Effects of quinoa protein Pickering emulsion on the properties, structure and intermolecular interactions of myofibrillar protein gel

Glioblastoma (GBM) is the most fatal primary brain cancer in adults. Despite extensive treatment, tumors inevitably recur, leading to an average survival time shorter than 1.5 years. The 18 kDa translocator protein (TSPO) is abundantly expressed throughout the body including the central nervous system. The expression of TSPO increases in states of inflammation and brain injury due to microglia activation. Not least due to its location in the outer mitochondrial membrane, TSPO has been implicated with a broad spectrum of functions. These include the regulation of proliferation, apoptosis, migration, as well as mitochondrial functions such as mitochondrial respiration and oxidative stress regulation. TSPO is frequently overexpressed in GBM. Its expression level has been positively correlated to WHO grade, glioma cell proliferation, and poor prognosis of patients. Several lines of evidence indicate that TSPO plays a functional part in glioma hallmark features such as resistance to apoptosis, invasiveness, and proliferation. This review provides a critical overview of how TSPO could regulate several aspects of tumorigenesis in GBM, particularly in the context of the hallmarks of cancer proposed by Hanahan and Weinberg in 2011.

The Role of Translocator Protein TSPO in Hallmarks of Glioblastoma.

The impact of high pressure homogenisation (HPH) on physico-chemical, microstructural, and rheological properties of quinoa protein isolate (QPI) suspensions were studied. Individual protein bands kept unchanged with HPH treatment up to 50 MPa, as revealed by SDS-PAGE. After HPH treatment at 50 MPa, large protein aggregates were disrupted, and particle size was substantially reduced from ~8.2–0.5 µm. Concurrently, water solubility, emulsifying, and foaming capability were significantly enhanced. QPI molecules after HPH treatment became more flexible with increased surface hydrophobicity and absorbed at the air-water and oil-water interfaces faster, resulting in a more rapid decrease of surface tension and interfacial tension. The secondary structure of QPI proteins was not significantly altered after HPH treatment as probed by FTIR. All QPI suspensions formed weak gels after thermal treatment (85 °C, 30 min), and HPH treated QPI suspensions resulted in a stronger gel strength with a more compact and homogeneous protein network microstructure. These results show that HPH treatment could be an excellent processing technique to modify the physico-chemical, techno-functional, and microstructural properties of QPI suspensions. 

Impact of high-pressure homogenization on physico-chemical, structural, and rheological properties of quinoa protein isolates

Radiation-induced brain injury (RIBI) after radiotherapy has become an increasingly important factor affecting the prognosis of patients with head and neck tumor. With the delivery of high doses of radiation to brain tissue, microglia rapidly transit to a pro-inflammatory phenotype, upregulate phagocytic machinery, and reduce the release of neurotrophic factors. Persistently activated microglia mediate the progression of chronic neuroinflammation, which may inhibit brain neurogenesis leading to the occurrence of neurocognitive disorders at the advanced stage of RIBI. Fully understanding the microglial pathophysiology and cellular and molecular mechanisms after irradiation may facilitate the development of novel therapy by targeting microglia to prevent RIBI and subsequent neurological and neuropsychiatric disorders.

/pdf/microglia-as-therapeutic-target-for-radiation-induced-brain-1l21c6f2.pdf

Microglia as Therapeutic Target for Radiation-Induced Brain Injury

Microglia, the innate immune cells of the central nervous system, play a pivotal role in the modulation of neuroinflammation. Neuroinflammation has been implicated in many diseases of the CNS, including Alzheimer’s disease and Parkinson’s disease. It is well documented that microglial activation, initiated by a variety of stressors, can trigger a potentially destructive neuroinflammatory response via the release of pro-inflammatory molecules, and reactive oxygen and nitrogen species. However, the potential anti-inflammatory and neuroprotective effects that microglia are also thought to exhibit have been under-investigated. The application of ionising radiation at different doses and dose schedules may reveal novel methods for the control of microglial response to stressors, potentially highlighting avenues for treatment of neuroinflammation associated CNS disorders, such as Alzheimer’s disease and Parkinson’s disease. There remains a need to characterise the response of microglia to radiation, particularly low dose ionising radiation.

Control of Neuroinflammation through Radiation-Induced Microglial Changes

Effect of NaCl and CaCl2 concentration on the rheological and structural characteristics of thermally-induced quinoa protein gels

The brain’s early response to low dose ionising radiation, as may be encountered during diagnostic procedures and space exploration, is not yet fully characterised. In the brain parenchyma, the mitochondrial translocator protein (TSPO) is constitutively expressed at low levels by endothelial cells, and can therefore be used to assess the integrity of the brain’s vasculature. At the same time, the inducible expression of TSPO in activated microglia, the brain’s in-trinsic immune cells, is a regularly observed early indicator of subtle or incipient brain pathology. Here, we explored the use of TSPO as a biomarker of brain tissue injury following whole body irradiation. Post-radiation responses were measured in C57BL/6 wild type (Tspo+/+) and TSPO knockout (Tspo-/-) mice 48 h after single whole body gamma irra-diations with low doses 0 Gy, 0.01 Gy and 0.1 Gy and a high dose of 2 Gy. Additionally, post-radiation responses of primary microglial cell cultures were measured at 1, 4, 24 and 48 h at an irradiation dose range of 0 Gy-2 Gy. TSPO mRNA and protein expression in the brain showed a decreased trend after 0.01 Gy relative to sham-irradiated con-trols, but remained unchanged after higher doses. Immunohistochemistry confirmed subtle decreases in TSPO ex-pression after 0.01 Gy in vascular endothelial cells of the hippocampal region and in ependymal cells, with no de-tectable changes following higher doses. Cytokine concentrations in plasma after whole body irradiation showed differential changes in IL-6 and IL-10 with some variations between Tspo-/- and Tspo+/+ animals. The in vitro meas-urements of TSPO in primary microglial cell cultures showed a significant reduction 1 hour after low dose irradiation (0.01 Gy). In summary, acute low and high doses of gamma irradiation up to 2 Gy reduced TSPO expression in the brain’s vascular compartment without de novo induction of TSPO expression in parenchymal microglia, while TSPO expression in directly irradiated, isolated, and thus highly activated microglia, too, was reduced after low dose ir-radiation. The potential link between TSPO, its role in mitochondrial energy metabolism and the selective radiation sensitivity, notably of cells with constitutive TSPO expression such as vascular endothelial cells, merits further ex-ploration.

/pdf/mitochondrial-translocator-protein-tspo-expression-in-the-358ub17w7z.pdf

Mitochondrial Translocator Protein (TSPO) Expression in the Brain After Whole Body Gamma Irradiation.

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Effect of NaCl and CaCl2 concentration on the rheological and structural characteristics of thermally-induced quinoa protein gels

Mitochondrial Translocator Protein (TSPO) Expression in the Brain After Whole Body Gamma Irradiation.