Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of immunologic markers for neurofilaments, neuropeptides of sensory nerve fibers (Calcitonin gene-related peptide and substance P), for noradrenergic innervation (neuropeptide Y and Tyrosine hydroxylase), and Neuron-specific protein 9.5 was evaluated in frozen tissue sections from normal skin (n = 34) and from skin biopsies manifesting urticaria (n = 6), leukocytoclastic vasculitis (n = 4), systemic lupus erythematosus (n = 23), and atopic dermatitis (n = 40, of which 16 were from lesions induced by epicutaneous atopic allergen patch tests). In some normal skin specimens immunoreactive nerve fibers expressing Neuron-specific protein 9.5 were observed in the epidermis, dermis, and around blood vessels. For the other markers, immunolabeling was mainly observed in the dermis around blood vessels. Neurofilaments, which are scarce in normal skin epidermis, were present in higher density in the epidermis of affected skin in all disease conditions. Biopsies from urticaria and systemic lupus erythematosus showed a decrease in density of fibers immunolabeled for neuropeptides substance P and Calcitonin gene-related peptide and for Neuropeptide Y. In biopsies from skin with atopic dermatitis, an increased density of fibers was observed for all markers except Neuropeptide Y and Tyrosine hydroxylase. In this group, biopsies from positive atopic allergen patch tests showed an enhanced density of fibers labeled by antibody to Neuron-specific protein 9.5 and a lower density in labeling for Tyrosine hydroxylase. The data indicate a potential role of innervation and neuropeptides in dermatoses like atopic dermatitis.
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PMID:Increased number of immunoreactive nerve fibers in atopic dermatitis. 138 6

Calcitonin gene-related peptide is a potent vasodilator neuropeptide that is localized in perivascular sensory nerves. To determine whether alpha-calcitonin gene-related peptide possesses protective activity against hypertension-induced end organ damage, hypertension was induced in alpha-calcitonin gene-related/calcitonin peptide knockout and wild-type mice by uninephrectomy, deoxycorticosteroid administration, and 0.9% saline drinking water. These mice were instrumented previously for long-term telemetric blood pressure recording. Control groups were sham-operated and given tap water. Mean arterial pressures were determined, and 3 weeks after initiation of each protocol, tissues were taken for histopathologic studies. The deoxycorticosteroid-salt protocol produced a significant 35% mean arterial pressure increase in both mouse strains. No pathological changes were observed in sections of aortas and femoral arteries from any of the groups studied. Likewise, heart and kidney sections from the hypertensive wild-type mice showed no pathological changes compared with their normotensive counterparts. In contrast, marked vasculitis was seen in the heart sections from the deoxycorticosteroid-salt-treated alpha-calcitonin gene-related peptide knockout mice with thickening and inflammation of the vessel walls. In addition, myocarditis and focal epicarditis with areas of myocardial necrosis were present. Kidneys of these mice exhibited prominent glomerular changes including congestion of the capillary loops, focal mesangial and crescent proliferation, and focal histocytic infiltration. Urinary microalbumin was significantly higher in the hypertensive alpha-calcitonin gene-related peptide knockout compared with hypertensive wild-type mice. These data suggest that deletion of the alpha-calcitonin gene-related peptide gene makes the heart and kidneys more vulnerable to hypertension-induced end organ damage.
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PMID:Calcitonin gene-related peptide protects against hypertension-induced heart and kidney damage. 1558 78