Premature thymic involution, observed at the ultrastructural level, in two lineages of human-SOD-1 transgenic mice

Nabarra, B; Casanova, M; Paris, Daniel; Paly, Evelyne; Toyoma, K.; Ceballos, I.; London, Jacqueline

doi:10.1016/s0047-6374(97)01892-7

Cited by 18 publications

(11 citation statements)

References 36 publications

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“…Several lines of evidence support the fact that differentiation of thymocytes is accelerated in Tg-SOD mice. First, as shown by the profile of TCRβ expression (Fig 2 A.), mature SP expressing high level of TCR were detected for both CD4 + and CD8 + cells in Tg-SOD mice as early as day 3 which is in accordance with the observation in DS thymus [21]. Second, using CD69 marker as an indicator of positive selection, we showed an earlier activation of both SP in Tg mice ( Fig 2B.) and greater numbers of CD69 + cells in DP and both SP lymphocytes until day 100 (Fig 2C.).…”

Section: Discussionsupporting

confidence: 83%

“…The colonization of the thymus was shown to happen earlier than in control, following a more rapid decrease from day 140. This observation could explain the earlier thymic architecture disorganization observed in these Tg-SOD mice [21]. Moreover, Tg-SOD mice exhibit productions of both CD4 + and CD8 + SP lymphocytes which appear earlier (Fig 1A.) and which are greater along the development until day 100 (Fig 1 B and C) as compared to ntg controls.…”

Section: Discussionmentioning

confidence: 80%

“…Homozygous mice from the same transgenic line used in the present study have been shown by electron microscopy to exhibit a premature thymic involution [20,21].This thymus premature involution is a characteristic for DS patients [3,37] and may be related to SOD1 gene dosage since SOD1 is mostly expressed in the human thymic medulla [38]. The involution of the thymus is recognized as the most prominent features of age-related immune senescence [13,39,40].…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies with hemizygous hSOD1 Tg (hSOD1/+) mice more than 6 months-old from the same line (KT) indicated an early involution of the thymus architecture [20,21].…”

Section: Activity Of Sod1 In the Tg-sod Mouse Thymusmentioning

confidence: 99%

“…To explore the possible role of SOD1 over-expression in the premature thymic involution and immune disorders observed in DS patients, transgenic mice over-expressing the human SOD1 gene (hSOD1 Tg mice) were generated [19]. Transgenic mice overexpressing SOD1 has been shown to have thymic abnormalities [20][21][22]. More recently the Ts65Dn mice, modeling human trisomy 21, has been shown also to have abnormal thymic apoptosis properties in which reactive oxygen species are involved [23].…”

Section: Introductionmentioning

confidence: 99%

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Early thymic T cell development in young transgenic mice overexpressing human Cu/Zn superoxide dismutase, a model of Down syndrome

Laurent¹,

Paly

Marche

et al. 2006

Free Radical Biology and Medicine

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. Early thymic T cell development in young transgenic mice overexpressing human Cu/Zn superoxide dismutase, a model of Down syndrome.: Early thymic development in SOD1 transgenic mice.. Free Radical Biology and Medicine, Elsevier, 2006Elsevier, , 40 (11), pp.1971Elsevier, -1980 ABSTRACTPrevious studies have shown that transgenic mice over-expressing Cu/Zn Superoxide dismutase, a model of Down's syndrome, exhibit premature thymic involution. We have performed an extensive multiparametric flow cytometry analysis of the developing thymus in these homozygous transgenic mice (hSOD1/hSOD1: Tg-SOD). Longitudinal follow-up analysis from day 3 to day 280 showed an early thymic development in Tg-SOD mice as compared with controls. This thymic early development was associated with an increased migration of mature T cells to peripheral lymphoid organs. BrdU labeling showed no difference between Tg-SOD and control mice, confirming that the greater number of peripheral T cells in Tg-SOD mice was not due to extensive proliferation of these cells but rather to a greater pool of emigrant T cells in Tg-SOD.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 99%

“…Previous studies with hemizygous hSOD1 Tg (hSOD1/+) mice more than 6 months-old from the same line (KT) indicated an early involution of the thymus architecture [20,21].…”

Section: Activity Of Sod1 In the Tg-sod Mouse Thymusmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Early thymic T cell development in young transgenic mice overexpressing human Cu/Zn superoxide dismutase, a model of Down syndrome

Laurent¹,

Paly

Marche

et al. 2006

Free Radical Biology and Medicine

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Overexpression of copper/zinc‐superoxide dismutase in transgenic mice markedly impairs regeneration and increases development of neuropathic pain after sciatic nerve injury

Kotulska

LePecheur

Marcol

et al. 2006

J of Neuroscience Research

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Despite the general capacity of peripheral nervous system to regenerate, peripheral nerve injury is often followed by incomplete recovery of function, sometimes with the burden of neuropathic pain. The mechanisms of both regeneration and nociception have not been clarified, but it is known that inflammatory reactions are involved. Cu/Zn-superoxide dismutase (SOD1) is an important scavenger protein that acts against oxidative stress. It has been shown to play an important role in apoptosis and inflammation. The aim of this study was to examine the role of SOD1 overexpression in peripheral nerve regeneration and neuropathic pain-related behavior in mice. Sciatic nerves of SOD1-overexpressing and FVB/N wild type-mice were transected and immediately resutured. Evaluation of motor and sensory function and autotomy was carried out during 4 weeks of followup. We found markedly worse sciatic function index outcome as well as more significant atrophy of denervated muscles in SOD1-overexpressing animals compared with wild type. Autotomy was markedly worse in SOD1 transgenic mice than in wild-type animals. Histological evaluation revealed that the intensity of regeneration features, including numbers of GAP-43-positive growth cones, Schwann cells, and macrophages in the distal stump of the transected nerve, was also decreased in transgenic mice. Neuroma formation at the injury site was significantly more prominent in this group. Taken together, our findings suggest that SOD1 overexpression is deleterious for nerve regeneration processes and aggravates neuropathic pain-like state in mice. This can be at least partially ascribed to disturbed inflammatory reactions at the injury site.

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Human Cu/Zn Superoxide Dismutase (SOD1) Overexpression in Mice Causes Mitochondrial Vacuolization, Axonal Degeneration, and Premature Motoneuron Death and Accelerates Motoneuron Disease in Mice Expressing a Familial Amyotrophic Lateral Sclerosis Mutant SOD1

Jaarsma

Haasdijk

Grashorn

et al. 2000

Neurobiology of Disease

300

219

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Premature thymic involution, observed at the ultrastructural level, in two lineages of human-SOD-1 transgenic mice

Cited by 18 publications

References 36 publications

Early thymic T cell development in young transgenic mice overexpressing human Cu/Zn superoxide dismutase, a model of Down syndrome

Early thymic T cell development in young transgenic mice overexpressing human Cu/Zn superoxide dismutase, a model of Down syndrome

Overexpression of copper/zinc‐superoxide dismutase in transgenic mice markedly impairs regeneration and increases development of neuropathic pain after sciatic nerve injury

Human Cu/Zn Superoxide Dismutase (SOD1) Overexpression in Mice Causes Mitochondrial Vacuolization, Axonal Degeneration, and Premature Motoneuron Death and Accelerates Motoneuron Disease in Mice Expressing a Familial Amyotrophic Lateral Sclerosis Mutant SOD1

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