Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Combined exposure of hamsters to 60% hyperoxia and the carcinogen diethylnitrosamine for 6 wk resulted in the development of lung tumors. This was associated with progressive loss of body weight as well as increases in the pulmonary-associated peptides, mammalian bombesin (MB) and immunoreactive calcitonin (iCT). After 3 wk of exposure, multiple bronchial epithelial hyperplastic foci were noted, along with increased lung levels of MB and iCT as well as increased serum levels of MB. At this time, immunocytochemistry revealed the presence of MB and iCT within hyperplastic pulmonary neuroendocrine (PNE) cells. In addition, the localization of MB to alveolar type II cells was noted, along with the presence of lamellar bodies and secretion granules in these cells on electron microscopy. After 6 wk of exposure, distinctive microscopic pulmonary tumorlets were seen. These tumorlets were associated with a marked increase in lung and serum MB, and to a lesser extent lung and serum iCT. At this time, MB and iCT were localized exclusively to these abnormal PNE cell sites. These results, which may have relevance in humans, suggest that endogenous peptides may be important components in the process of development of neuroendocrine cancer.
Am J Respir Cell Mol Biol 1990 Jan
PMID:Pulmonary bombesin and calcitonin in hamsters during exposure to hyperoxia and diethylnitrosamine. 230 67

The calcitonin gene related peptide (CGRP) gene is a complex transcription unit that is expressed in a highly restricted pattern in both the nervous system, particularly in sensory ganglia and brainstem, and in the thyroid C cells of the endocrine system, with tissue-specific alternative RNA processing events generating transcripts encoding either the hormone, calcitonin, or the neuropeptide, CGRP. This pattern of expression in neural and endocrine tissues raises the question whether similar or distinct genomic elements are responsible for activation in both neural and endocrine cell types. We have identified a complex enhancer element, located more than 1 kilobase 5' of the transcription initiation site of the calcitonin/CGRP gene that functions in cells of neuronal or C cell origin, but not in any other cell type tested. At least two complementary regulatory sequences are required for the function of the cell-specific enhancer.
Mol Endocrinol 1990 Mar
PMID:A tissue-specific enhancer in the rat-calcitonin/CGRP gene is active in both neural and endocrine cell types. 234 82

Multiple molecular weight forms of the potent vasodilator peptide calcitonin gene-related peptide (CGRP) are present in the circulation in man. The monomeric form of CGRP(1-37) and CT(1-32) account for only a fraction of the total immunoreactive CGRP and calcitonin (CT) in the circulation. In vivo release of various molecular weight forms of CGRP and CT, including the monomeric form, into the circulation was demonstrated by gel-permeation chromatography, following stimulation of the gastrointestinal tract by a meal, and C-cells of the thyroid gland with pentagastrin. Following these stimulations an increase of the levels of C-terminal fragment of CGRP was also observed indicating a rapid metabolic breakdown of CGRP in vivo. In addition to a number of endogenous peptides and other substances, acute release of monomeric CGRP into the circulation may also contribute to the vasodilation observed following ingestion of food and administration of pentagastrin in man.
Mol Cell Endocrinol 1990 May 28
PMID:Effects of in vivo stimulation on molecular forms of circulatory calcitonin and calcitonin gene-related peptide in man. 236 32

Calcitonin-induced changes in gene expression at the level of protein synthesis were examined in cultured porcine kidney cells (LLC-PK1) using two-dimensional gel electrophoresis of [35S]methionine-labeled polypeptides. Twelve intracellular polypeptides showed reproducible changes in the relative intensity of labeling. From that set of polypeptides ten showed an increase and two a decrease in the labeling intensity after calcitonin treatment. One of the induced polypeptides was identified as plasminogen activator and two others were shown to be related to cytokeratins. The labeling of two induced and well-separated polypeptides of 70K and 95K Mr was quantitated and correlated with an increase in secretion of plasminogen activator.
Mol Cell Endocrinol 1985 May
PMID:Hormonal regulation of protein synthesis in cultured kidney cells. 240 39

Immunization of rabbits with elastin peptides prepared from purified bovine ligamentum nuchae elastin produces calcified arteriosclerotic lesions and fragmentation of elastic lamellae. Simultaneous administration of porcine calcitonin largely prevents the development of lesions. Experiments were carried out to clarify the mechanisms involved in the development of lesions as well as those involved in the preventive effect of calcitonin. Control experiments were carried out using bovine serum albumin (BSA) as antigen. Circulating antibodies and soluble immune complexes increased steadily in the sera of animals immunized with elastin peptides or BSA. The cellular immune reaction was weak as assessed by [3H]thymidine incorporation into lymphocytes in the presence of antigen or phytohemagglutinin. Arterial lesions appeared only in the animals immunized with elastin peptides, not in those immunized with BSA. Ion flux measurements were also carried out on strips of aorta obtained from immunized and control animals. Immunization with elastin peptides significantly increased the ouabain-insensitive 22Na+ efflux, the 86Rb efflux (indicator of K+ efflux), and the 45Ca2+ influx. Simultaneous calcitonin administration prevented the increase in Ca2+ influx but did enhance passive permeability to Na+ and K+ as well as the sodium pump. When calcitonin was administered without immunization, it decreased arterial smooth muscle permeability to Na+ and K+ and also decreased the basal Ca2+ influx. It is concluded that the pathological modifications of the arterial wall triggered by immunization with elastin peptides is at least partly mediated by the effect of antielastin antibodies and immune complexes on the ion permeability of arterial smooth muscle. Prevention of the increased Ca2+ influx by calcitonin is probably a key effect in the prevention of the development of lesions. The fact that calcitonin alone can modify the ion permeability of arterial smooth muscle suggests that this hormone may play a role in the regulation of vascular homeostasis.
Exp Mol Pathol 1987 Jun
PMID:Prevention by calcitonin of the pathological modifications of the rabbit arterial wall induced by immunization with elastin peptides: effect on vascular smooth muscle permeability to ions. 243 69

Since the development of molecular biology, knowledge about polypeptide hormones has increased rapidly. Recombinant DNA techniques have made it possible to establish the structure of genes encoding polypeptide hormones. The results have provided insight into the mechanisms underlying the increasing diversity of polypeptide hormones. Comparison of nucleotide sequences of various genes has revealed surprising similarities and variations. The calcitonin (CT) genes offered an opportunity for speculation about the evolutionary origin on one hand and relationships between these genes on the other.
Mol Cell Endocrinol 1988 May
PMID:Evolutionary pathways of the calcitonin genes. 245 32

The extracellular ionized calcium concentration (Ca2+) is a main regulator of calcitonin (CT) release. Calcium-induced CT secretion differs for acute versus long-term alterations of Ca2+. Using the rat C cell line rMTC 6-23 we have investigated the effect of repetitive stimulation by Ca2+ on CT release. After a Ca-induced initial rise of CT secretion, repetitive Ca stimulation led to a decline of CT release to unstimulated levels (after about 4 h). Reversing the high Ca2+ concentration (2.0 mM) to basal (1.1 mM) for 2 h and then increasing Ca2+ again resulted in a restored stimulatory action of Ca2+ (about 100% increase above the control). In contrast, repetitive stimulation with the dihydropyridine Ca channel agonist Bay K-8644 showed an unchanged stimulatory effect, as observed for the cAMP analog 8-bromo-cAMP, too. The results indicate that the reversible desensitization of Ca-induced CT secretion might be due to a modification of the voltage-dependent Ca channels proximal to or at the site of Bay K-8644 action.
Mol Cell Endocrinol 1989 May
PMID:Reversible desensitization of calcitonin secretion by repetitive stimulation with calcium. 247 33

This report describes a series of studies on the regulation of teleocalcin secretion by primary cultures of rainbow trout corpuscles of Stannius, endocrine glands believed to be unique to bony fishes. Teleocalcin release by these cultured cells was stimulated specifically by calcium in a dose-related fashion. Magnesium did not mimic the effects of added calcium and varying the osmotic pressure had no effect on hormone release. The addition of either ethyleneglycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) or cobalt chloride blocked the stimulatory effects of added calcium, whereas the calcium ionophore A23187 mimicked the effects of calcium on hormone release. Mammalian and piscine pituitary hormones (prolactin, growth hormone and gonadotrophic hormone) had no effect on teleocalcin secretion. Inconclusive results were obtained with the calcium channel blockers, verapamil and nifedipine. The results are discussed in relation to calcium-regulated secretion of calcitonin and parathyroid hormone, as well as the known physiological effects of teleocalcin in fish.
Mol Cell Endocrinol 1989 Mar
PMID:Primary culture of teleocalcin cells from rainbow trout corpuscles of Stannius: regulation of teleocalcin secretion by calcium. 250 Nov 23

Adenylate cyclase (AC) activity was studied in whole homogenates of normal and otosclerotic bone cell cultures. When Mn2+ or Ca2+ was added to the medium there was a similar increase in AC activity in both cell types. F- provoked a greater rise in normal than in pathological cells, whereas 0.01 mM guanosine triphosphate (GTP) significantly raised cAMP synthesis in otosclerotic cells only. Mn2+ + calcitonin (Ct) increased AC activity in both cell preparations. With Ca2+ as cofactor there was no significant rise in either normal or pathological cells. However, while the combination Ca2+ + Ct + GTP had little effect on normal cells, it markedly increased cAMP synthesis in the pathological cells. 1 microgram/ml of the beta-blocker propranolol inhibited the effect Ct exerts on AC in normal cells, but enhanced it in otosclerotic cells. It would, therefore, seem that the pathogenesis of otosclerosis could be associated with an alteration in the AC system associated with Ct receptors.
Mol Cell Endocrinol 1989 Mar
PMID:Altered adenylate cyclase activity in human otosclerotic bone cell cultures. 254 83

Endocrine cells were investigated in human Bartholin's glands by use of histochemical, immunohistochemical and ultrastructural methods. Endocrine cells represent normal constituents of these glands, being mainly distributed throughout the transitional epithelium of the major excretory duct; however, single elements are dispersed among the acinar lobules. Serotonin-, calcitonin-, katacalcin-, bombesin- and alpha-hCG-immunoreactive cells were recognized, with serotonin-immunoreactive cells predominating. Co-expression of calcitonin, katacalcin or alpha-hCG with serotonin was observed in single endocrine cells. At the ultrastructural level, these cells are richly granulated and show typical neuroendocrine features. Bartholin's glands display an endocrine profile quite similar to that of other cloacal-derived tissues.
Virchows Arch B Cell Pathol Incl Mol Pathol 1989
PMID:Endocrine cells in human Bartholin's glands. An immunohistochemical and ultrastructural analysis. 256 49


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