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Trans-synaptic regulation of calmodulin gene expression after experimentally induced orofacial inflammation and subsequent corticosteroid treatment in the principal sensory and motor trigeminal nuclei of the rat.

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The cutaneous and mucosal surfaces in the infraorbital region around the whisker pad are innervated by the maxillary division of the afferent fibers of the trigeminal nerve, while certain ganglion cells project to the principal sensory trigeminal nucleus (Pr5). In turn, some of the neurons in the

Calcium/Calmodulin-Dependent Protein Kinase IV (CaMKIV) Mediates Acute Skeletal Muscle Inflammatory Response.

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The objective of this study is to investigate the role of Calmodulin-dependent protein kinase IV (CaMKIV) in Cardiotoxin (CTX)-induced mice muscle inflammation. CTX injection i.m. was performed to induce B6 mice acute tibialis anterior (TA) muscle injury. The mice were then injected i.p. with the

Reversal of chronic inflammatory pain by acute inhibition of Ca2+/calmodulin-dependent protein kinase II.

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Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is a major protein kinase that is capable of regulating the activities of many ion channels and receptors. In the present study, the role of CaMKII in the complete Freund's adjuvant (CFA)-induced inflammatory pain was investigated.

Spasmolytic and calmodulin inhibitory effect of non-steroidal anti-inflammatory drugs in vitro.

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The effect of several anti-inflammatory drugs (NSAIDs), the calmodulin inhibitor W-7 and cortisol on vanadate-induced tonic contraction and on calmodulin dependent cAMP-phosphodiesterase activity have been assayed. Indomethacin, diclofenac, phenylbutazone, mefenamic acid, naproxen, tolmetin,

Mechanisms underlying the anti-inflammatory effects of the Ca2+/calmodulin antagonist CV-159 in cultured vascular smooth muscle cells.

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CV-159 is a unique dihydropyridine Ca(2+) antagonist with an anti-calmodulin (CaM) action. A pathogenic feature of atherosclerosis is vascular inflammatory change. In the present study, we examined whether CV-159 exerts protective effects on smooth muscle inflammatory responses. After pretreatment

Effects of a calmodulin inhibitor on bleomycin-induced lung inflammation in hamsters. Biochemical, morphometric, and bronchoalveolar lavage data.

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Previous studies have shown that bleomycin-induced pulmonary fibrosis is accompanied by elevated levels of calcium and calmodulin, which are important in the regulation of many biologic processes. The authors have further extended these observations and assessed the effect of a calmodulin inhibitor,

Anti-inflammatory actions of benzoyl peroxide: effects on the generation of reactive oxygen species by leucocytes and the activity of protein kinase C and calmodulin.

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For many years, benzoyl peroxide has been used as a topical treatment for acne. Although the drug has been shown to interfere with a variety of pathways, believed to be of importance in the aetiopathogenesis of acne, its mechanism of action is thought to be principally antibacterial. Recent

Inhibition of calcium-calmodulin-dependent phosphodiesterase (PDE1) suppresses inflammatory responses.

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A novel, potent, and highly specific inhibitor of calcium-calmodulin-dependent phosphodiesterases (PDE) of the PDE1 family, ITI-214, was used to investigate the role of PDE1 in inflammatory responses. ITI-214 dose-dependently suppressed lipopolysaccharide (LPS)-induced gene expression of

Calcium/calmodulin-dependent protein kinase kinase 2 regulates macrophage-mediated inflammatory responses.

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Calcium/calmodulin-dependent kinase kinase 2 (CaMKK2) plays a key role in regulating food intake and energy expenditure at least in part by its actions in hypothalamic neurons. Previously, we showed that loss of CaMKK2 protected mice from high-fat diet (HFD)-induced obesity and glucose intolerance.

Calmodulin-dependent signalling pathways are activated and mediate the acute inflammatory response of injured skeletal muscle.

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KEY POINTS

There is a close relationship between skeletal muscle physiology and Ca²⁺ /CaM signalling. Despite the effects of Ca²⁺ /CaM signalling on immune and inflammatory responses have been extensively explored, few studies have investigated the role of

Inflammation and NLRP3 Inflammasome Activation Initiated in Response to Pressure Overload by Ca2+/Calmodulin-Dependent Protein Kinase II δ Signaling in Cardiomyocytes Are Essential for Adverse Cardiac Remodeling.

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BACKGROUND

Inflammation is associated with cardiac remodeling and heart failure, but how it is initiated in response to nonischemic interventions in the absence of cell death is not known. We tested the hypothesis that activation of Ca²⁺/calmodulin-dependent protein

Calcium/Calmodulin-Dependent Kinase IV Facilitates the Recruitment of Interleukin-17-Producing Cells to Target Organs Through the CCR6/CCL20 Axis in Th17 Cell-Driven Inflammatory Diseases.

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The recruitment of interleukin-17 (IL-17)-producing T helper (Th17) cells to inflammatory sites has been implicated in the development of organ damage in inflammatory and autoimmune diseases including systemic lupus erythematosus (SLE). To define the mechanism of calcium/calmodulin-dependent kinase

Clozapine reduces Toll-like receptor 4/NF-κB-mediated inflammatory responses through inhibition of calcium/calmodulin-dependent Akt activation in microglia.

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Clozapine is an atypical antipsychotic agent used in the treatment of schizophrenia and severe mood disorders. Accumulating evidence suggests that neuroinflammation is closely associated with the pathogenesis of various neurodegenerative diseases and psychiatric disorders. Clozapine exerts

miR-125a-5p alleviates dysfunction and inflammation of pentylenetetrazol-induced epilepsy through targeting calmodulin-dependent protein kinase IV (CAMK4).

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MicroRNAs (miRNA) are known as a key role in the etiology and treatment of epilepsy through controlling the expression of gene. However, miR-125a-5p in the epilepsy is little known. The epilepsy rat models were induced by pentylenetetrazol (PTZ) and miR-125a-5p profiles in the

Calcium/calmodulin-dependent kinase IV in immune and inflammatory responses: novel routes for an ancient traveller.

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Ca(2+) is a pivotal second messenger controlling the activation of lymphocytes. Crucial events in the social life of immunocytes are regulated by the calcium/calmodulin complex (Ca(2+)/CaM), which controls the activation status of many enzymes, including the Ca(2+)/CaM-dependent Ser-Thr kinases

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