the phenylethanolamine N-methyltransferase GRE plays a necessary, but not sufficient role in the transcriptional aspects to the control mechanism. Analyses implicate the participation of sequences in the distal 5´promoter of this gene.
epinephrine is an important neurotransmitter and hormone, and epinephrine is required for normal blood pressure and cardiac filling responses to stress, but is not required for tachycardia during stress or normal cardiovascular function at rest
epinephrine is an important neurotransmitter and hormone, and epinephrine is required for normal blood pressure and cardiac filling responses to stress, but is not required for tachycardia during stress or normal cardiovascular function at rest
the phenylethanolamine N-methyltransferase GRE plays a necessary, but not sufficient role in the transcriptional aspects to the control mechanism. Analyses implicate the participation of sequences in the distal 5´promoter of this gene.
pheochromocytomas are tumors of adrenal chromaffin cells. Phenylethanolamine N-methyltransferase mRNA levels are markedly increased by glucocorticoid administration. Dexamethasone elicites approximately 800fold increases in phenylethanolamine N-methyltransferase mRNA levels in mouse pheochromocytoma 862L cells and approximately 75fold increases for mouse pheochromocytoma 10/9CR1 cells. Glial cell line-derived neurotrophic factor and cpt-cAMP alone each produce little or no change in baseline phenylethanolamine N-methyltransferase mRNA levels. In both cell lines, dexamethasone-stimulated increases in phenylethanolamine N-methyltranferase mRNA levels are reduced approximately 90% by prior tratment with cAMP. Glial cell line-derived neurotrophic factor reduces dexamethasone effects on phenylethanolamine N-methyltransferase mRNA levels by 40% in mouse pheochromocytoma 862L cells, while not supressing the dexamethasone response in mouse pheochromocytoma 10/9CRC1 cells. Pretreatment with cAMP and afterwards treatment with glial cell line-derived neurotrophic factor before additon of dexamethasone reduced phenylethanolamine N-methyltransferase expression in mouse pheochromocytoma 862L and 10/9CRC1 cells to 0.1% and 5.5% of their corresponding DEX induced maxima.
higher levels of phenylethanolamine N-methyltransferase in stellate ganglia of mice compared with rats. There are differences in noradrenaline and adrenaline concentration in stellate ganglia between wild type and knock out mice under basal and under stress conditons. Phenylethanolamine N-methyltransferase mRNA is present in stellate ganglia. There is an increase in phenylethanolamine N-methyltransferase mRNA levels in stellate ganglia of WT mice after exposure to single and also an increase in phenylethanolamine N-methyltransferase mRNA and protein levels after repeated immobilization compared with the unstressed control group. In corticotropin-releasing hormone knockout mice, no increase in phenylethanolamine N-methyltransferase gene expression and protein level occurs either after single or after repeated immobilization stress exposure.
construction of enzyme knockout mutant mice, that show resting cardiovascular function, including blood pressure, heart rate, and cardiac output similar to that in wild-type mice, and the basal norepinephrine plasma level is unaltered. However, inhibition of sympathetic innervation with the ganglion blocker hexamethonium causes a 54% smaller decrease in blood pressure in KO mice compared to wild-type mice, and treadmill exercise causes an 11% higher increase in blood pressure, both suggesting impaired vasodilation in KO mice, the enzyme knockout does not change the heart rate response to ganglionic blockade and exercise. KO mice have an increased ratio of left ventricular posterior wall thickness to internal dimensions but do not have cardiac hypertrophy, in restrained, awake KO mice, heart rate and ejection fraction remain unaltered, but cardiac output is significantly reduced because of diminished end-diastolic volume, phenotype, overview
construction of PNMT promoter constructs using nested deletion constructs treated with DEX or sequentially with GDNF/cAMP/DEX, the suppression of PNMT induction is reversible
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CLONED (Commentary)
ORGANISM
UNIPROT
LITERATURE
expression analysis, transcriptional response of the PNMT gene to GDNF and cpt-cAMP involves distal portions of the PNMT promoter, transient expression of PNMT promoter constructs in MPC 10/9CRC1 cultures