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Cells May 2024Heart failure is the common concluding pathway for a majority of cardiovascular diseases and is associated with cardiac dysfunction. Since heart failure is invariably... (Review)
Review
Heart failure is the common concluding pathway for a majority of cardiovascular diseases and is associated with cardiac dysfunction. Since heart failure is invariably preceded by adaptive or maladaptive cardiac hypertrophy, several biochemical mechanisms have been proposed to explain the development of cardiac hypertrophy and progression to heart failure. One of these includes the activation of different neuroendocrine systems for elevating the circulating levels of different vasoactive hormones such as catecholamines, angiotensin II, vasopressin, serotonin and endothelins. All these hormones are released in the circulation and stimulate different signal transduction systems by acting on their respective receptors on the cell membrane to promote protein synthesis in cardiomyocytes and induce cardiac hypertrophy. The elevated levels of these vasoactive hormones induce hemodynamic overload, increase ventricular wall tension, increase protein synthesis and the occurrence of cardiac remodeling. In addition, there occurs an increase in proinflammatory cytokines and collagen synthesis for the induction of myocardial fibrosis and the transition of adaptive to maladaptive hypertrophy. The prolonged exposure of the hypertrophied heart to these vasoactive hormones has been reported to result in the oxidation of catecholamines and serotonin via monoamine oxidase as well as the activation of NADPH oxidase via angiotensin II and endothelins to promote oxidative stress. The development of oxidative stress produces subcellular defects, Ca-handling abnormalities, mitochondrial Ca-overload and cardiac dysfunction by activating different proteases and depressing cardiac gene expression, in addition to destabilizing the extracellular matrix upon activating some metalloproteinases. These observations support the view that elevated levels of various vasoactive hormones, by producing hemodynamic overload and activating their respective receptor-mediated signal transduction mechanisms, induce cardiac hypertrophy. Furthermore, the occurrence of oxidative stress due to the prolonged exposure of the hypertrophied heart to these hormones plays a critical role in the progression of heart failure.
Topics: Heart Failure; Humans; Cardiomegaly; Signal Transduction; Animals; Angiotensin II; Oxidative Stress
PubMed: 38786079
DOI: 10.3390/cells13100856 -
Frontiers in Neural Circuits 2022Neuropeptides, a diverse class of signaling molecules in the nervous system, modulate various biological effects including membrane excitability, synaptic transmission... (Review)
Review
Neuropeptides, a diverse class of signaling molecules in the nervous system, modulate various biological effects including membrane excitability, synaptic transmission and synaptogenesis, gene expression, and glial cell architecture and function. To date, most of what is known about neuropeptide action is limited to subcortical brain structures and tissue outside of the central nervous system. Thus, there is a knowledge gap in our understanding of neuropeptide function within cortical circuits. In this review, we provide a comprehensive overview of various families of neuropeptides and their cognate receptors that are expressed in the prefrontal cortex (PFC). Specifically, we highlight dynorphin, enkephalin, corticotropin-releasing factor, cholecystokinin, somatostatin, neuropeptide Y, and vasoactive intestinal peptide. Further, we review the implication of neuropeptide signaling in prefrontal cortical circuit function and use as potential therapeutic targets. Together, this review summarizes established knowledge and highlights unknowns of neuropeptide modulation of neural function underlying various biological effects while offering insights for future research. An increased emphasis in this area of study is necessary to elucidate basic principles of the diverse signaling molecules used in cortical circuits beyond fast excitatory and inhibitory transmitters as well as consider components of neuropeptide action in the PFC as a potential therapeutic target for neurological disorders. Therefore, this review not only sheds light on the importance of cortical neuropeptide studies, but also provides a comprehensive overview of neuropeptide action in the PFC to serve as a roadmap for future studies in this field.
Topics: Neuropeptide Y; Neuropeptides; Prefrontal Cortex; Synaptic Transmission; Vasoactive Intestinal Peptide
PubMed: 35800635
DOI: 10.3389/fncir.2022.796443 -
Pediatric Critical Care Medicine : a... Aug 2022To compare the prevalence of adverse events related to vasoactive drug infusions administered via a peripheral venous catheter versus a central venous or intraosseous... (Observational Study)
Observational Study
OBJECTIVES
To compare the prevalence of adverse events related to vasoactive drug infusions administered via a peripheral venous catheter versus a central venous or intraosseous catheter.
DESIGN
Retrospective observational study.
SETTING
A pediatric critical care transport team, and the PICUs and regional hospitals within the North Thames and East Anglia regions of the United Kingdom.
PATIENTS
Children (up to 18 yr old) transported by the Children's Acute Transport Service receiving an infusion of a vasoactive drug (epinephrine, dobutamine, dopamine, norepinephrine, and vasopressin).
INTERVENTIONS
None.
MEASUREMENTS AND MAIN RESULTS
The medical records of all children transported between April 2017 and May 2020 receiving a vasoactive drug infusion were reviewed and cross-referenced with the service critical incident database. The outcome measure was anatomic catheter-related adverse events (including extravasation) reported during transport or in the first 24 hours on the PICU. During the study period, the service undertook 3,836 transports. Vasoactive drugs were administered during 558 patient transports (14.5%). During 198 of 558 transports (35.5%), vasoactive drugs were administered via a peripheral venous catheter, with seven of 198 (3.5%) adverse events. One extravasation event resulted in tissue necrosis. The median time to injury after the infusion was commenced was 60 minutes (interquartile range, 30-60 min). During 360 of 558 transports (64.5%), vasoactive infusions were administered by central venous or intraosseous catheter, with nine of 360 (2.5%) adverse events.
CONCLUSIONS
During pediatric critical care transport, we did not find a difference in prevalence of adverse events following the administration of vasoactive drugs via peripheral venous catheters or via central venous and intraosseous catheters.
Topics: Child; Critical Care; Dobutamine; Dopamine; Epinephrine; Humans; Norepinephrine; Retrospective Studies
PubMed: 35481954
DOI: 10.1097/PCC.0000000000002972 -
Current Medicinal Chemistry 2021Parkinson's disease is one of the most common neurodegenerative disorders and although its aetiology is not yet fully understood, neuroinflammation has been identified...
BACKGROUND
Parkinson's disease is one of the most common neurodegenerative disorders and although its aetiology is not yet fully understood, neuroinflammation has been identified as a key factor in the progression of the disease. Vasoactive intestinal peptide and pituitary adenylate-cyclase activating polypeptide are two neuropeptides that exhibit anti-inflammatory and neuroprotective properties, modulating the production of cytokines and chemokines and the behaviour of immune cells. However, the role of chemokines and cytokines modulated by the endogenous receptors of the peptides varies according to the stage of the disease.
METHODS
We present an overview of the relationship between some cytokines and chemokines with vasoactive intestinal peptide, pituitary adenylate cyclase activating polypeptide and their endogenous receptors in the context of Parkinson's disease neuroinflammation and oxidative stress, as well as the modulation of microglial cells by the peptides in this context.
RESULTS
The two peptides exhibit neuroprotective and anti-inflammatory properties in models of Parkinson's disease, as they ameliorate cognitive functions, decrease the level of neuroinflammation and promote dopaminergic neuronal survival. The peptides have been tested in a variety of in vivo and in vitro models of Parkinson's disease, demonstrating the potential for therapeutic application.
CONCLUSION
More studies are needed to establish the clinical use of vasoactive intestinal peptide and pituitary adenylate cyclase activating polypeptide as safe candidates for treating Parkinson's disease, as the use of the peptides in different stages of the disease could produce different results concerning effectiveness.
Topics: Humans; Parkinson Disease; Pituitary Adenylate Cyclase-Activating Polypeptide; RNA, Messenger; Receptors, Vasoactive Intestinal Polypeptide, Type I; Vasoactive Intestinal Peptide
PubMed: 32196442
DOI: 10.2174/0929867327666200320162436 -
Endocrine, Metabolic & Immune Disorders... 2020Rheumatoid arthritis (RA) is an autoimmune inflammatory disease comparing the inflammation of synovium. Macrophage-like synoviocytes and fibroblast-like synoviocytes... (Review)
Review
Rheumatoid arthritis (RA) is an autoimmune inflammatory disease comparing the inflammation of synovium. Macrophage-like synoviocytes and fibroblast-like synoviocytes (synoviocytes) are crucial ingredients of synovium. Therein, a lot of research has focused on synoviocytes. Researches demonstrated that TLR1, TLR2, TLR3, TLR4, TLR5, TLR6 TLR7 and TLR9 are expressed in synoviocyte. Additionally, the expression of TLR2, TLR3, TLR4 and TLR5 is increased in RA synoviocyte. In this paper, we review the exact role of TLR2, TLR3, TLR4 and TLR5 participate in regulating the production of inflammatory factors in RA synoviocyte. Furthermore, we discuss the role of vasoactive intestinal peptide (VIP), MicroRNA, Monome of Chinese herb and other cells (Monocyte and T cell) influence the function of synoviocyte by regulating TLRs. The activation of toll-like receptors (TLRs) in synoviocyte leads to the aggravation of arthritis, comparing with angiogenesis and bone destruction. Above all, TLRs are promising targets for managing RA.
Topics: Animals; Antirheumatic Agents; Arthritis, Rheumatoid; Humans; MicroRNAs; RANK Ligand; Synovial Membrane; Synoviocytes; T-Lymphocytes; Toll-Like Receptors; Vasoactive Intestinal Peptide
PubMed: 32338225
DOI: 10.2174/1871530320666200427115225 -
Blood Transfusion = Trasfusione Del... Oct 2017Here we review recent data and the evolving understanding of the role of red blood cell-derived microparticles (RMPs) in normal physiology and in disease progression.... (Review)
Review
Here we review recent data and the evolving understanding of the role of red blood cell-derived microparticles (RMPs) in normal physiology and in disease progression. Microparticles (MPs) are small membrane vesicles derived from various parent cell types. MPs are produced in response to a variety of stimuli through several cytoskeletal and membrane phospholipid changes. MPs have been investigated as potential biomarkers for multiple disease processes and are thought to have biological effects, most notably in: promotion of coagulation, production and handling of reactive oxygen species, immune modulation, angiogenesis, and in apoptosis. Specifically, RMPs are produced normally during RBC maturation and their production is accelerated during processing and storage for transfusion. Several factors during RBC storage are known to trigger RMP production, including: increased intracellular calcium, increased potassium leakage, and energy failure with ATP depletion. Of note, RMP composition differs from that of intact RBCs, and the nature and composition of RMP components are affected by both storage duration and the character of storage solutions. Recognised RMP bioactivities include: promotion of coagulation, immune modulation, and promotion of endothelial adhesion, as well as influence upon vasoregulation via nitric oxide (NO) scavenging. Of particular relevance, RMPs are more avid NO scavengers than intact RBCs and this feature has been proposed as a mechanism for the impaired oxygen delivery homeostasis that has been observed following transfusion. Preliminary human studies demonstrate that circulating RMP abundance increases with RBC transfusion and is associated with altered plasma vasoactivity and abnormal vasoregulation. In summary, RMPs are submicron particles released from stored RBCs, with demonstrated vasoactive properties that appear to disturb oxygen delivery homeostasis. The clinical impact of RMPs in transfusion recipients is an area of continued investigation.
Topics: Animals; Apoptosis; Biomarkers; Blood Coagulation; Blood Preservation; Blood Transfusion; Cell Communication; Cell-Derived Microparticles; Erythrocytes; Homeostasis; Humans; Inflammation; Nitric Oxide; Oxidative Stress; Oxygen; Vasodilation
PubMed: 28686154
DOI: 10.2450/2017.0353-16 -
Journal of Neurochemistry Sep 2021One of the urgent tasks of neuroscience is to understand how neuronal circuits operate, what makes them fail, and how to repair them when needed. Achieving this goal... (Review)
Review
One of the urgent tasks of neuroscience is to understand how neuronal circuits operate, what makes them fail, and how to repair them when needed. Achieving this goal requires identifying the principal circuitry elements and their interactions with one another. However, what constitutes 'an atom' of a neuronal circuit, a neuronal type, is a complex question. In this review we focus on a class of cortical neurons that are exclusively identified by the expression of vasoactive intestinal polypeptide (VIP) and choline acetyltransferase (ChAT). The genetic profile of these VIP /ChAT interneurons suggests that they can release both γ-aminobutyric acid (GABA) and acetylcholine (ACh). This hints to a specific potential role in the cortical circuitry. Yet the VIP /ChAT interneurons are sparse (a mere 0.5% of the cortical neurons), which raises questions about their potential to significantly affect the circuit function. In view of recent developments in genetic techniques that allow for direct manipulation of these neurons, we provide a thorough and updated picture of the properties of the VIP /ChAT interneurons. We discuss their genetic profile, their physiological and structural properties, and their input-output mapping in sensory cortices and the medial prefrontal cortex (mPFC). Then, we examine possible amplification mechanisms for mediating their function in the cortical microcircuit. Finally, we discuss directions for further exploration of the VIP /ChAT population, focusing on its function during behavioral tasks as compared to the VIP /ChAT population.
Topics: Animals; Cerebral Cortex; Choline O-Acetyltransferase; Humans; Interneurons; Transcriptome; Vasoactive Intestinal Peptide
PubMed: 33301603
DOI: 10.1111/jnc.15263 -
Neuropeptides Jun 2023Multiple factors regulate the regeneration of craniofacial bone defects. The nervous system is recognized as one of the critical regulators of bone mass, thereby... (Review)
Review
Multiple factors regulate the regeneration of craniofacial bone defects. The nervous system is recognized as one of the critical regulators of bone mass, thereby suggesting a role for neuronal pathways in bone regeneration. However, in the context of craniofacial bone regeneration, little is known about the interplay between the nervous system and craniofacial bone. Sensory and sympathetic nerves interact with the bone through their neuropeptides, neurotransmitters, proteins, peptides, and amino acid derivates. The neuron-derived factors, such as semaphorin 3A (SEMA3A), substance P (SP), calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY), and vasoactive intestinal peptide (VIP), possess a remarkable role in craniofacial regeneration. This review summarizes the roles of these factors and recently published factors such as secretoneurin (SN) and spexin (SPX) in the osteoblast and osteoclast differentiation, bone metabolism, growth, remodeling and discusses the novel application of nerve-based craniofacial bone regeneration. Moreover, the review will facilitate understanding the mechanism of action and provide potential treatment direction for the craniofacial bone defect.
Topics: Calcitonin Gene-Related Peptide; Neuropeptide Y; Vasoactive Intestinal Peptide; Neurons; Bone and Bones; Substance P
PubMed: 36827755
DOI: 10.1016/j.npep.2023.102328 -
Journal of Pharmacy Practice Aug 2020The objective of this article is to discuss the pharmacology, side effects, and clinical application of vasoactive therapy in the management of adult septic shock. (Review)
Review
PURPOSE
The objective of this article is to discuss the pharmacology, side effects, and clinical application of vasoactive therapy in the management of adult septic shock.
SUMMARY
Sepsis is one of the most common reasons for admission to an intensive care unit with the incidence estimated to be greater than 750 000 cases per year in the United States. Clinicians should understand the basic pharmacology of available vasoactive agents to allow for routine and complex management of septic shock.
CONCLUSION
While advances in research, identification, and early implementation of best practices for the treatment of sepsis has reduced mortality, rates remain high. Vasopressors and inotropes remain part of the core therapeutic modalities of sepsis management. Norepinephrine is the first-line vasopressor of choice for septic shock, though secondary vasopressors can be used depending on the patient's circumstances.
Topics: Adult; Humans; Intensive Care Units; Norepinephrine; Shock, Septic; Vasoconstrictor Agents
PubMed: 31057085
DOI: 10.1177/0897190019844124 -
Developmental Neuroscience 2021GABAergic inhibitory interneurons of the cerebral cortex expressing vasoactive intestinal peptide (VIP-INs) are rapidly emerging as important regulators of network... (Review)
Review
GABAergic inhibitory interneurons of the cerebral cortex expressing vasoactive intestinal peptide (VIP-INs) are rapidly emerging as important regulators of network dynamics and normal circuit development. Several recent studies have also identified VIP-IN dysfunction in models of genetically determined neurodevelopmental disorders (NDDs). In this article, we review the known circuit functions of VIP-INs and how they may relate to accumulating evidence implicating VIP-INs in the mechanisms of prominent NDDs. We highlight recurring VIP-IN-mediated circuit motifs that are shared across cerebral cortical areas and how VIP-IN activity can shape sensory input, development, and behavior. Ultimately, we extract a set of themes that inform our understanding of how VIP-INs influence pathogenesis of NDDs. Using publicly available single-cell RNA sequencing data from the Allen Institute, we also identify several underexplored disease-associated genes that are highly expressed in VIP-INs. We survey these genes and their shared related disease phenotypes that may broadly implicate VIP-INs in autism spectrum disorder and intellectual disability rather than epileptic encephalopathy. Finally, we conclude with a discussion of the relevance of cell type-specific investigations and therapeutics in the age of genomic diagnosis and targeted therapeutics.
Topics: Autism Spectrum Disorder; Cerebral Cortex; Humans; Interneurons; Vasoactive Intestinal Peptide
PubMed: 33794534
DOI: 10.1159/000515264