Expression of alpha-adrenoceptors in a human transformed lymphoblastoid cell line
| Autor: | Enri Borda, Leonor Sterin-Borda, Claudia Perez Leiros, de Bracco Mm |
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| Rok vydání: | 1990 |
| Předmět: |
Agonist
Male medicine.medical_specialty Adrenergic receptor medicine.drug_class Immunology Population Indomethacin Biology In Vitro Techniques Clonidine Cell Line Internal medicine Adrenergic antagonist medicine Prazosin Immunology and Allergy Animals Humans Adrenergic agonist Lymphocytes education education.field_of_study Rats Inbred Strains Receptors Adrenergic alpha Myocardial Contraction Raji cell Yohimbine Rats Endocrinology Cell Transformation Neoplastic Neurology Neurology (clinical) Adrenergic alpha-Agonists Cell Division medicine.drug |
| Zdroj: | Journal of neuroimmunology. 29(1-3) |
| ISSN: | 0165-5728 |
| Popis: | The presence of α-adrenergic receptors (absent in normal lymphocytes) has been demonstrated in transformed human lymphocytes of the Raji cell line. Binding properties of β-adrenergic receptors were similar to those reported for normal lymphocytes. A single population of α 2 -adrenergic receptors was characterized in intact Raji lymphoblasts by binding and saturation assays with the α 2 -adrenergic antagonist yohimbine. Competition curves with [ 3 H]yohimbine indicate the presence of typical α 2 -adrenoceptors. Reaction of Raji with the α 2 -adrenergic agonist clonidine (10 −6 M) stimulated their growth rate. In contrast, the α 1 -adrenergic agonist methoxamine (10 −6 M) had no effect. Previous work indicates that Raji can actively produce thromboxanes (TX) and that these decreased atrium contractility. In agreement with these results and with the binding studies, it is now shown that clonidine stimulation enhanced the negative inotropic effects of Raji on isolated rat atria. This reaction was prevented by incubation of Raji with yohimbine (10 −6 M) but not with the α 1 -adrenergic antagonist prazosin (10 −6 M) or the β-adrenergic antagonist propranolol (10 −7 M). The biologic effect of Raji on rat atria was probably due to production of cyclooxygenase metabolites of arachidonic acid, because it was blocked by preincubation of the cells with the cyclooxygenase inhibitors indomethacin (10 −6 M) and aspirin (10 −4 M) or the thromboxane synthetase inhibitors nictindol (10 −5 M) and imidazole (10 −4 M). The presence of α-adrenoceptors on transformed Raji cells may play a role in the regulation of cell growth and biologic activity, since α 2 -adrenergic stimulation can change the balance of the intracellular signals involved in triggering cell division and function. |
| Databáze: | OpenAIRE |
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