Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q13519 (OFQ)
 1,265 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study characterized the contributions of protein tyrosine kinase and mitogen-activated protein kinase in nociceptin/orphanin FQ induced impairment of NMDA dilation after cerebral hypoxia/ischemia in anesthetized newborn pigs equipped with a closed cranial window. Topical nociceptin/orphanin FQ, in a concentration observed after hypoxia/ischemia, impaired NMDA pial artery vasodilation. Co-administration either of the protein tyrosine kinase inhibitor genistein or the mitogen activated protein kinase inhibitor U0126 with nociceptin/orphanin FQ partially prevented the inhibition of NMDA dilation compared to that observed in their absence. After exposure to hypoxia/ischemia, pial artery dilation in response to NMDA was reversed to vasoconstriction but pretreatment with either genistein or U0126 partially protected such impairment. These data show that protein tyrosine kinase and mitogen activated protein kinase activation contribute to nociceptin/orphanin FQ induced impairment of NMDA dilation. These data suggest that protein tyrosine and mitogen activated protein kinase are involved in the mechanism by which nociceptin/orphanin FQ impairs NMDA dilation following hypoxia/ischemia.
 ...
PMID:Newborn pig nociceptin/orphanin FQ activates protein tyrosine kinase and mitogen activated protein kinase to impair NMDA cerebrovasodilation after ischemia. 1259 29

Mild traumatic brain injury (mTBI) diagnoses have increased due to aggressive sports and blast-related injuries, but the cellular mechanisms and pathology underlying mTBI are not completely understood. Previous reports indicate that Nociceptin Orphanin/FQ (N/OFQ), an endogenous neuropeptide, contributes to post-injury ischemia following mechanical brain injury, yet its specific role in cerebral hypoxia, vestibulomotor function and injury marker expression following blast-induced TBI is not known. This study is the first to identify a direct association of N/OFQ and its N/OFQ peptide (NOP) receptor with TBI-induced changes following a single 80psi head blast exposure in male rats. N/OFQ and NOP receptor expression increased in brain tissue and plasma following TBI, concurrent with vestibular dysfunction but preceding hypoxia and appearance of injury markers compared to sham rats. A single post-blast treatment with the NOP receptor antagonist, SB-612111, transiently improved acute vestibulomotor performance. It also prevented increases in markers of TBI-induced hypoxia, pro-apoptotic proteins and injury seen 8-10days post-blast. This study reveals an apparent role for the N/OFQ-NOP receptor system in blast TBI and suggests potential therapeutic utility of NOP receptor antagonists for mTBI.
 ...
PMID:Post-blast treatment with Nociceptin/Orphanin FQ peptide (NOP) receptor antagonist reduces brain injury-induced hypoxia and signaling proteins in vestibulomotor-related brain regions. 2779 33

Exposure of the organism to a hostile stimulus results in a series of coordinated reactions that aim to avoid the aversive effect and maintain or restore homeostasis of the organism. In response to noxious stimuli corticotropin-releasing factor (CRF), the primary mediator of stress responses is released from the paraventricular nucleus resulting in activation of the hypothalamic-pituitary-adrenocortical axis and coordination of the endocrine, autonomic, behavioral and immune responses to stress. Several other neuropeptides, released in a coordinated way are also involved in the regulation of the stress response. However, besides the development of adaptive physiological, beneficial reactions, pathological, non-desired somatic and psychic responses can also develop, among others: gastric mucosal damage, erosion and ulceration. The mechanism of stress-related gastric mucosal injury is not fully understood; both mucosal injurious and protective mechanisms are activated in response to stress. Decreased mucosal circulation due to redistribution of blood flow from the visceral region toward the vital organs seems to be the primary mechanism of gastric mucosal damage. Mucosal hypoperfusion can result in mucosal ischemia, free radical formation and gastric hypomotiliy. On the other hand, several stressrelated neuropeptides, such as CRF, SP, N/OFQ, opioids, oxytocin and prolactin have been reported to inhibit the stress- and other ulcerogenic stimulus-induced mucosal lesions independently on their effect on other stressrelated symptoms. Consequently, neuropeptides released during stress, besides their numerous physiological and pathophysiological functions, may initiate adaptive mechanisms as well as counteract the stress-induced gastric mucosal injury.
 ...
PMID:Stress, Neuropeptides and Gastric Mucosa. 2785 11


<< Previous 1 2