scholarly journals Antimicrobial Properties of α-MSH and Related Synthetic Melanocortins

2006 ◽  
Vol 6 ◽  
pp. 1241-1246 ◽  
Author(s):  
A. Catania ◽  
G. Colombo ◽  
C. Rossi ◽  
A. Carlin ◽  
A. Sordi ◽  
...  
Keyword(s):  
Antimicrobial Peptides ◽  
Mammalian Cells ◽  
Antimicrobial Properties ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Natural Antimicrobial ◽  
Melanocyte Stimulating Hormone ◽  
Evolutionary Spectrum ◽  
The Central Nervous System ◽  
Anti Inflammatory

The natural antimicrobial peptides are ancient host defense effector molecules, present in organisms across the evolutionary spectrum. Several properties of α-melanocyte stimulating hormone (α-MSH) suggested that it could be a natural antimicrobial peptide. α-MSH is a primordial peptide that appeared during the Paleozoic era, long before adaptive immunity developed and, like natural antimicrobial molecules, is produced by barrier epithelia, immunocytes, and within the central nervous system. α-MSH was discovered to have antimicrobial activity against two representative pathogens,Staphylococcus aureusandCandida albicans. The candidacidal influences of α-MSH appeared to be mediated by increases in cell cyclic adenosine monophosphate (cAMP). The cAMP-inducing capacity of α-MSH likely interferes with the yeast's own regulatory mechanisms of this essential signaling pathway. It is remarkable that this mechanism of action in yeast mimics the influences of α-MSH in mammalian cells in which the peptide binds to G-protein-linked melanocortin receptors, activates adenylyl cyclase, and increases cAMP. When considering that most of the natural antimicrobial peptides enhance the local inflammatory reaction, the anti-inflammatory and antipyretic effects of α-MSH confer unique properties to this molecule relative to other natural antimicrobial molecules. Synthetic derivatives, chemically stable and resistant to enzymatic degradation, could form the basis for novel therapies that combine anti-inflammatory and antimicrobial properties.

scholarly journals Anti-Allergic and Anti-Inflammatory Effects of Undecane on Mast Cells and Keratinocytes

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1554
Author(s):  
Dabin Choi ◽  
Wesuk Kang ◽  
Taesun Park
Keyword(s):  
Mast Cells ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Allergic Diseases ◽  
Intracellular Camp ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Skin Conditions ◽  
Factor Α ◽  
Camp Levels

The critical roles of keratinocytes and resident mast cells in skin allergy and inflammation have been highlighted in many studies. Cyclic adenosine monophosphate (cAMP), the intracellular second messenger, has also recently emerged as a target molecule in the immune reaction underlying inflammatory skin conditions. Here, we investigated whether undecane, a naturally occurring plant compound, has anti-allergic and anti-inflammatory activities on sensitized rat basophilic leukemia (RBL-2H3) mast cells and HaCaT keratinocytes and we further explored the potential involvement of the cAMP as a molecular target for undecane. We confirmed that undecane increased intracellular cAMP levels in mast cells and keratinocytes. In sensitized mast cells, undecane inhibited degranulation and the secretion of histamine and tumor necrosis factor α (TNF-α). In addition, in sensitized keratinocytes, undecane reversed the increased levels of p38 phosphorylation, nuclear factor kappaB (NF-κB) transcriptional activity and target cytokine/chemokine genes, including thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC) and interleukin-8 (IL-8). These results suggest that undecane may be useful for the prevention or treatment of skin inflammatory disorders, such as atopic dermatitis, and other allergic diseases.

Effects of hormones on 3', 5' -cyclic adenosine monophosphate in choroid plexus.

1977 ◽  
Vol 232 (4) ◽  
pp. E353
Author(s):  
D Rudman ◽  
B M Hollins ◽  
N C Lewis ◽  
J W Scott
Keyword(s):  
Effective Dose ◽  
Choroid Plexus ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Tyrode Solution ◽  
Minimal Effective Dose ◽  
Camp Content ◽  
Melanocyte Stimulating Hormone ◽  
Stimulating Hormone

Choroid plexus of rabbit and rat was incubated for 2-30 min at 37 degrees C under 95% O2-5% CO2 in Tyrode solution containing 10 mM glucose and 1 mM theophylline with these agents: epinephrine, norepinephrine, isoproterenol, dopamine, histamine, serotonin, arginine, and lysine vasopressins, oxytocin, angiotensin, adrenocorticotropin (ACTH), beta-melanocyte-stimulating hormone, and choroid plexus peptide IIF. After incubation, tissue and medium were analyzed for 3', 5' -cyclic adenosine monophosphate (cAMP) content. Each amine or peptide was tested initially at 1,000 microng/ml. Only ACTH and serotonin affected cAMP content of rabbit choroid plexus. At 1,000 microng/ml, these agents caused a 10 and 4 times (respectively) increase in cAMP content of tissue + medium at 2-10 min with decline in content at 10-30 min. More than 90% of the increment was located in tissue, less than 10% in medium. Minimal effective dose (MED) to cause a significant (P less than .05) accumulation of cAMP was 0.1 microng/ml (2.2 x 10(-8) M) for ACTH and 10 microng/ml (5.7 x10(-3) M) for serotonin. Only isoproterenol, epinephrine, and norepinephrine influenced cAMP content of rat choroid plexus. MED's for this effect by isoproterenol, epinephrine, and norepinephrine were .001, .01, and 10 microng/ml (4.7 x 10(-9), 5.5 x 10(-8), and 5.9 x 10(-5) M), respectively.

scholarly journals Differential Signaling Profiles of MC4R Mutations with Three Different Ligands

2020 ◽  
Vol 21 (4) ◽  
pp. 1224 ◽  
Author(s):  
Sarah Paisdzior ◽  
Ioanna Maria Dimitriou ◽  
Paul Curtis Schöpe ◽  
Paolo Annibale ◽  
Patrick Scheerer ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
G Protein ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Loss Of Function ◽  
Melanocyte Stimulating Hormone ◽  
Melanocortin 4 Receptor ◽  
Erk Phosphorylation ◽  
Extracellular Regulated Kinase ◽  
Peptide Agonist

The melanocortin 4 receptor (MC4R) is a key player in hypothalamic weight regulation and energy expenditure as part of the leptin–melanocortin pathway. Mutations in this G protein coupled receptor (GPCR) are the most common cause for monogenetic obesity, which appears to be mediated by changes in the anorectic action of MC4R via GS-dependent cyclic adenosine-monophosphate (cAMP) signaling as well as other signaling pathways. To study potential bias in the effects of MC4R mutations between the different signaling pathways, we investigated three major MC4R mutations: a GS loss-of-function (S127L) and a GS gain-of-function mutant (H158R), as well as the most common European single nucleotide polymorphism (V103I). We tested signaling of all four major G protein families plus extracellular regulated kinase (ERK) phosphorylation and β-arrestin2 recruitment, using the two endogenous agonists, α- and β-melanocyte stimulating hormone (MSH), along with a synthetic peptide agonist (NDP-α-MSH). The S127L mutation led to a full loss-of-function in all investigated pathways, whereas V103I and H158R were clearly biased towards the Gq/11 pathway when challenged with the endogenous ligands. These results show that MC4R mutations can cause vastly different changes in the various MC4R signaling pathways and highlight the importance of a comprehensive characterization of receptor mutations.

scholarly journals Rottlerin Reduces cAMP/CREB-Mediated Melanogenesis via Regulation of Autophagy

2019 ◽  
Vol 20 (9) ◽  
pp. 2081 ◽  
Author(s):  
Nurinanda Prisky Qomaladewi ◽  
Mi-Yeon Kim ◽  
Jae Youl Cho
Keyword(s):  
Signaling Pathway ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Camp Response Element Binding ◽  
Sequential Process ◽  
Camp Response Element ◽  
Melanin Production ◽  
Melanocyte Stimulating Hormone ◽  
Cellular Autophagy

Melanogenesis is the sequential process of melanin production by melanocytes in order to protect the skin from harmful stimuli. Melanogenesis is disrupted by radiation exposure, which results in the differentiation of melanocytes into melanoma. Recently, some methods have been developed to maintain the instability of melanogenesis in melanoma by activating cellular autophagy. However, there is still a lack of knowledge about how autophagy is involved in the regulation of melanogenesis in melanoma cells. Here, we used rottlerin as an autophagy inducer to investigate the role of the cyclic adenosine monophosphate (cAMP)/cAMP response element binding (CREB) signaling pathway in melanogenesis. We found that rottlerin can inhibit melanin production by targeting cAMP, which is initially activated by alpha-melanocyte stimulating hormone (α-MSH). Our findings suggest that rottlerin has a pivotal role as an autophagy inducer in the regulation of melanogenesis by targeting the cAMP/CREB signaling pathway.

Concentration of 3′,5′ cyclic adenosine monophosphate in ventricular CSF of patients following severe head trauma

1977 ◽  
Vol 47 (4) ◽  
pp. 517-524 ◽  
Author(s):  
Alan S. Fleischer ◽  
Daniel R. Rudman ◽  
C. Babson Fresh ◽  
George T. Tindall
Keyword(s):  
Head Trauma ◽  
Lateral Ventricle ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Content Type ◽  
Therapeutic Implications ◽  
Level Of Consciousness ◽  
The Central Nervous System ◽  
Camp Metabolism ◽  
Coma Grade

✓ Previous studies have demonstrated that cerebrospinal fluid (CSF) from the lateral ventricle of patients without disturbance of sensorium or intracranial pressure, contains 15 to 30 nM 3′,5′ cyclic adenosine monophosphate (cAMP). The concentration of this cyclic nucleotide was measured by radioimmunoassay in 133 samples of CSF from the lateral ventricle of 26 patients who were comatose following acute head trauma for periods up to 40 days. Concentration of CSF cAMP in diminishing coma Grades V, IV, III, II, and I was 1.5 ± 0.1 nM; 1.24 ± 0.34 nM; 3.14 ± 0.7 nM; 10.06 ± 3.47 nM; and 13.36 ± 1.38 nM, respectively. After the sensorium cleared (coma Grade 0), cAMP was 22.0 ± 1.7 nM. The correlation between the grade of coma and cAMP concentration was −0.80 (p > 0.01). These results imply that alteration in the level of consciousness following head trauma is associated with a disturbance of cAMP metabolism within the central nervous system. Possible mechanisms explaining this observation as well as therapeutic implications are discussed.

scholarly journals Alpha-Melanocyte Stimulating Hormone: An Emerging Anti-Inflammatory Antimicrobial Peptide

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Madhuri Singh ◽  
Kasturi Mukhopadhyay
Keyword(s):  
Antimicrobial Activity ◽  
Antimicrobial Peptides ◽  
Antimicrobial Peptide ◽  
Bacterial Pathogens ◽  
Melanocyte Stimulating Hormone ◽  
Antimicrobial Potential ◽  
Anti Inflammatory ◽  
Infective Agent ◽  
Stimulating Hormone

The alpha-melanocyte stimulating hormone (α-MSH) is a neuropeptide belonging to the melanocortin family. It is well known for its anti-inflammatory and antipyretic effects and shares several characteristics with antimicrobial peptides (AMPs). There have been some recent reports about the direct antimicrobial activity ofα-MSH against various microbes belonging to both fungal and bacterial pathogens. Similar toα-MSH’s anti-inflammatory properties, its C-terminal residues also exhibit antimicrobial activity parallel to that of the entire peptide. This review is focused on the current findings regarding the direct antimicrobial potential and immunomodulatory mechanism ofα-MSH and its C-terminal fragments, with particular emphasis on the prospects ofα-MSH based peptides as a strong anti-infective agent.

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