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1.
PLoS One ; 17(1): e0262500, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35030225

RESUMEN

With their ability of CO2 fixation using sunlight as an energy source, algae and especially microalgae are moving into the focus for the production of proteins and other valuable compounds. However, the valorization of algal biomass depends on the effective disruption of the recalcitrant microalgal cell wall. Especially cell walls of Chlorella species proved to be very robust. The wall structures that are responsible for this robustness have been studied less so far. Here, we evaluate different common methods to break up the algal cell wall effectively and measure the success by protein and carbohydrate release. Subsequently, we investigate algal cell wall features playing a role in the wall's recalcitrance towards disruption. Using different mechanical and chemical technologies, alkali catalyzed hydrolysis of the Chlorella vulgaris cells proved to be especially effective in solubilizing up to 56 wt% protein and 14 wt% carbohydrates of the total biomass. The stepwise degradation of C. vulgaris cell walls using a series of chemicals with increasingly strong conditions revealed that each fraction released different ratios of proteins and carbohydrates. A detailed analysis of the monosaccharide composition of the cell wall extracted in each step identified possible factors for the robustness of the cell wall. In particular, the presence of chitin or chitin-like polymers was indicated by glucosamine found in strong alkali extracts. The presence of highly ordered starch or cellulose was indicated by glucose detected in strong acidic extracts. Our results might help to tailor more specific efforts to disrupt Chlorella cell walls and help to valorize microalgae biomass.


Asunto(s)
Pared Celular/química , Pared Celular/fisiología , Chlorella vulgaris/metabolismo , Biomasa , Carbohidratos/análisis , Pared Celular/patología , Celulosa/análisis , Chlorella vulgaris/patogenicidad , Microalgas/metabolismo , Almidón/análisis
2.
Mol Biol Rep ; 47(1): 369-379, 2020 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-31642042

RESUMEN

Human diploid fibroblasts (HDFs) cultured in vitro have limited capacity to proliferate after population doubling is repeated several times, and they enter into a state known as replicative senescence or cellular senescence. This study aimed to investigate the effect of Chlorella vulgaris on the replicative senescence of HDFs by determining the expression of senescence-associated genes. Young and senescent HDFs were divided into untreated control and C. vulgaris-treated groups. A senescence-associated gene transcription analysis was carried out with qRT-PCR. Treatment of young HDFs with C. vulgaris reduced the expression of SOD1, CAT and CCS (p < 0.05). In addition, the expression of the SOD2 gene was increased with C. vulgaris treatment in young, pre-senescent and senescent HDFs (p < 0.05). Treatment of senescent HDFs with C. vulgaris resulted in the downregulation of TP53 gene expression. The expression of the CDKN2A gene was significantly decreased upon C. vulgaris treatment in young and senescent HDFs. C. vulgaris treatment was also found to significantly upregulate the expression of the MAPK14 gene in pre-senescent HDFs. In addition, the expression of MAPK14 was significantly upregulated compared to that in the untreated senescent HDFs (p < 0.05). In summary, the expression of senescence-associated genes related to antioxidants and the insulin/insulin-like growth factor-1 signalling, DNA damage-associated signalling, cell differentiation and cell proliferation pathways was modulated by C. vulgaris during replicative senescence of human diploid fibroblasts.


Asunto(s)
Senescencia Celular/efectos de los fármacos , Senescencia Celular/genética , Chlorella vulgaris/metabolismo , Antioxidantes/metabolismo , Catalasa/genética , Catalasa/metabolismo , Diferenciación Celular/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Células Cultivadas , Senescencia Celular/fisiología , Chlorella vulgaris/patogenicidad , Daño del ADN/efectos de los fármacos , Diploidia , Fibroblastos/metabolismo , Expresión Génica/efectos de los fármacos , Genes p53/genética , Humanos , Masculino , Proteína Quinasa 14 Activada por Mitógenos/genética , Chaperonas Moleculares/genética , Chaperonas Moleculares/metabolismo , Cultivo Primario de Células , Transducción de Señal/efectos de los fármacos , Superóxido Dismutasa/metabolismo , Superóxido Dismutasa-1/genética , Superóxido Dismutasa-1/metabolismo
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