Severe hypoxia and malnutrition collectively contribute to scar fibroblast inhibition and cell apoptosis

Lynam, Emily; Xie, Yun; Dawson, Rebecca; McGovern, Jacqui A.; Upton, Zee; Wang, Xiqiao

doi:10.1111/wrr.12343

Cited by 17 publications

(10 citation statements)

References 31 publications

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“…Importantly, malnutrition has been frequently associated with increased apoptosis and immune system activation both clinically and in animal models. 51,52 Moreover, poor nutritional status is known to accelerate CD/dementia in aging human populations, 53 and altered apoptosis could represent one of the mechanisms of action contributing to CD/dementia risk. Indeed, in our sample, we find a significant indirect effect of reduced prealbumin levels on future CD mediated by increased cell death during differentiation, emphasizing that the observed association between apoptosis and CD is influenced by the negative effect of poor overall nutrition.…”

Section: Discussionmentioning

confidence: 99%

The serum metabolome mediates the concert of diet, exercise, and neurogenesis, determining the risk for cognitive decline and dementia

Preez

Lefèvre‐Arbogast

Houghton

et al. 2021

Alzheimer's & Dementia

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Introduction: Diet and exercise influence the risk of cognitive decline (CD) and dementia through the food metabolome and exercise-triggered endogenous factors, which use the blood as a vehicle to communicate with the brain. These factors might act in concert with hippocampal neurogenesis (HN) to shape CD and dementia.Methods: Using an in vitro neurogenesis assay, we examined the effects of serum samples from a longitudinal cohort (n = 418) on proxy HN readouts and their association with future CD and dementia across a 12-year period.Results: Altered apoptosis and reduced hippocampal progenitor cell integrity were associated with exercise and diet and predicted subsequent CD and dementia. The effects of exercise and diet on CD specifically were mediated by apoptosis.Discussion: Diet and exercise might influence neurogenesis long before the onset of CD and dementia. Alterations in HN could signify the start of the pathological process and potentially represent biomarkers for CD and dementia.

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Section: Discussionmentioning

confidence: 99%

The serum metabolome mediates the concert of diet, exercise, and neurogenesis, determining the risk for cognitive decline and dementia

Preez

Lefèvre‐Arbogast

Houghton

et al. 2021

Alzheimer's & Dementia

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“…Figure 3D illustrated the increase in HDF viability under hypoxic conditions after treatment with CM collected from P6 hMSCs and AuFe NP-treated P12 hMSCs. Previous research showed that fibroblasts play important roles in the wound healing process [41,42,43]. Through mimicking the hypoxic condition of the skin wound environment in vitro before the in vivo test, the result showing the viability and proliferation of fibroblasts could provide the possibility of improved therapeutic effect induced by CMs.…”

Section: Discussionmentioning

confidence: 99%

Enhancing the Wound Healing Effect of Conditioned Medium Collected from Mesenchymal Stem Cells with High Passage Number Using Bioreducible Nanoparticles

Kim

et al. 2019

IJMS

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Injecting human mesenchymal stem cells (hMSCs) at wound sites is known to have a therapeutic effect; however, hMSCs have several limitations, such as low viability and poor engraftment after injection, as well as a potential risk of oncogenesis. The use of a conditioned medium (CM) was suggested as an alternative method for treating various wounds instead of direct hMSC administration. In addition to not having the adverse effects associated with hMSCs, a CM can be easily mass produced and can be stored for long-term, thereby making it useful for clinical applications. In general, a CM is collected from hMSCs with low passage number; whereas, the hMSCs with high passage number are usually discarded because of their low therapeutic efficacy as a result of reduced angiogenic factor secretion. Herein, we used a CM collected from high passage number (passage 12, P12) hMSCs treated with gold-iron nanoparticles (AuFe NPs). Our AuFe NPs were designed to release the iron ion intracellularly via endocytosis. Endosomes with low pH can dissolve iron from AuFe NPs, and thus, the intracellularly released iron ions up-regulate the hypoxia-inducible factor 1α and vascular endothelial growth factor (VEGF) expression. Through this mechanism, AuFe NPs improve the amount of VEGF expression from P12 hMSCs so that it is comparable to the amount of VEGF expression from low passage number (passage 6, P6), without treatment. Furthermore, we injected the CM retrieved from P12 MSCs treated with AuFe NPs in the mouse skin wound model (AuFe P12 group). AuFe P12 group revealed significantly enhanced angiogenesis in the mouse skin wound model compared to the high passage hMSC CM-injected group. Moreover, the result from the AuFe P12 group was similar to that of the low passage hMSC CM-injected group. Both the AuFe P12 group and low passage hMSC CM-injected group presented significantly enhanced re-epithelization, angiogenesis, and tissue remodeling compared to the high passage hMSC CM-injected group. This study reveals a new strategy for tissue regeneration based on CM injection without considering the high cell passage count.

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“…To date, more and more studies have been performed, and the mechanism of damage in hypoxic cardiomyocytes has been analyzed, but the results are not systematic and all-sided [20, 21]. Hypoxia is a major risk factor for apoptosis [22–24]. Maintaining the production of ATP and modulating apoptosis are two major functions of mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor receptor-associated protein 1 regulates hypoxia-induced apoptosis through a mitochondria-dependent pathway mediated by cytochrome c oxidase subunit II

Fei

et al. 2019

Burns &Amp; Trauma

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Background Tumor necrosis factor receptor-associated protein 1 (TRAP1) plays a protective effect in hypoxic cardiomyocytes, but the precise mechanisms are not well clarified. The study is aimed to identify the mechanism of TRAP1 on hypoxic damage in cardiomyocytes. Methods In this study, the effects of TRAP1 and cytochrome c oxidase subunit II (COXII) on apoptosis in hypoxia-induced cardiomyocytes were explored using overexpression and knockdown methods separately. Results Hypoxia induced cardiomyocyte apoptosis, and TRAP1 overexpression notably inhibited apoptosis induced by hypoxia. Conversely, TRAP1 silencing promoted apoptosis in hypoxic cardiomyocytes. Further investigation revealed that the proapoptotic effects caused by the silencing of TRAP1 were prevented by COXII overexpression, whereas COXII knockdown reduced the antiapoptotic function induced by TRAP1 overexpression. Additionally, changes in the release of cytochrome c from mitochondria into the cytosol and the caspase-3 activity in the cytoplasm, as well as reactive oxygen species production, were found to be correlated with the changes in apoptosis. Conclusions The current study uncovered that TRAP1 regulates hypoxia-induced cardiomyocyte apoptosis through a mitochondria-dependent apoptotic pathway mediated by COXII, in which reactive oxygen species presents as an important component.

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Severe hypoxia and malnutrition collectively contribute to scar fibroblast inhibition and cell apoptosis

Cited by 17 publications

References 31 publications

The serum metabolome mediates the concert of diet, exercise, and neurogenesis, determining the risk for cognitive decline and dementia

The serum metabolome mediates the concert of diet, exercise, and neurogenesis, determining the risk for cognitive decline and dementia

Enhancing the Wound Healing Effect of Conditioned Medium Collected from Mesenchymal Stem Cells with High Passage Number Using Bioreducible Nanoparticles

Tumor necrosis factor receptor-associated protein 1 regulates hypoxia-induced apoptosis through a mitochondria-dependent pathway mediated by cytochrome c oxidase subunit II

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