Apoptosis and White Matter Injury in Preterm Infants

Chamnanvanakij, Sangkae; Margraf, Linda R.; Burns, Dennis K.; Perlman, Jeffrey M.

doi:10.1007/s10024-001-0205-0

Cited by 13 publications

(12 citation statements)

References 16 publications

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“…Apoptosis was detected in our human cases as previously reported in infants suffering intrauterine cerebral injury [34] , preterm infants [35,36] and mature perinatal deaths [37] following hypoxic injuries. Apoptotic features in Vim-positive astrocytes and clasmatodendrotic features in both Vim-and GFAP-positive cells without TUNELpositive (apoptotic) nuclei were observed in both rat and human (present in all studied cases) brain sections.…”

Section: Discussionmentioning

confidence: 63%

Astrocytic Demise in the Developing Rat and Human Brain after Hypoxic-Ischemic Damage

et al. 2009

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In order to approach the physiopathological mechanism underlying the selective susceptibility of the immature brain to hypoxia-ischemia (HI), we have compared the lesions experimentally induced in postnatal day 7 rats using a model of neonatal stroke with those occurring in human fetal and neonatal brains. We first observed that gray and white matter lesions demonstrated a similar organization (core with cell loss and/or cavity and penumbra) and evolutionary pattern between experimental and human HI lesions. We then observed that, in the intermediate white matter, GFAP- and vimentin-positive astrocytes exhibited clasmatodendrosis and represent a major cell population involved in cell death in human brains (56.3 and 67.9%, respectively). In rat brains, GFAP- and TUNEL-positive astrocytes were also highly vulnerable, increasing between 6 (31%) and 72 (58%) hours after ischemia. Together, these results indicate that astroglial dysfunction may play a critical role in determining the progress and outcome of acute hypoxic-ischemic injury particularly in the developing brain.

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Section: Discussionmentioning

confidence: 63%

Astrocytic Demise in the Developing Rat and Human Brain after Hypoxic-Ischemic Damage

et al. 2009

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“…Apoptosis has been reported to be a contributing mechanism for cell death in infants with WM injury (29). As previously demonstrated in pregnant rabbits and guinea pigs, E. coli inoculation into the uterine horns or into the cervix resulted in abundant PCD in the WM 2 d later (16,30).…”

Section: Discussionmentioning

confidence: 69%

Maternal Exposure to LPS Induces Hypomyelination in the Internal Capsule and Programmed Cell Death in the Deep Gray Matter in Newborn Rats

et al. 2006

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Epidemiologic and experimental findings implicate maternal infection in the etiology of injury to brain white matter, which may lead to cerebral palsy in preterm newborns. In the present study, inflammation and brain damage in 1-and 7-d-old rats were investigated after maternal inflammation. Intraperitoneal injection of 300 g/kg of Escherichia coli lipopolysaccharide was administered to pregnant Wistar rats at d 19 and 20 of gestation (LPS group). Control females received a saline injection. Proinflammatory cytokines IL-1␤, tumor necrosis factor-␣, and IL-6 expression in the fetal brain were determined by reverse transcription quantitative polymerase chain reaction. Brain injury was examined in 16-m coronal brain sections by GFAP, MBP, caspase-3 immunohistochemistry, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling. Expression of IL-1␤ was significantly increased 3 d after maternal administration (P1). A significant increase in cell death occurred at P1 and P7 in specific brain areas, i.e. in the subventricular striatal zone at P1, and in 1) the periventricular striatum, 2) the periventricular white matter, and 3) the germinative ventricular zone at P7. We also observed typical astrogliosis and strong hypomyelination in the external and internal capsule in the LPS group at P7. These results demonstrate that maternal LPS treatment induces persistent fetal inflammatory reactions associated with significant white matter injury in progeny at P1 and P7. This model should be relevant for the study of the pathophysiological mechanisms involved in cerebral white matter damage in preterm human newborns and in the development of therapeutic strategies. (Pediatr Res 59: [428][429][430][431][432][433] 2006)

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“…Nuclear blebbing and karyorrhexis were observed in glial cells within the white matter after intraventricular hemorrhage in preterm infants [68]. Astrocytic loss temporally preceded vascular injury after experimental ICH [28, 62] and focal astrocyte loss increased microvascular damage and induced transient BBB opening [69].…”

Section: Discussionmentioning

confidence: 99%

Necrostatin-1 Reduces Neurovascular Injury after Intracerebral Hemorrhage

King

Whitaker-Lea

Campbell

et al. 2014

International Journal of Cell Biology

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Intracerebral hemorrhage (ICH) is the most common form of hemorrhagic stroke, accounting for 15% of all strokes. ICH has the highest acute mortality and the worst long-term prognosis of all stroke subtypes. Unfortunately, the dearth of clinically effective treatment options makes ICH the least treatable form of stroke, emphasizing the need for novel therapeutic targets. Recent work by our laboratory identified a novel role for the necroptosis inhibitor, necrostatin-1, in limiting neurovascular injury in tissue culture models of hemorrhagic injury. In the present study, we tested the hypothesis that necrostatin-1 reduces neurovascular injury after collagenase-induced ICH in mice. Necrostatin-1 significantly reduced hematoma volume by 54% at 72 h after-ICH, as compared to either sham-injured mice or mice administered an inactive, structural analogue of necrostatin-1. Necrostatin-1 also limited cell death by 48%, reduced blood-brain barrier opening by 51%, attenuated edema development to sham levels, and improved neurobehavioral outcomes after ICH. These data suggest a potential clinical utility for necrostatin-1 and/or novel necroptosis inhibitors as an adjunct therapy to reduce neurological injury and improve patient outcomes after ICH.

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Apoptosis and White Matter Injury in Preterm Infants

Cited by 13 publications

References 16 publications

Astrocytic Demise in the Developing Rat and Human Brain after Hypoxic-Ischemic Damage

Astrocytic Demise in the Developing Rat and Human Brain after Hypoxic-Ischemic Damage

Maternal Exposure to LPS Induces Hypomyelination in the Internal Capsule and Programmed Cell Death in the Deep Gray Matter in Newborn Rats

Necrostatin-1 Reduces Neurovascular Injury after Intracerebral Hemorrhage

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