Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously reported that the potent tumor-promoting agent 12-O-tetradecanoylphorbol-13-acetate (TPA) and a factor from fetal calf serum (FCS) markedly enhance the transformation of mouse C3H 10T1/2 and Rat 6 fibroblasts, when added to cultures following transfection with plasmid pT24 DNA that contains an activated c-Ha-ras oncogene. In the present study, we examined possible enhancing or inhibiting effects of various chemicals on the transformation of Rat 6 fibroblasts by T24 DNA when tested in the presence of calf serum, calf serum plus TPA or FCS. We found that, like TPA, the chemicals mezerein, 1-oleoyl-2-acetylglycerol, and phospholipase C increased the yield of T24-induced foci, thus further implicating protein kinase C as a critical constituent in this process. Low concentrations (10(-6)-10(-7)M) of retinoic acid (both trans and 13-cis) also stimulated cell transformation. Several compounds inhibited T24-induced transformation. These included nontoxic concentrations of the calcium ionophore A23187, indomethacin, and epsilon-amino-n-caproic acid. Compounds that failed to exert a significant reproducible effect included vasopressin, vitamin D3, selenium, antipain, Bowman-Birk inhibitor, vitamin B12, epidermal growth factor, platelet-derived growth factor, insulin, and transferrin. These findings suggest that this simple in vitro system might be useful for detecting enhancers and inhibitors of ras oncogene-induced cell transformation and also elucidating their mechanisms of action.
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PMID:Effects of various chemical agents on the transformation of rat fibroblasts by an activated c-Ha-ras oncogene. 266 19

Normal cells require growth factors to multiply. One group of growth factors such as platelet-derived growth factor, bombesin and vasopressin in fibroblasts or antigen in lymphocytes uses a specific inositol lipid as part of a transduction mechanism for generating intracellular mitogenic signals. These growth factors stimulate the hydrolysis of phosphatidylinositol 4,5-bisphosphate to give diacylglycerol (DG) and inositol 1,4,5-trisphosphate (Ins1,4,5P3). The DG remains within the plane of the membrane to activate protein kinase C, one function of which is to increase intracellular pH by switching on a Na+/H+ exchanger. The other product, Ins1,4,5P3, functions as a second messenger to mobilize calcium from intracellular stores. These two ionic events, the increase in pH and calcium, contribute to the onset of DNA synthesis. The hydrolysis of an inositol lipid is a key event in this signal pathway which mediates the action of competence factors. A separate signal pathway, perhaps based on tyrosine phosphorylation, carries out the effects of progression growth factors such as epidermal growth factor (EGF) and insulin. It is argued that oncogenes may be arranged into groups associated with specific signal pathways. For example, the sis oncogene encodes platelet-derived growth factor which might use the src gene product as part of its transduction mechanism to generate the second messengers DG, Ins1,4,5P3 and calcium. These last then act to stimulate the transcription of myc and fos. On the other hand, the erbB gene encodes a protein which resembles the receptor for EGF. The function of the ras protein remains a major unsolved problem but there is indirect evidence for proposing that it may mediate the action of progression factors such as EGF or insulin.
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PMID:Growth factors, oncogenes and inositol lipids. 377 62

Using molecular hybridization, left ventricular ras oncogene expression was examined in the hypertrophic heart of rat or during injection of vasopressin or alpha-receptor agonist neosynephrine. Results showed that ras oncogene expression of left ventricle could be potentiated by neosynephrine but not by vasopressin. Furthermore, expression of both nucleic oncogene myc and membrane oncogene ras were increased during chronic cardiac pressure overload, with the former occurring in early loading stage and the latter staying the whole loading stage.
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PMID:[Ras oncogene expression of left ventricle in hypertrophic rat heart and during induction by vasopressin and neosynephrine]. 824 34

Neuropeptides are often ectopically expressed by non-endocrine tumours. We used transgenic mice to assess the effect of ectopic expression of the neuropeptide, vasopressin, in mammary tumours induced by the transgenetic expression of an activated ras oncogene. Mice bearing a mouse mammary tumour virus-vasopressin (MMTV-VP) fusion transgene synthesise authentic VP in mammary ducts and alveoli. Bitransgenic mice bearing both MMTV-VP and MMTV-v-Ha-ras transgenes developed tumours that were histologically indistinguishable from those of single MMTV-v-Ha-ras animals. However, tumour onset was significantly delayed in the bitransgenic animals. These data provide evidence that an ectopic neuropeptide can slow the development of ras tumours in vivo.
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PMID:Ectopic vasopressin expression in MMTV-v-Ha-ras transgenic mice delays the onset of mammary tumorigenesis. 869 19

We have reported that lovastatin attenuates the development of hypertension in spontaneously hypertensive rats (SHR). The fall in arterial pressure is associated with an elevation in renal medullary blood flow, normalization of the pressure-natriuresis relationship, and diminished hypertrophy of renal arterioles. However, the mechanism by which lovastatin alters renal vascular tone is unknown. The present study examined the effects of lovastatin on renal vascular tone and the expression of G proteins. Four-week-old SHR were chronically treated with lovastatin (20 mg/kg/day) or vehicle by gavage for 4 weeks. At the end of the study, mean arterial pressure averaged 131 +/- 4 (n = 5) and 160 +/- 4 mm Hg (n = 6) in lovastatin- and vehicle-treated SHR, respectively. Renal arterioles isolated from lovastatin-treated SHR were significantly less responsive to norepinephrine and vasopressin than those obtained from vehicle-treated rats (ED50: 5.0 v 1.8 x 10(-7) mol/L for norepinephrine, and 8.0 v 5.2 x 10(-10) mol/L for vasopressin). The fall in renal vascular reactivity in lovastatin-treated SHR was associated with reduced levels of ras and rho proteins in renal arterioles, whereas the expressions of heterotrimeric G proteins (Gs Gq, Gi) were similar in renal arterioles from vehicle- and lovastatin-treated SHR. Overnight culture of renal arterioles with media containing lovastatin also diminished the expression of ras and rho proteins and the response to vasoconstrictors. These findings indicate that lovastatin diminishes the response to vasoconstrictors and the expression of small G proteins in the renal vasculature of SHR and suggest that a fall in the levels of ras and rho proteins in these vessels may contribute to the antihypertensive effects of lovastatin.
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PMID:Lovastatin reduces renal vascular reactivity in spontaneously hypertensive rats. 979 39

Expression of genes that encode oxytocin (OXT) and vasopressin (AVP) and their cognate receptors in normal and diseased prostates are only partially characterized. Reverse transcription and PCR were used to examine the expression of these genes in normal prostate epithelial and stromal cell lines, k-ras-transformed prostate epithelial cell lines, and in four prostate cancer cell lines. Secreted and cell-associated OXT peptide was measured by an enzyme immunoassay. OXT and its receptor (OXTR) were expressed in all eight prostate cell lines. Cell-associated OXT peptide was also found in all prostate epithelial cell lines except in DU145 cells. Neither AVP nor its cognate receptors (V1a receptor and V2 receptor) were expressed in any prostate cell line examined. These data point to the OXTR as the primary target of OXT and AVP, and suggest that OXT might be an autocrine/paracrine regulator in human prostate. We found that OXT induces the migration of PC3 and PC3M, but not DU145 prostate cancer cells. The effect of OXT is distinct from the epidermal growth factor (EGF)-induced migration of prostate cancer cells, in which ERK1/2 and EGF receptor kinase activities were required. When cells were pretreated with pertussis toxin, the effect of OXT, but not EGF, on cell migration was abolished. Pretreatment with the cyclic AMP analogue, 8-Br-cAMP, did not affect OXT-induced cell migration, which eliminated the nonspecific effect of pertussis toxin. We conclude that a Gi-dependent mechanism is involved in OXTR-mediated migration of prostate cancer cells, and indicates a role for OXTR in prostate cancer metastasis.
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PMID:Oxytocin induces the migration of prostate cancer cells: involvement of the Gi-coupled signaling pathway. 2066 60

The 99mTc-labeled conjugates of the vasopressin (AVP) peptide and of its analogue d(CH2)5[D-Tyr(Et2)-Ile4-Eda9]AVP (AVP(an)) have been synthesized using the technetium complexes with tetradentate tripodal chelator (the tris(2-mercaptoethyl)amine (NS3)) and the monodentate isocyanide ligand (CN-peptide). The conjugates exhibit high stability in the presence of 100 times the molar excess of standard amino acids cysteine or histidine and also satisfactory stability in human serum. The 99mTc(NS3)(CN-AVP) and 99mTc(NS3)(CN-AVP(an)) ability of binding to small-cell lung cancer (SCLC) cell line H69 was studied in vitro. The results suggest that the novel vasopressin conjugate 99mTc(NS3)(CN-AVP(an)) is a desirable compound for imaging oncogene receptors overexpressed in SCLC cells and can be an important basis for further consideration the conjugate as a potential diagnostic radiopharmaceutical for patients suffering from small-cell lung cancer.
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PMID:99mTc-labeled vasopressin peptide as a radiopharmaceutical for small-cell lung cancer (SCLC) diagnosis. 2497 71