Increased expression and colocalization of GAP43 and CASP3 after brain ischemic lesion in mouse

Gorup, Dunja; Bohaček, Ivan; Miličević, Tena; Pochet, Roland; Mitrečić, Dinko; Križ, Jasna; Gajović, Srećko

doi:10.1016/j.neulet.2015.04.042

Cited by 49 publications

(37 citation statements)

References 19 publications

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“…According to this, other studies did not show any age-related changes in SYP1 brain levels [58,59], while others reported significantly decreased SYP1 with age [60][61][62]. GAP43, another nervous tissue-specific protein, is mainly involved in neurite outgrowth and elongation during the neuronal development and is also regarded as a marker for neural plasticity [63][64][65]. In our study, GAP43 was highly expressed in brains of 3-month-old animals which is in accordance with findings from Rosskothen-Kuhl and Illing who found the highest expression of GAP43 during the early development of the nervous system [66].…”

Section: Momentioning

confidence: 85%

Cerebral Mitochondrial Function and Cognitive Performance during Aging: A Longitudinal Study in NMRI Mice

Reutzel

Grewal

Dilberger

et al. 2020

Oxidative Medicine and Cellular Longevity

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Brain aging is one of the major risk factors for the development of several neurodegenerative diseases. Therefore, mitochondrial dysfunction plays an important role in processes of both, brain aging and neurodegeneration. Aged mice including NMRI mice are established model organisms to study physiological and molecular mechanisms of brain aging. However, longitudinal data evaluated in one cohort are rare but are important to understand the aging process of the brain throughout life, especially since pathological changes early in life might pave the way to neurodegeneration in advanced age. To assess the longitudinal course of brain aging, we used a cohort of female NMRI mice and measured brain mitochondrial function, cognitive performance, and molecular markers every 6 months until mice reached the age of 24 months. Furthermore, we measured citrate synthase activity and respiration of isolated brain mitochondria. Mice at the age of three months served as young controls. At six months of age, mitochondria-related genes (complex IV, creb-1, β-AMPK, and Tfam) were significantly elevated. Brain ATP levels were significantly reduced at an age of 18 months while mitochondria respiration was already reduced in middle-aged mice which is in accordance with the monitored impairments in cognitive tests. mRNA expression of genes involved in mitochondrial biogenesis (cAMP response element-binding protein 1 (creb-1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1-α), nuclear respiratory factor-1 (Nrf-1), mitochondrial transcription factor A (Tfam), growth-associated protein 43 (GAP43), and synaptophysin 1 (SYP1)) and the antioxidative defense system (catalase (Cat) and superoxide dismutase 2 (SOD2)) was measured and showed significantly decreased expression patterns in the brain starting at an age of 18 months. BDNF expression reached, a maximum after 6 months. On the basis of longitudinal data, our results demonstrate a close connection between the age-related decline of cognitive performance, energy metabolism, and mitochondrial biogenesis during the physiological brain aging process.

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Section: Momentioning

confidence: 85%

Cerebral Mitochondrial Function and Cognitive Performance during Aging: A Longitudinal Study in NMRI Mice

Reutzel

Grewal

Dilberger

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…The overexpression of GAP43 in a neurodegenerative disease or a traumatic injury in a mouse model showed a significant improvement in the dysfunction of the mouse. [ 16 ] Figure 3c shows a pandect of immunofluorescence images of different groups after a culture of 10 days. The nuclei are fluorescently stained in blue and the GAP 43 in green.…”

Section: Resultsmentioning

confidence: 99%

3D‐Printed Soft Magnetoelectric Microswimmers for Delivery and Differentiation of Neuron‐Like Cells

Dong

Wang

Chen

et al. 2020

Adv Funct Materials

206

191

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Neurodegenerative diseases generally result in irreversible neuronal damage and neuronal death. Cell therapy shows promise as a potential treatment for these diseases. However, the therapeutic targeted delivery of these cells and the in situ provision of a suitable microenvironment for their differentiation into functional neuronal networks remain challenging. A highly integrated multifunctional soft helical microswimmer featuring targeted neuronal cell delivery, on-demand localized wireless neuronal electrostimulation, and post-delivery enzymatic degradation is introduced. The helical soft body of the microswimmer is fabricated by two-photon lithography of the photocurable gelatin-methacryloyl (GelMA)-based hydrogel. The helical body is then impregnated with composite multiferroic nanoparticles displaying magnetoelectric features (MENPs). While the soft GelMA hydrogel chassis supports the cell growth, and is degraded by enzymes secreted by cells, the MENPs allow for the magnetic transportation of the bioactive chassis, and act as magnetically mediated electrostimulators of neuron-like cells. The unique combination of the materials makes these microswimmers highly integrated devices that fulfill several requirements for their future translation to clinical applications, such as cargo delivery, cell stimulation, and biodegradability. The authors envision that these devices will inspire new avenues for targeted cell therapies for traumatic injuries and diseases in the central nervous system.

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“…On the contrary, the highest expression levels of SYP and PSD-95 in MDP Group show most synaptogenesis which corresponds to the results in the TEM depicting. SYP, GAP-43mRNA and MAP-2 are associated with presynaptic and postsynaptic plasticity as well as the neuronal cytoskeletons [32], they play crucial roles in neuroplasticity and recovery from a stroke [38,39,40]. The synchronous changes of these three markers reflect the consistency of genes, molecules and cell regulation in NVU.…”

Section: Discussionmentioning

confidence: 99%

The experimental research on neuroplasticity in rats’ hippocampus subjected to chronic cerebral hypoperfusion and interfered by Modified Dioscorea Pills

Liang

Zhou

2020

Heliyon

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A B S T R A C TBackground: Chronic Cerebral Hypoperfusion (CCH) is a common, crucial and tough problem for old people. It easily leads to Lacunar Infarction and even Vascular Dementia (VD). Western medicine has the advantage to relieve some VD symptoms but fails to cure it. Some classic Chinese medicines have good efficacies to treat and delay the cerebral functional decline resulted from CCH. Among them Modified Dioscorea Pills (MDP) has been proven to have a convincing effect in curing VD. So far the knowledge about neuroplasticity in CCH is little known and the underlying interfered mechanism by MDP on neuroplasticity has not yet been explored. This study explores the changes of neuroplasticity involving neurogenesis, angiogenesis and synaptogenesis in CCH and interfered by MDP. Methods: 40 male SD rats were divided into the Sham operated Group, the Model Group and the MDP Group according to a Random Number Table. Bilateral Common Carotid Arteries Occlusion (BCCAO) was adopted to prepare CCH models. MDP condense decoction had been administered by gavage to rats in the MDP Group (10g⋅Kg-1⋅d-1) for 45 days; Rats in the other two groups were accepted normal salts as substitution with same dosage and course. Through Morris Water Maze (MWM) test, pathological observation of hippocampus, ultrastructural study on synapse, Real Time Polymerase Chain Reaction (RT-PCR) and immunohistochemistry detection, the capacities of intelligence of rats, the morphological character of hippocampus CA1 zone and the synapse associated protein and gene such as Growth Associated Protein (GAP-43) mRNA, Vascular Endothelial Growth Factor (VEGF) mRNA, Microtubule-associated Protein (MAP)-2, Synaptophysin (SYP), Postsynaptic Density protein (PSD)-95 and Micro Vessel Density (MVD) were determined. Through one-way ANOVA the data was analyzed and when P＜0.05 the result was considered significant. Results: Compared to the Model Group, rats in the MDP Group achieved much better behavioral performance (P＜ 0.05); more neurons and more synapses regenerated; the expression of SYP, PSD-95and MAP-2 up-regulated (P＜ 0.05); The expressions of GAP-43 mRNA and VEGF mRNA in the Model Group were higher than those in the Sham operated Group (P＜0.05), but they reached the highest in the MDP Group (P＜0.05); The count of MVD in the Sham operated Group is the lowest, it is higher in the MDP Group and it reaches highest in the Model Group (P＜ 0.05). Conclusions: Some key genes promoting neuroplasticity such as GAP-43 mRNA and VEGF mRNA remarkably upregulated in CCH, they only boost angiogenesis but fail to facilitate neurogenesis and synaptogenesis in CCH. However, accompanied by furtherly up-regulation of these two key genes, MDP obviously improves neurogenesis, synaptogenesis and temperate angiogenesis in CCH which may be underlying its good efficacy.

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Increased expression and colocalization of GAP43 and CASP3 after brain ischemic lesion in mouse

Cited by 49 publications

References 19 publications

Cerebral Mitochondrial Function and Cognitive Performance during Aging: A Longitudinal Study in NMRI Mice

Cerebral Mitochondrial Function and Cognitive Performance during Aging: A Longitudinal Study in NMRI Mice

3D‐Printed Soft Magnetoelectric Microswimmers for Delivery and Differentiation of Neuron‐Like Cells

The experimental research on neuroplasticity in rats’ hippocampus subjected to chronic cerebral hypoperfusion and interfered by Modified Dioscorea Pills

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