Modulation of Intracellular Formation of Reactive Oxygen Intermediates in Peritoneal Macrophages and Microglia/Brain Macrophages by Propentofylline

Bánati, Richard B.; Schubert, Peter; Rothe, Gregor; Gehrmann, Jochen; Rudolphi, Karl Asmund; Valet, G.; Kreutzberg, Georg W.

doi:10.1038/jcbfm.1994.19

Cited by 105 publications

(42 citation statements)

References 35 publications

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“…In acute human stroke, PPF posttreatment increased cerebral energy metabolism (54). Additional protective actions of PPF may include a decrease in production of oxygen free radicals by activated microglia (55), and a potentiation of A, adenosine receptor-mediated actions secondary to phosphodiesterase inhibition (46).…”

Section: Dcf-treated Animalsmentioning

confidence: 99%

Reduction in Cerebral Ischemic Injury in the Newborn Rat by Potentiation of Endogenous Adenosine

et al. 1995

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Because of ontogenic influences on the pathophysiologic mechanisms of brain injury in the perinatal brain, and in particular, the incomplete development of adenosine receptor systems, we investigated the potential for adenosine to provide cerebroprotection in a well established newborn rat model of hypoxiaischemia. Fifteen litters of postnatal d 7 animals were subjected to unilateral carotid ligation and exposure to hypoxia (8% oxygen) for 3 h. Immediately after hypoxia-ischemia, animals received either the adenosine deaminase inhibitor deoxycoformycin (DCF; 2.5 mg/kg intraperitoneally) or the adenosine uptake inhibitor propentofylline (PPF; 10 mg/kg intraperitoneally); paired littermates received an equivalent volume of normal saline. On postnatal d 14, injury or protection was assessed by differences in hemispheric weights, morphometric determinations of infarct area, and histopathologic analyses. DCF resulted in a 34% (p = 0.02) and 31% ( p = 0.03) reduction in hemispheric weight disparities and infarct area, respectively; for PPF, these reductions were 46% ( p = 0.03) and 32% ( p = 0.04), Although the brain of the newborn exhibits a higher tolerance to ischemia than that of the adult, morbidity and mortality from hypoxic-ischemic encephalopathy in the perinatal period remain high (1). Although the general pathophysiologic mechanisms underlying cerebral ischemic injury are probably similar between age groups, the unique characteristics of energy and glucose metabolism (2), glutamate receptor physiology (3, 4), and vascular regulation (5, 6) in the newborn brain may dictate separate therapeutic regimens for affected neonates relative to adults.In recent years, experimental evidence has accumulated from adult animal models attesting to the neuroprotective properties of the purine nucleoside adenosine in the setting of Received February 3, 1995; accepted April 6, 1995 7 for review), and the mechanistic basis for such an adenosine-mediated reduction in ischemic brain injury has been outlined (8). Ontogenic studies of the brains of fetal and newborn animals indicate that the requisite metabolic enzymes and transporters for adenosine are fully matured at birth or earlier (9-12). There is also consistent evidence that cerebral adenosine production increases in response to perinatal hypoxia-ischemia (13-16). Although cerebral vessels in fetal and newborn animals exhibit the characteristic vasodilatative response to adenosine (17, 18), significant development of neuronal adenosine receptors, particularly in terms of density and coupling to second messengers, may occur postnatally (12,19,20). Thus, adenosinebased treatments may not provide therapeutic efficacy against cerebral hypoxia-ischemia in the perinatal period. To address this possibility, we used two different drugs to determine whether potentiating endogenous adenosine would confer cerebroprotection in a neonatal model of hypoxia-ischemia.

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Section: Dcf-treated Animalsmentioning

confidence: 99%

Reduction in Cerebral Ischemic Injury in the Newborn Rat by Potentiation of Endogenous Adenosine

et al. 1995

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“…However, no regional correlation has been found between SP and Aß vascular deposits within the cerebral cortex in AD [111]. Microglial-like perivascular cells within the vascular basement membrane express APP and may thus represent a possible source of vascular amyloid [105,112,113]. In large vessels, Aß protein may be produced in both APP-containing degenerating vascular muscle cells and microglial-like perivascular cells [103,113].…”

Section: Aß Deposits In Ad Vesselsmentioning

confidence: 99%

Reevaluating the Role of Vascular Changes in the Differential Diagnosis of Alzheimer’s Disease and Vascular Dementia

1998

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Alzheimer’s disease (AD) and vascular dementia (VaD) are the two most common causes of dementia, and much effort has been devoted to their differential diagnosis. However, current epidemiological, clinical and neuropathological evidence points to a substantial overlap between AD and VaD and suggests that vascular pathology, the traditional cornerstone of the differential diagnosis between the two entities, may not represent as clear a line of demarcation as originally believed. It may be time to reevaluate the dichotomy between AD and VaD.

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“…ϩ , or head-kidney cells triggered by PMA was measured as the dihydrorhodamine 1,2,3-dependent fluorescence, using flow cytometry [15].…”

Section: Roi Production Assaymentioning

confidence: 99%

Professional phagocytic granulocytes of the bony fish gilthead seabream display functional adaptation to testicular microenvironment

Chaves-Pozo

Mulero

Meseguer

et al. 2005

Journal of Leukocyte Biology

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It has been shown previously that professional phagocytic granulocytes are present in the testis of the gilthead seabream, a seasonal breeding teleost that offers an excellent model for studying the testicular regression process that occurs in seasonal testicular involution and sex change. It is unexpected that testicular granulocytes produce interleukin-1␤, a regulator for spermatogonia proliferation in mammals, but are not involved in the elimination of degenerative germ cells. Here, we show that phagocytosis and reactive oxygen intermediate (ROI) production were suppressed dramatically in testicular phagocytic granulocytes, compared with their level of activity in the head-kidney, the main hematopoietic organ in fish. Furthermore, testicular-conditioned media modulated migration, phagocytosis, and ROI production of head-kidney phagocytic granulocytes, and the addition of testicular cells impaired their ROI production capacity. Until now, monocytes/ macrophages were believed to be the only innate immune cells able to develop into functional subsets, whereas neutrophils only infiltrate the tissues upon infection or inflammation. Our findings demonstrate, however, that fish professional phagocytic granulocytes also display functional adaptation to different microenvironments and strongly suggest a role for these cells in the reorganization of the testis during post-spawning. J. Leukoc. Biol. 78: 345-351; 2005.

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Modulation of Intracellular Formation of Reactive Oxygen Intermediates in Peritoneal Macrophages and Microglia/Brain Macrophages by Propentofylline

Cited by 105 publications

References 35 publications

Reduction in Cerebral Ischemic Injury in the Newborn Rat by Potentiation of Endogenous Adenosine

Reduction in Cerebral Ischemic Injury in the Newborn Rat by Potentiation of Endogenous Adenosine

Reevaluating the Role of Vascular Changes in the Differential Diagnosis of Alzheimer’s Disease and Vascular Dementia

Professional phagocytic granulocytes of the bony fish gilthead seabream display functional adaptation to testicular microenvironment

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