Metallothionein 3 attenuated the apoptosis of neurons in the CA1 region of the hippocampus in the senescence-accelerated mouse/PRONE8 (SAMP8)

Ma, Fei; Wang, Hu; Chen, Bin; Wang, Feng; Xu, Haixiong

doi:10.1590/s0004-282x2011000100020

Cited by 22 publications

(18 citation statements)

References 23 publications

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“…For the regulation of apoptosis, there were significant levels of neuronal apoptosis were observed in the hippocampus of SAMP8 mice, which was comparable with those in the SMAR1 mice (Ma et al, 2011; Lou et al, 2012). The number of hippocampal neurons was decreased in the hippocampus of SAMP8 mice (Yaguchi et al, 2010; Hu et al, 2012), and there was an increase in the number of condensed nuclei in primary culture cerebellar neurons from SAMP8 mice (Tajes et al, 2008).…”

Section: Discussionsupporting

confidence: 71%

Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model

Cheng¹,

Cui

Zheng³

et al. 2013

Front. Aging Neurosci.

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Harboring the behavioral and histopathological signatures of Alzheimer's disease (AD), senescence accelerated mouse-prone 8 (SAMP8) mice are currently considered a robust model for studying AD. However, the underlying mechanisms, prioritized pathways and genes in SAMP8 mice linked to AD remain unclear. In this study, we provide a biological interpretation of the molecular underpinnings of SAMP8 mice. Our results were derived from differentially expressed genes in the hippocampus and cerebral cortex of SAMP8 mice compared to age-matched SAMR1 mice at 2, 6, and 12 months of age using cDNA microarray analysis. On the basis of PPI, MetaCore and the co-expression network, we constructed a distinct genetic sub-network in the brains of SAMP8 mice. Next, we determined that the regulation of synaptic transmission and apoptosis were disrupted in the brains of SAMP8 mice. We found abnormal gene expression of RAF1, MAPT, PTGS2, CDKN2A, CAMK2A, NTRK2, AGER, ADRBK1, MCM3AP, and STUB1, which may have initiated the dysfunction of biological processes in the brains of SAMP8 mice. Specifically, we found microRNAs, including miR-20a, miR-17, miR-34a, miR-155, miR-18a, miR-22, miR-26a, miR-101, miR-106b, and miR-125b, that might regulate the expression of nodes in the sub-network. Taken together, these results provide new insights into the biological and genetic mechanisms of SAMP8 mice and add an important dimension to our understanding of the neuro-pathogenesis in SAMP8 mice from a systems perspective.

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Section: Discussionsupporting

confidence: 71%

Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model

Cheng¹,

Cui

Zheng³

et al. 2013

Front. Aging Neurosci.

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“…In addition, the immunohistochemical analysis for cleaved caspase 3 has also confirmed the increased apoptosis in SAMP8 mice hearts compared with SAMR1 mice. Several reports are available to show the relationship between aging and apoptotic cell loss in various organs such as pancreas , brain , and spleen . In consistent with these reports, our present study has confirmed the involvement of apoptotic cell death in the accelerated aging induced cardiac dysfunction.…”

Section: Discussionsupporting

confidence: 92%

Role of MAPK‐mediated endoplasmic reticulum stress signaling in the heart during aging in senescence‐accelerated prone mice

et al. 2016

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Heart failure is typically related to aging as there is a definite relationship between age-related changes in the heart and the pathogenesis of heart failure. We have previously reported the involvement of p38 mitogen-activated protein kinase protein in cardiac function using animal models of heart failure. To further understand its relationship with aging-induced heart failure, we have compared its expression in the hearts of senescence accelerated-prone (SAMP8) mice and their control (SAMR1) with normal aging behavior. We have identified its activation along with reduced expression of 14-3-3η protein in SAMP8 mice hearts than in SAMR1 mice. To reveal the downstream signaling, we have measured the endoplasmic reticulum stress marker proteins along with some inflammatory and apoptosis markers and identified a significant increase in SAMP8 mice hearts than that of SAMR1. In addition, we have performed comet assay and revealed a significant DNA damage in the cardiomyocytes of SAMP8 mice when compared with SAMR1 mice. All these results demonstrate the role of 14-3-3η protein and the downstream mitogen-activated protein kinase-mediated endoplasmic reticulum stress, and apoptosis and DNA damage in aging-induced cardiac malfunction in SAMP8 mice. Thus targeting this signaling might be effective in treating age-related cardiac dysfunction. © 2016 BioFactors, 42(4):368-375, 2016.

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“…The sections were deparaffined, dehydrated and treated with 1% H 2 O 2 as decribed [41] Antigen retrieval was carried out using citrate buffer (0.01 M; pH 6.0). The sections were then incubated with the primary antibody recognizing Aβ (1–40/42) (Millipore; 1∶100) overnight at 4°C followed by incubation with biotinylated goat anti-rabbit IgG.…”

Section: Methodsmentioning

confidence: 99%

WNT5A Signaling Contributes to Aβ-Induced Neuroinflammation and Neurotoxicity

Zhong

Yang

et al. 2011

PLoS ONE

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Neurodegenration is a pathological hallmark of Alzheimer's disease (AD), but the underlying molecular mechanism remains elusive. Here, we present evidence that reveals a crucial role of Wnt5a signaling in this process. We showed that Wnt5a and its receptor Frizzled-5 (Fz5) were up-regulated in the AD mouse brain, and that beta-amyloid peptide (Aβ), a major constituent of amyloid plaques, stimulated Wnt5a and Fz5 expression in primary cortical cultures; these observations indicate that Wnt5a signaling could be aberrantly activated during AD pathogenesis. In support of such a possibility, we observed that inhibition of Wnt5a signaling attenuated while activation of Wnt5a signaling enhanced Aβ-evoked neurotoxicity, suggesting a role of Wnt5a signaling in AD-related neurodegeneration. Furthermore, we also demonstrated that Aβ-induced neurotoxicity depends on inflammatory processes, and that activation of Wnt5a signaling elicited the expression of proinflammatory cytokines IL-1β and TNF-α whereas inhibition of Wnt5a signaling attenuated the Aβ-induced expression of the cytokines in cortical cultures. Our findings collectively suggest that aberrantly up-regulated Wnt5a signaling is a crucial pathological step that contributes to AD-related neurodegeneration by regulating neuroinflammation.

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Metallothionein 3 attenuated the apoptosis of neurons in the CA1 region of the hippocampus in the senescence-accelerated mouse/PRONE8 (SAMP8)

Cited by 22 publications

References 23 publications

Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model

Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model

Role of MAPK‐mediated endoplasmic reticulum stress signaling in the heart during aging in senescence‐accelerated prone mice

WNT5A Signaling Contributes to Aβ-Induced Neuroinflammation and Neurotoxicity

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