Neuroendocrine and cardiac metabolic dysfunction and NLRP3 inflammasome activation in adipose tissue and pancreas following chronic spinal cord injury in the mouse
| العنوان: | Neuroendocrine and cardiac metabolic dysfunction and NLRP3 inflammasome activation in adipose tissue and pancreas following chronic spinal cord injury in the mouse |
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| المؤلفون: | Valerie Bracchi-Ricard, Gregory E. Bigford, Mark S. Nash, John R. Bethea, Robert W. Keane |
| المصدر: | ASN NEURO ASN Neuro, Vol 5 (2013) |
| سنة النشر: | 2013 |
| مصطلحات موضوعية: | ROCK, Rho-associated kinase, RHOA, Pro-Opiomelanocortin, Inflammasomes, Adipose tissue, Mice, MYPT1, myosin phosphatase target subunit 1, cardiovascular disease, Neuropeptide Y, pathophysiology, biology, General Neuroscience, HRP, horseradish peroxidase, VAT, visceral adipose tissue, Inflammasome, S11, NLRP3, NOD-like receptor family, pyrin domain containing 3, STAT, signal transducer and activator of transcription, Adipose Tissue, DAMPS, damage–associated molecular pattern molecules, Receptors, Leptin, Female, Signal transduction, medicine.symptom, JAK, Janus kinase, signal transduction, medicine.drug, Research Article, STAT3 Transcription Factor, medicine.medical_specialty, Hypothalamus, NPY, neuropeptide Y, Adipokine, Inflammation, ASC, apoptosis-associated speck-like protein containing a caspase recruitment domain (CARD, q.v.), S8, CVD, cardiovascular disease, S3, CNS, central nervous system, IACUC, Institutional Animal Care and Use Committee, lcsh:RC321-571, ARC, arcuate nucleus, SCI, spinal cord injury, POMC, proopiomelanocortin, Internal medicine, NLR Family, Pyrin Domain-Containing 3 Protein, medicine, Animals, neuroendocrine, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Pancreas, Spinal Cord Injuries, Leptin receptor, Myocardium, Janus Kinase 2, RBD, Rho-binding domain, spinal cord injury, IL, interleukin, Mice, Inbred C57BL, Endocrinology, biology.protein, Neurology (clinical), PFA, paraformaldehyde, Janus kinase, Carrier Proteins, rhoA GTP-Binding Protein, metabolism, FAO, fatty acid oxidation, PVN, paraventricular nucleus |
| الوصف: | CVD (cardiovascular disease) represents a leading cause of mortality in chronic SCI (spinal cord injury). Several component risk factors are observed in SCI; however, the underlying mechanisms that contribute to these risks have not been defined. Central and peripheral chronic inflammation is associated with metabolic dysfunction and CVD, including adipokine regulation of neuroendocrine and cardiac function and inflammatory processes initiated by the innate immune response. We use female C57 Bl/6 mice to examine neuroendocrine, cardiac, adipose and pancreatic signaling related to inflammation and metabolic dysfunction in response to experimentally induced chronic SCI. Using immunohistochemical, -precipitation, and -blotting analysis, we show decreased POMC (proopiomelanocortin) and increased NPY (neuropeptide-Y) expression in the hypothalamic ARC (arcuate nucleus) and PVN (paraventricular nucleus), 1-month post-SCI. Long-form leptin receptor (Ob-Rb), JAK2 (Janus kinase)/STAT3 (signal transducer and activator of transcription 3)/p38 and RhoA/ROCK (Rho-associated kinase) signaling is significantly increased in the heart tissue post-SCI, and we observe the formation and activation of the NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome in VAT (visceral adipose tissue) and pancreas post-SCI. These data demonstrate neuroendocrine signaling peptide alterations, associated with central inflammation and metabolic dysfunction post-SCI, and provide evidence for the peripheral activation of signaling mechanisms involved in cardiac, VAT and pancreatic inflammation and metabolic dysfunction post-SCI. Further understanding of biological mechanisms contributing to SCI-related inflammatory processes and metabolic dysfunction associated with CVD pathology may help to direct therapeutic and rehabilitation countermeasures. |
| تدمد: | 1759-0914 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1b63202e6d83a48dcfcd5252f49ab0c4 https://pubmed.ncbi.nlm.nih.gov/23924318 |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....1b63202e6d83a48dcfcd5252f49ab0c4 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 17590914 |
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