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#28942595   2017/09/24 Save this To Up

Oxytocin Signaling in Pain: Cellular, Circuit, System, and Behavioral Levels.

Originally confined to the initiation of parturition and milk ejection after birth, the hypothalamic nonapeptide oxytocin (OT) is now recognized as a critical determinant of social behavior and emotional processing. It accounts for the modulation of sensory processing and pain perception as OT displays a potent analgesic effect mediated by OT receptors (OTRs) expressed in the peripheral and central nervous systems. In our chapter, we will first systemically analyze known efferent and afferent OT neuron projections, which form the anatomical basis for OT modulation of somatosensory and pain processing. Next, we will focus on the synergy of distinct types of OT neurons (e.g., magno- and parvocellular OT neurons) which efficiently control acute inflammatory pain perception. Finally, we will describe how OT signaling mechanisms in the spinal cord control nociception, as well as how OT is able to modulate emotional pain processing within the central amygdala. In the conclusions at the end of the chapter, we will formulate perspectives in the study of OT effects on pain anticipation and pain memory, as well as propose some reasons for the application of exogenous OT for the treatment of certain types of pain in human patients.

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#28942553   2017/09/24 Save this To Up

Clinacanthus nutans Mitigates Neuronal Apoptosis and Ischemic Brain Damage Through Augmenting the C/EBPβ-Driven PPAR-γ Transcription.

Clinacanthus nutans Lindau (C. nutans) is a traditional herbal medicine widely used in Asian countries for treating a number of remedies including snake and insect bites, skin rashes, viral infections, and cancer. However, the underlying molecular mechanisms for its action and whether C. nutans can offer protection on stroke damage in brain remain largely unknown. In the present study, we demonstrated protective effects of C. nutans extract to ameliorate neuronal apoptotic death in the oxygen-glucose deprivation model and to reduce infarction and mitigate functional deficits in the middle cerebral artery occlusion model, either administered before or after hypoxic/ischemic insult. Using pharmacological antagonist and siRNA knockdown approaches, we demonstrated ability for C. nutans extract to protect neurons and ameliorate ischemic injury through promoting the anti-apoptotic activity of peroxisome proliferator-activated receptor-gamma (PPAR-γ), a stress-induced transcription factor. Reporter and chromatin immunoprecipitation promoter analysis further revealed C. nutans extract to selectively increase CCAAT/enhancer binding protein (C/EBP)β binding to specific C/EBP binding site (-332~-325) on the PPAR-γ promoter to augment its transcription. In summary, we report a novel transcriptional activation involving C/EBPβ upregulation of PPAR-γ expression to suppress ischemic neuronal apoptosis and brain infarct. Recognition of C. nutans to enhance the C/EBPβ → PPAR-γ neuroprotective signaling pathway paves a new way for future drug development for prevention and treatment of ischemic stroke and other neurodegenerative diseases.

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#28942514   2017/09/24 Save this To Up

Intrauterine hyperglycemia-induced inflammatory signalling via the receptor for advanced glycation end products in the cardiac muscle of the infants of diabetic mother rats.

Gestational diabetes is associated with increased risk to the health of the mother and her offspring. In particular, the infants of diabetic mothers (IDMs) exhibit elevated levels of preterm birth, macrosomia, hypoglycemia, hypocalcemia, and cardiomyopathy. We have previously reported that IDMs showed abnormalities in cardiac Akt-related insulin signalling, and that these deficiencies in Akt-related signalling were attenuated by supplementing the maternal diet with fish-oil. Herein, we investigated whether the eicosapentaenoic acid (EPA) found in fish oil can be used to attenuate diabetes associated impairments in cardiomyocyte signalling.

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#28942487   2017/09/24 Save this To Up

Erratum to: The crystal structure of Ac-AChBP in complex with α-conotoxin LvIA reveals the mechanism of its selectivity towards different nAChR subtypes.

In the original publication of the article the keywords are incorrectly online published. The correct keywords should read as α-Conotoxin; Nicotinc acetylcholine receptor; Acetylcholine binding protein; X-ray crystallography".

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#28942479   2017/09/24 Save this To Up

Tumor necrosis factor-associated periodic syndrome in adults.

Tumor necrosis factor-associated periodic syndrome is an autoinflammatory disorder classified under hereditary periodic fever syndromes. Mutations in the tumor necrosis factor receptor contribute to tumor necrosis factor-associated periodic syndrome. Decreased shedding of receptors and increased mitochondrial reactive oxygen species production leading to elevated proinflammatory cytokines are documented. Inflammation in various organs is hallmark of tumor necrosis factor-associated periodic syndrome and manifests as spiking fever, abdominal pain, conjunctivitis and polyserositis in adults. The ongoing challenge is to diagnose the disease early in its course to prevent amyloidosis. The treatment options have evolved from use of nonsteroidal anti-inflammatory drugs and corticosteroids to targeted therapy like tumor necrosis factor receptor inhibitors and interleukin-1 blockers. The aim of this review is to give an overview of the pathogenesis, clinical features and the various treatment modalities available for tumor necrosis factor-associated periodic syndrome and aid physicians in recognizing the signs of the disease earlier.

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#28942449   2017/09/24 Save this To Up

FSHR and LHR Expression and Signaling as Well as Maturation and Apoptosis of Cumulus-Oocyte Complexes Following Treatment with FSH Receptor Binding Inhibitor in Sheep.

Currently, it remains unknown whether FSH receptor binding inhibitor (FRBI) influences follicular development and reproduction functions in humans and animals. The present study aimed to investigate FRBI effects on in vitro maturation (IVM) and apoptosis of cumulus-oocyte complexes (COCs) of sheep, to determine the effect of FRBI on mRNA and protein levels of FSHR and LHR in COCs, and to elucidate the signal pathway of FRBI effects.

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#28942427   2017/09/24 Save this To Up

Binding of FUNDC1 with Inositol 1,4,5-Trisphosphate Receptor in Mitochondria-Associated Endoplasmic Reticulum (ER) Membranes Maintains Mitochondrial Dynamics and Function in Hearts In Vivo.

Background -FUN14 domain containing 1 (FUNDC1) is a highly conserved outer mitochondrial membrane protein. The aim of this study is to examine if FUNDC1 modulates the mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs), mitochondrial morphology, and function in cardiomyocytes and in intact hearts. Methods -The impacts of FUNDC1 on MAMs formation and cardiac functions were studied in mouse neonatal cardiomyocytes, in mice with cardiomyocyte-specific Fundc1 gene knockout (Fundc1(f/Y)/Cre(αMyHC+/-) ), and in the cardiac tissues of the patients with heart failure. Results -In mouse neonatal cardiomyocytes and intact hearts, FUNDC1 was localized in MAMs by binding to ER-resided inositol 1,4,5-trisphosphate type 2 receptor (IP3R2). Fundc1 ablation disrupted MAMs, reduced the levels of IP3R2 and Ca(2+) in both mitochondria and cytosol whereas overexpression of Fundc1 increased the levels of IP3R2 and Ca(2+) in both mitochondria and cytosol. Consistently, Fundc1 ablation increased Ca(2+) levels in ER whereas Fundc1 overexpression lowered ER Ca(2+) levels. Further, Fundc1 ablation in cardiomyocytes elongated mitochondria, and compromised mitochondrial functions. Mechanistically, we found that Fundc1 ablation-induced reduction of intracellular Ca(2+) levels suppressed mitochondrial fission 1 protein (Fis1) expression and mitochondrial fission by reducing the binding of the cAMP response element binding protein (CREB) in the Fis1 promoter. Fundc1(f/Y)/Cre(αMyHC+/-) mice but not their littermate control mice (Fundc1(wt/Y)/Cre(αMyHC+/-)) exhibited cardiac dysfunction. The ligation of the left ventricle artery of Fundc1(f/Y)/Cre(αMyHC+/-) mice caused more severe cardiac dysfunction than those in sham-treated Fundc1(f/Y)/Cre(αMyHC+/-) mice. Finally, we found that the FUNDC1/MAMs/CREB/Fis1 signaling axis was significantly suppressed in the patients with heart failure. Conclusions -We conclude that FUNDC1 binds to IP3R2 to modulate ER Ca(2+) release into mitochondria and cytosol and that a disruption of FUNDC1 and IP3R2 interaction lowers the levels of Ca(2+) in mitochondria and cytosol, both of which instigate aberrant mitochondrial fission, mitochondrial dysfunction, cardiac dysfunction, and heart failure.

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#28942366   2017/09/24 Save this To Up

T-regulatory cells mediate local immunosuppression in lymphedema.

Patients who suffer from lymphedema have impaired immunity and, as a result, are at an increased risk for infections. Furthermore, previous studies have shown that lymphadenectomy impairs acquisition of adaptive immune responses and antibody production in response to foreign antigens. Although it is clear that antigen presentation in lymph nodes plays a key role in adaptive immunity, the cellular mechanisms that regulate impaired immune responses in patients with lymphedema or following lymphatic injury remain unknown. We have previously found that axillary lymph node dissection (ALND), both clinically and in a mouse model, results in a marked increase in the number of T-regulatory cells (Tregs) in the ipsilateral limb. In this study, we focus on the role of Tregs in immunosuppression and show that Treg proliferation in tissues distal to site of lymphatic injury contributes to impaired innate and adaptive immune responses. More importantly, using Foxp3-diptheria toxin receptor (Foxp3-DTR) transgenic mice, we show that depletion of Tregs in the setting of lymphatic injury restores these critical immune-mediated responses. These findings provide additional evidence that immune responses following lymphatic injury play a key role in mediating the pathology of lymphedema.

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#28942364   2017/09/24 Save this To Up

Toll-like receptor-mediated upregulation of CXCL16 in psoriasis orchestrates neutrophil activation.

Innate immune processes are central in the development of the chronic inflammatory skin disease psoriasis. Studying stimulation of keratinocytes, monocytes and dendritic cells by type I interferons or ligation of toll-like receptors TLR1/2, TLR2/6 or TLR7, but not TLR7/8, resulted in enhanced surface expression and secretion of the chemokine CXCL16. The corresponding receptor CXCR6 was expressed on neutrophils whose recruitment into skin is important especially in early psoriatic disease. Using the recently developed technique real-time deformability cytometry demonstrated that CXCL16 and IL-8 decreased the stiffness and enhanced deformation of neutrophils facilitating transmigration through vessel wall. In addition, CXCL16 potently induced migration of neutrophils and enhanced the chemotactic effect of IL-8. The positive feedback loop was supported by IL-8 enhancing CXCL16 production of neutrophils. Blocking of CXCL16 expression by effective treatment of psoriasis patients with TNF-α blockers further supported the pathogenic role of this chemokine. In summary, the data link innate immune stimulation to CXCL16 upregulation and neutrophil infiltration into skin. CXCL16 could therefore represent a potent future target for treatment of psoriasis.

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#28942351   2017/09/24 Save this To Up

Sphingosine 1-phosphate and cancer.

The bioactive lipid, sphingosine 1-phosphate (S1P) is produced by phosphorylation of sphingosine and this is catalysed by two sphingosine kinase isoforms (SK1 and SK2). Here we discuss structural functional aspects of SK1 (which is a dimeric quaternary enzyme) that relate to coordinated coupling of membrane association with phosphorylation of Ser225 in the 'so-called' R-loop, catalytic activity and protein-protein interactions (e.g. TRAF2, PP2A and Gq). S1P formed by SK1 at the plasma-membrane is released from cells via S1P transporters to act on S1P receptors to promote tumorigenesis. We discuss here an additional novel mechanism that can operate between cancer cells and fibroblasts and which involves the release of the S1P receptor, S1P2 in exosomes from breast cancer cells that regulates ERK-1/2 signalling in fibroblasts. This novel mechanism of signalling might provide an explanation for the role of S1P2 in promoting metastasis of cancer cells and which is dependent on the micro-environmental niche.

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