title: Changes and role of adrenoceptors in PC12 cells after phenylephrine administration and apoptosis induction.
abstract: The present study addresses the hypothesis that adrenergic regulation modulates the effect of apoptosis. Therefore we studied, whether α1-adrenergic receptor's agonist phenylephrine (PE) can affect or induce apoptosis in rat pheochromocytoma (PC12) cells. We have shown that PE treatment did not increase level of the apoptosis, or level of the caspase 3 mRNA. When apoptosis was induced in the presence of PE, caspase 3 mRNA was significantly increased, while the percentage of apoptotic cells remained unchanged compared to apoptotic group without PE. During this process, α1D-, β2- and β3-adrenergic receptors (ARs) were upregulated. Since all these three types of ARs are differently localized in the cell, we assume that mutual communication of all three ARs is crucial to participate in this signaling and during development of apoptosis, some of these systems might translocate. Another important system in handling noradrenaline during apoptosis might be noradrenaline transporter (NET), since it was downregulated in apoptotic cells treated with PE, compared to untreated apoptotic cells. However, precise mechanism of mutual communication among all these systems remains to be elucidated.
authors.affiliation: Institute of Molecular Physiology and Genetics, Center of Excellence for Cardiovascular Research, Slovak Academy of Sciences, Vlarska 5, 833 34 Bratislava, Slovak Republic.
authors.forename: Lubomira
authors.initials: L
authors.lastname: Lencesova
authors.forename: Marta
authors.initials: M
authors.lastname: Sirova
authors.forename: Lucia
authors.initials: L
authors.lastname: Csaderova
authors.forename: Marcela
authors.initials: M
authors.lastname: Laukova
authors.forename: Zdena
authors.initials: Z
authors.lastname: Sulova
authors.forename: Richard
authors.initials: R
authors.lastname: Kvetnansky
authors.forename: Olga
authors.initials: O
authors.lastname: Krizanova
mesh_terms: D058646:Adrenergic alpha-1 Receptor Agonists / Q000494:pharmacology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D002452:Cell Count; D006863:Hydrogen-Ion Concentration / Q000187:drug effects; D007424:Intracellular Fluid / Q000187:drug effects / Q000502:physiology; D009336:Necrosis; D009474:Neurons / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D016716:PC12 Cells; D010656:Phenylephrine / Q000008:administration & dosage* / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D018343:Receptors, Adrenergic, beta-2 / Q000502:physiology*
chemical_list: D058646:Adrenergic alpha-1 Receptor Agonists; D012333:RNA, Messenger; D018340:Receptors, Adrenergic, alpha-1; D018343:Receptors, Adrenergic, beta-2; D010656:Phenylephrine; C505410:Casp3 protein, rat; D053148:Caspase 3