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Aldo-keto reductase family 1 member A (AKR1A) is an NADPH-dependent aldehyde reductase widely expressed in mammalian tissues. In this study induced differentiation of MC3T3-E1 preosteoblasts was found to increase AKR1A gene expression concomitantly increased N[O.sub.x]- (nitrite + nitrate), increased glucose uptake, increased [NAD[(P).sup.+]]/[NAD(P)H] and lactate production but decreased reactive oxygen species (ROS) without changes in endothelial nitric oxide synthase (eNOS) expression in differentiated osteoblasts (OBs). A study using gain- and loss-of-function MC3T3-E1 cells indicated that AKR1A is essential for modulating OB differentiation and gene expression of collagen 1 A1, receptor activator of nuclear factor kappa-B ligand, and osteoprotegerin in OBs. Immunofluorescence microscopy also revealed that changes in AKR1A expression altered extracellular collagen formation in differentiated OBs. Consistently analyses of alkaline phosphatase activity and calcium deposits of matrix mineralization by Alizarin Red S staining verified that AKR1A is involved in the regulation of OB differentiation and bone matrix formation. In addition, AKR1A gene alterations affected the levels of N[O.sub.x]-, eNOS expression, glucose uptake, [NAD[(P).sup.+]]/[NAD(P)H] dinucleotide redox couples, lactate production, and ROS in differentiated OBs. Herein, we report that AKR1A-mediated denitrosylation may play a role in the regulation of lactate metabolism as well as redox homeostasis in cells, providing an efficient way to quickly gain energy and to significantly reduce oxidative stress for OB differentiation. Key words: aldo-keto reductase family 1 member A (AKR1A), osteoblastogenesis, NADPH-dependent aldehyde reductase, alkaline phosphatase activity, Alizarin Red S staining L'aldéhyde réductase AKR1A (Aldo-keto reductase family 1 member A) est une aldéhyde réductase NADPH-dépendante largement exprimée dans les tissus des mammifères. Dans cette étude, les auteurs ont constaté que l'induction de la différenciation des préostéoblastes MC3T3-E1 accroissait l'expression du gène AKR1A, augmentait de façon concomitante les N[O.sub.x] - (nitrite + nitrate), augmentait l'absorption du glucose, augmentait la production de [NAD[(P).sup.+]]/[NAD(P)H] et de lactate, mais diminuait les dérivés réactifs de l'oxygène (DRO) sans modifier l'expression de l'eNOS (oxyde nitrique synthase endothéliale) dans les ostéoblastes différenciés. Une étude utilisant des cellules MC3T3-E1 avec gain ou perte de fonction indiquait que AKR1A est essentiel pour moduler la différenciation des OB et l'expression génique du collagène 1 Al, du récepteur de l'activateur du ligand du facteur nucléaire kappa (RANKL) et de l'ostéoprotégérine dans les OB. La microscopie par immunofluorescence a également révélé que les changements dans l'expression d'AKRIA modifiaient la formation de collagène extracellulaire dans les OB différenciés. De même, les analyses de l'activité de la phosphatase alcaline et des dépôts de calcium de la matrice minéralisée par coloration au rouge d'alizarine S confirmaient que AKR1A est impliqué dans la régulation de la différenciation des OB et de la formation de la matrice osseuse. En outre, les altérations du gène AKR1A affectaient les niveaux de N[O.sub.x]-, l'expression d'eNOS, l'absorption du glucose, les couples de dinucléotides redox [NAD[(P).sup.+]]/[NAD(P)H], la production de lactate et les DRO dans les OB différenciés. Les auteurs rapportent ici que la dénitrosylation médiée par AKR1A peut jouer un rôle dans la régulation du métabolisme du lactate ainsi que dans l'homéostasie redox dans les cellules, offrant ainsi un moyen efficace de gagner rapidement de l'énergie et de réduire significativement le stress oxydant pour la différenciation des OB. [Traduit par la Rédaction] Mots-clés : AKR1A, ostéoblastogenèse, aldéhyde réductase NADPH-dépendante, activité phosphatase alcaline, coloration rouge alizarine S, Introduction Aldo-keto reductase family 1 member A (AKR1A) is known to play roles in catalyzing intermediary metabolism, maintaining cellular redox homeostasis, and detoxifying toxic aldehydes (e.g., acrolein) due to its [...]

Significant research has been conducted in the field of high-strength RC. This body of work encompasses a wide range of topics from material behavior to seismic performance, which has been instrumental in shaping design codes for high-strength RC structures. However, a notable gap remains in understanding the postfire seismic behavior of high-strength RC members. This study addressed this gap by conducting experimental tests to explore the seismic behavior of high-strength RC columns after fire exposure. The experimental program subjected column specimens to both fire exposure and cyclic loading tests, with key variables including varying concrete strengths and a standard 2-h fire exposure. This study extensively analyzed the impact of fire exposure on seismic performance, focusing on temperature gradients, damage patterns, load-displacement hysteresis responses, displacement composition, and plastic region length. The results indicated that fire exposure caused more significant structural degradation in high-strength concrete (HSC) columns compared with normal-strength concrete (NSC) columns. Specifically, fire exposure moderately reduced the peak strength of NSC and HSC columns by 8% and 12%, respectively, and significantly decreased their initial stiffness by 48% and 55%, respectively. Despite considerable spalling in the cover concrete of the HSC column, the core concrete and longitudinal reinforcement remained largely intact, effectively sustaining the postpeak behavior under cyclic loading. Complementing the experimental work, the study also proposed suitable computational models to simulate the postfire seismic responses of NSC and HSC columns. These models aim to enhance the predictive understanding of structural behavior in postfire scenarios, contributing valuable insights for the design and assessment of fire-affected RC structures. [ABSTRACT FROM AUTHOR]