Hippocampal neural stem cells rapidly change their metabolic profile during neuronal differentiation &amp;nbsp; in cell culture &amp;nbsp;

Hruzova, Martina; Zamboni, Nicola; Jessberger, Sebastian

doi:10.19185/matters.201603000016

Cited by 2 publications

(2 citation statements)

References 27 publications

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“…Most studies that have investigated a role for metabolic factors in the pathology of ALS/FTLD were performed in vivo in animal models, which have supported and advanced clinical findings in humans, where it is more difficult to control for various factors. Immortalized cancer cell lines and in neural stem cells are also excellent models to study; however, they can show metabolic adaptations that complicate interpretation of data derived from them [ 23 , 68 ]. Other systems that may be excellent for studying metabolic effects in real time include alternative ex vivo systems, such as organotypic slice culture models [ 88 ], induced pluripotent stem cells (iPSCs)-derived neurons [ 108 ] or long-term complex neuronal cultures [ 159 ].…”

Section: Discussionmentioning

confidence: 99%

Disease-modifying effects of metabolic perturbations in ALS/FTLD

Jawaid

Khan

Polymenidou

et al. 2018

Mol Neurodegeneration

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Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) are two fatal neurodegenerative disorders with considerable clinical, pathological and genetic overlap. Both disorders are characterized by the accumulation of pathological protein aggregates that contain a number of proteins, most notably TAR DNA binding protein 43 kDa (TDP-43). Surprisingly, recent clinical studies suggest that dyslipidemia, high body mass index, and type 2 diabetes mellitus are associated with better clinical outcomes in ALS. Moreover, ALS and FTLD patients have a significantly lower incidence of cardiovascular disease, supporting the idea that an unfavorable metabolic profile may be beneficial in ALS and FTLD. The two most widely studied ALS/FTLD models, super-oxide dismutase 1 (SOD1) and TAR DNA binding protein of 43 kDA (TDP-43), reveal metabolic dysfunction and a positive effect of metabolic strategies on disease onset and/or progression. In addition, molecular studies reveal a role for ALS/FTLD-associated proteins in the regulation of cellular and whole-body metabolism. Here, we systematically evaluate these observations and discuss how changes in cellular glucose/lipid metabolism may result in abnormal protein aggregations in ALS and FTLD, which may have important implications for new treatment strategies for ALS/FTLD and possibly other neurodegenerative conditions.

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Section: Discussionmentioning

confidence: 99%

Disease-modifying effects of metabolic perturbations in ALS/FTLD

Jawaid

Khan

Polymenidou

et al. 2018

Mol Neurodegeneration

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“…We used CFD modeling of O 2 diffusion and consumption to simulate the gradient variation of O 2 levels in the gap area (1.33 cm) between the media and media + O 2 supply channels (diameter, 1 mm) of the chip: 2 cm (W ) by 2 cm (D) by 5 mm (H ). When the O 2 gradient in the chip was calculated by computational modeling, we considered the O 2 consumption of BMSCs along with the O 2 supply through media to set up the chip circulation system (see Supplementary Text) (55)(56)(57). Color coding from contour and volume rendering via quantitative analyses of 3D modeling showed the O 2 levels.…”

Section: Cfd Modelingmentioning

confidence: 99%

O ₂ variant chip to simulate site-specific skeletogenesis from hypoxic bone marrow

Kim

et al. 2023

Sci. Adv.

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The stemness of bone marrow mesenchymal stem cells (BMSCs) is maintained by hypoxia. The oxygen level increases from vessel-free cartilage to hypoxic bone marrow and, furthermore, to vascularized bone, which might direct the chondrogenesis to osteogenesis and regenerate the skeletal system. Hence, oxygen was diffused from relatively low to high levels throughout a three-dimensional chip. When we cultured BMSCs in the chip and implanted them into the rabbit defect models of low-oxygen cartilage and high-oxygen calvaria bone, (i) the low oxygen level (base) promoted stemness and chondrogenesis of BMSCs with robust antioxidative potential; (ii) the middle level (two times ≥ low) pushed BMSCs to quiescence; and (iii) the high level (four times ≥ low) promoted osteogenesis by disturbing the redox balance and stemness. Last, endochondral or intramembranous osteogenesis upon transition from low to high oxygen in vivo suggests a developmental mechanism–driven solution to promote chondrogenesis to osteogenesis in the skeletal system by regulating the oxygen environment.

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Hippocampal neural stem cells rapidly change their metabolic profile during neuronal differentiation   in cell culture

Cited by 2 publications

References 27 publications

Disease-modifying effects of metabolic perturbations in ALS/FTLD

Disease-modifying effects of metabolic perturbations in ALS/FTLD

O ₂ variant chip to simulate site-specific skeletogenesis from hypoxic bone marrow

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Hippocampal neural stem cells rapidly change their metabolic profile during neuronal differentiation &nbsp; in cell culture &nbsp;

Cited by 2 publications

References 27 publications

Disease-modifying effects of metabolic perturbations in ALS/FTLD

Disease-modifying effects of metabolic perturbations in ALS/FTLD

O 2 variant chip to simulate site-specific skeletogenesis from hypoxic bone marrow

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Hippocampal neural stem cells rapidly change their metabolic profile during neuronal differentiation in cell culture

O ₂ variant chip to simulate site-specific skeletogenesis from hypoxic bone marrow