Adrenergic Modulation of Apoptosis in Splenocytes of <i>Xenopus laevis</i> in vitro

Abstract

Impaired and healthy cells undergo suicide using an intrinsic genetic program. Exposure to stress-related α₂- or β-adrenergics for 4 or 20 h in vitro had no effect on apoptosis in splenocytes of adult Xenopus laevis, while a 4-hour coincubation of clonidine, an α₂-agonist, with a calcium ionophore (A23187) or a phorbol diester (PMA), enhanced apoptosis induced by each apoptogen alone. Clonidine did not affect apoptosis stimulated with dexamethasone (DEX), however. Comparable in vitro exposures to isoproterenol, a β-agonist, reduced apoptotic levels stimulated by all three apoptogens alone. Following 20 h coexposure, clonidine no longer affected A23187-induced apoptosis, but reduced PMA-induced apoptosis, while isoproterenol enhanced apoptosis stimulated with both. Neither agonist modulated apoptosis induced by 20 h of exposure to DEX. Thus, adrenergic agonists modulated apoptosis in cells coexposed to A23187 and PMA, in a time-dependent and adrenoceptor class-dependent fashion. These stress-induced products can affect concurrent apoptosis reversibly over time in vitro, and thus possibly in vivo.

In Response to a Punctual Stress Male and Female Tyrosine Hydroxylase Haploinsufficient Mice Show a Deteriorated Behavior, Immunity, and Redox State

“…These differences between the experimental groups in their catecholamine concentrations explain the results obtained when the different functions are evaluated given the close relationship between catecholamines and the homeostatic systems [ 7 , 39 ]. Regarding immunity, stress and catecholamine release regulate many functions of the immune system, such as cytokine production [ 40 , 41 ], proliferation [ 42 ], apoptosis of splenic cells [ 43 ], changes in leukocyte subsets [ 44 , 45 ], splenic macrophage phagocytosis [ 46 ], and NK cell cytotoxicity [ 12 ], thus catecholamines can be said to play a key role in the regulation of innate and adaptive immunity [ 13 ]. In this sense, the regulation of the immune system is mainly mediated by noradrenaline and dopamine, moreover, the immune cells themselves are able to synthesize noradrenaline through dopamine beta-hydroxylase [ 13 ], which could justify the decrease in this in WT males after stress, since they would be dealing dopamine to the synthesis of noradrenaline, trying to maintain their immune function.…”