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Yildiz, A. B.

Publications and source records attributed to Yildiz, A. B..

2 recordsLinked to original sources

The Arabidopsis Class I formin AtFH5 contributes to seedling resistance to salt stress.

The family of formins, evolutionarily conserved multidomain proteins engaged in the control of actin and microtubule cytoskeleton organization, exhibits considerable diversity in plants. Angiosperms have two formin clades consisting of multiple paralogs, Class I and Class II, the former being often transmembrane proteins located at the plasmalemma or endomembranes. According to available transcriptome data, the Arabidopsis thaliana Class I transmembrane formin AtFH5 (At5g54650) exhibits a distinct pattern of transcript abundance in various seedling root tissues with massive increase of transcript level upon salinity stress. To examine a possible role of AtFH5 in NaCl stress response, we generated transgenic plants expressing green fluorescent protein (GFP)-tagged AtFH5 under its native promoter and characterized its tissue and intracellular localization under standard culture conditions and under NaCl stress. While we confirmed the induction of AtFH5 expression by salt treatment, the distribution of tagged protein, with maxima in the border-like cells of the root cap, in the phloem and at lateral root emergence sites, did not reflect previously reported transcript abundance, suggesting posttranscriptional regulation of gene expression. Subcellular localization studies employing also membrane trafficking inhibitors suggested that AtFH5 protein level may be modulated by endocytosis and autophagy. Notably, loss-of-function atfh5 mutants exhibited increased sensitivity to NaCl stress, indicating that AtFH5 contributes to the development of seedling salt tolerance. These findings highlight the functional importance of AtFH5 in abiotic stress responses.

plant biology↗

Impact of Butyrate on Small and Large Airways: Effects on Cell Viability, Inflammatory Changes and Permeability

Chronic airway diseases, such as Chronic Obstructive Pulmonary Disease (COPD) and asthma pose a significant global health burden. The pathophysiology involves chronic inflammation, with oxidative stress playing a crucial role in disease severity. Current treatments, especially for COPD, have limitations, necessitating exploration of alternative therapeutic approaches. In this study, we investigated the potential effects of butyrate, a short-chain fatty acid, on airway epithelial cells. Human bronchial epithelial cells (BEAS-2B) and bronchiolar epithelial carcinoma cells (A549) were cultured and exposed to hydrogen peroxide (H2O2) to induce oxidative stress. Butyrate was then applied at various concentrations, and the impact on cell viability, epithelial permeability, inflammatory cytokines, and gene expression was assessed. Our cell viability experiments revealed a dose-dependent reduction in viability with H2O2, while butyrate was found to be safe as it did not affect cell viability. Additionally, butyrate showed decrease in small airway permeability. Butyrate demonstrated anti- inflammatory properties, suppressing H2O2-induced release of interleukin (IL)-6, IL-8, and granulocyte macrophage colony-stimulating factor (GM-CSF) in large airways. Gene expression analysis further highlighted complex regulatory effects of butyrate on inflammatory pathways. Our study suggests that butyrate may have potential therapeutic benefits in chronic airway diseases by modulating inflammation, permeability, and gene expression. However, further research, including in vivo studies and exploration of endogenous butyrate utilization, is needed to fully understand its pharmacodynamics and clinical relevance. Our findings contribute to the understanding of short-chain fatty acids as potential candidates for respiratory disease treatment.

cell biology↗