and synthesis of specific cytokines. These interconnected responses in human activated neutrophils, that have been evaluated from a morphofunctional and quantitative viewpoint, represent primitive, but potent, innate defence mechanisms. In invertebrates, circulating phagocytic immune cells, when activated, show responses similar to those described previously for activated human neutrophils. Invertebrate cells within endoplasmic reticulum cisternae produce a fibrillar material which is then assembled into an amyloidogenic scaffold utilized to convey melanin close to the invader. These findings, in consideration to the critical role played by NET in the development of several pathologies, could explain the structural resistance of these scaffolds and could provide the basis for developing new diagnostic and therapeutic approaches in immunomediated diseases in which the innate branch of the immune system has a pivotal role.

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“…These molecules have a direct role in immune defences. ACTH is widely expressed in various tissues (as well demonstrated in immunocytochemical localizations) and it is synthesized not only by cells of nervous system but also by nonneural cells [17][18][19]. ACTH expression is induced in stress conditions (such as ROS increase, lipopolysaccharide (LPS) administration, presence of bacteria and proinflammatory cytokine administration) to regulate the immune cellular functions influencing proliferation, migration, production of immune mediators, and trafficking of immunocytes.…”

Section: Types Of Cells and Subcellular Districts Involved In Amyloidmentioning

confidence: 99%

Amyloidogenesis and Responses to Stress

Eguileor¹,

Girardello²,

Grimaldi³

et al. 2016

Exploring New Findings on Amyloidosis

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Amyloidogenesis is a primitive, physiological response that seems to be an ancient process widely distributed in different cell types of evolutionary distant organisms. The amyloid fibril synthesis is part of a more general inflammatory response to stressful conditions all entailing overproduction of reactive oxygen species (ROS). Interestingly, this event has been integrated into additional physiological functions: (i) the formation of a scaffold promoting the activation and packaging of melanin; (ii) the formation of a scaffold to compartmentalize hormones in the cytoplasm; (iii) the ability to reversibly link different types of molecules to drive close to the nonself; (iv) the construction of a framework to close body lesions. Amyloid fibril formation is a cellular response harmonically integrated with the stress response but for a deregulation in assembling/dismantling, dangerous depots, as in a lot of pathologies, can occur.

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Melanocortins: Anti-Inflammatory and Neuroprotective Peptides

Cited by 6 publications

References 180 publications

Neuropeptides and Microglial Activation in Inflammation, Pain, and Neurodegenerative Diseases

Neuropeptides and Microglial Activation in Inflammation, Pain, and Neurodegenerative Diseases

NET amyloidogenic backbone in human activated neutrophils

Amyloidogenesis and Responses to Stress

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