Upregulation of calcium binding protein, S100A6, in activated astrocytes is linked to glutamate toxicity

Yamada, Jun; Jinno, Shozo

doi:10.1016/j.neuroscience.2012.08.068

Cited by 14 publications

(18 citation statements)

References 52 publications

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“…Whereas the biological actions of S100A6 in the brain remain largely undefined, expression of S100A6 is increased within astrocytes in response to glutamate excitotoxicity within the axotomized hypoglossal nucleus in mice [134]. Notably, reduced S100A6 expression in the hippocampus was associated with subsequent cognitive decline after lateral head acceleration-induced TBI whereas a delayed elevation of S100A6 was associated with cognitive recovery [135].…”

Section: Damage Associated Molecular Patterns (Damps): Mediators Omentioning

confidence: 99%

White matter damage after traumatic brain injury: A role for damage associated molecular patterns

Braun

Vaibhav

Saad

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Traumatic brain injury (TBI) is a leading cause of mortality and long-term morbidity worldwide. Despite decades of pre-clinical investigation, therapeutic strategies focused on acute neuroprotection failed to improve TBI outcomes. This lack of translational success has necessitated a reassessment of the optimal targets for intervention, including a heightened focus on secondary injury mechanisms. Chronic immune activation correlates with progressive neurodegeneration for decades after TBI; however, significant challenges remain in functionally and mechanistically defining immune activation after TBI. In this review, we explore the burgeoning evidence implicating the acute release of damage associated molecular patterns (DAMPs), such as adenosine 5′-triphosphate (ATP), high mobility group box protein 1 (HMGB1), S100 proteins, and hyaluronic acid in the initiation of progressive neurological injury, including white matter loss after TBI. The role that pattern recognition receptors, including toll-like receptor and purinergic receptors, play in progressive neurological injury after TBI is detailed. Finally, we provide support for the notion that resident and infiltrating macrophages are critical cellular targets linking acute DAMP release with adaptive immune responses and chronic injury after TBI. The therapeutic potential of targeting DAMPs and barriers to clinical translational, in the context of TBI patient management, are discussed.

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Section: Damage Associated Molecular Patterns (Damps): Mediators Omentioning

confidence: 99%

White matter damage after traumatic brain injury: A role for damage associated molecular patterns

Braun

Vaibhav

Saad

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…The protein appears to be regulated by calcium which binds to two EF-hand calcium binding sites within the protein. The binding of calcium is thought to induce conformational change in the protein which is involved in the regulation of a number of processes including cell proliferation and differentiation, calcium homeostasis, cell degeneration, and cytoskeletal dynamics via signal transduction pathways (21,22).…”

Section: Resultsmentioning

confidence: 99%

S100A6 expression in cutaneous smooth muscle neoplasms

Idriss

Elston

2015

APMIS

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The S100A6 protein is expressed in a variety of tissues and distinct staining patterns in S100A6 immunohistochemistry may be useful in the differential diagnosis of difficult lesions. We evaluated the staining pattern of the S100A6 antibody in 22 cases each of pilar leiomyoma (LM), angioleiomyoma (ALM), and cutaneous leiomyosarcoma (LMS). S100A6 labeled both the nucleus and cytoplasm of myocytes in positive cases. About 64% of LM and 86% ALM had positive staining to the S100A6 antibody but predominantly in a weak staining pattern. In contrast, 95% of the LMS exhibited moderate to strong staining with the S100A6 antibody. The difference in the frequency of positive cases was statistically significant in the LM vs LMS comparison (p = 0.025), but we found intensity of staining to be of greatest practical utility. Analysis between the groups taking in to consideration differences in intensity of staining using the nonparametric rank sum (Mann-Whitney U test) demonstrated that there was a statistically significant difference between LM and LMS and between ALM and LMS. Weak or absent S100A6 staining supports a diagnosis of LM, whereas strong positive staining supports a diagnosis of LMS.

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“…A recent study reported for the first time that up-regulation of S100A6 in activated astrocytes may be linked to glutamate toxicity in the hippocampus of two mouse models of brain aging and epilepsy, and in the axotomized hypoglossal nucleus of one mouse model [13]. The authors noted that no causal conclusions could be drawn based on their correlative findings.…”

Section: Discussionmentioning

confidence: 99%

“…The authors noted that no causal conclusions could be drawn based on their correlative findings. Despite this weakness, the authors suggested that their data provided some insights into the association between astrocytic S100A6 and glutamate-induced neuronal damage under pathophysiological conditions [13]. …”

Section: Discussionmentioning

confidence: 99%

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Expression of S100A6 in Rat Hippocampus after Traumatic Brain Injury Due to Lateral Head Acceleration

Fang

Ming

Yang

et al. 2014

IJMS

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In a rat model of traumatic brain injury (TBI), we investigated changes in cognitive function and S100A6 expression in the hippocampus. TBI-associated changes in this protein have not previously been reported. Rat S100A6 was studied via immunohistochemical staining, Western blot, and reverse transcription-polymerase chain reaction (RT-PCR) after either lateral head acceleration or sham. Reduced levels of S100A6 protein and mRNA were observed 1 h after TBI, followed by gradual increases over 6, 12, 24, and 72 h, and then a return to sham level at 14 day. Morris water maze (MWM) test was used to evaluate animal spatial cognition. TBI- and sham-rats showed an apparent learning curve, expressed as escape latency. Although TBI-rats displayed a relatively poorer cognitive ability than sham-rats, the disparity was not significant early post-injury. Marked cognitive deficits in TBI-rats were observed at 72 h post-injury compared with sham animals. TBI-rats showed decreased times in platform crossing in the daily MWM test; the performance at 72 h post-injury was the worst. In conclusion, a reduction in S100A6 may be one of the early events that lead to secondary cognitive decline after TBI, and its subsequent elevation is tightly linked with cognitive improvement. S100A6 may play important roles in neuronal degeneration and regeneration in TBI.

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Upregulation of calcium binding protein, S100A6, in activated astrocytes is linked to glutamate toxicity

Cited by 14 publications

References 52 publications

White matter damage after traumatic brain injury: A role for damage associated molecular patterns

White matter damage after traumatic brain injury: A role for damage associated molecular patterns

S100A6 expression in cutaneous smooth muscle neoplasms

Expression of S100A6 in Rat Hippocampus after Traumatic Brain Injury Due to Lateral Head Acceleration

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