Repozytorium
Danych Badawczych
Uniwersytetu Rzeszowskiego

 

Recent Submissions

Item
Body composition, lifestyle and nutrients on adiponectin and resistin levels and AR index in obese individuals
(2024) Polak-Szczybyło, Ewelina; Tabarkiewicz, Jacek
Background: Low-grade inflammation resulting from processes occurring in the adipose tissue of obese people is a factor in the occurrence of numerous diseases. Current research focuses on ways to regulate immunological mechanisms in adipose tissue in order to minimize the consequences for the health. Methods: Body composition analysis using BIA was performed among 84 adults with obesity (BMI ≥ 30 kg/m2). Serum was collected to analyze the concentration of adiponectin (ApN) and resistin. The subjects additionally completed a food frequency questionnaire FFQ-6 and a three-days food diary. Adiponectin-resistin index (AR index) was calculated. Results: Re-sistin showed a positive correlation with BMI and subcutaneous adipose tissue content. AR index value was also positively associated with the amount of adipose tissue and body mass. Adi-ponectin level in the blood of the studied individuals decreased with the content of lean tissue. Adiponectin level also decreased with the amount of carbohydrates, e.g. starch, and glycemic load of the diet. Resistin decreased in patients who frequently consumed white pasta and red meat, while AR index was positively associated with the amount of white rice and SFA and MUFA fatty acids consumed and negatively with the frequent consumption of carbohydrates, including starch. Physical activity was negatively correlated with adiponectin levels and AR index. Con-clusion: Body composition significantly affected the AR index and concentration of resistin and adiponectin in the blood of the subjects. Dietary factors also had a significant effect.
Item
Dataset used in research paper entitled "Plasma Circular-RNA 0005567 as a Potential Marker of Disease Activity in Rheumatoid Arthritis"
(MDPI, 2023-12-28) Cieśla, Marek
Circular RNAs (circRNAs) are noncoding molecules and are generated through back splicing. The 3′ and 5′ ends of the RNAs are covalently linked and form a loop structure, making it resistant to RNA exonucleases. Thus, circRNAs are biologically stable and may be considered as potential molecular markers of various diseases in tissues and biofluids. CircRNAs may regulate gene expression levels by acting as a microRNA sponge or by interacting with RNA binding proteins. The aim of the study was to find an association between plasma concentration of selected circRNAs and disease activity in patients with RA.
Item
Upregulation of GRP78 is accompanied by decreased antioxidant response and mitophagy promotion in streptozotocin-induced type 1 diabetes in rats - original data
(Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2024-09-25) Kaniuka, Olena; Deręgowska, Anna; Bandura, Yurii; Sabadashka, Mariya; Chala, Dariya; Kulachkovskyi, Olexandr; Kubis, Hubert; Adamczyk-Grochala, Jagoda; Sybirna, Nataliia
Endoplasmic reticulum stress, oxidative stress, and mitochondrial dysfunction are interconnected processes involved in the pathogenesis of diabetes mellitus (DM). In the present study, we demonstrate a distinct unfolded protein response (UPR) signaling pathways in two mammalian models of DM: β-TC-6 cell line and streptozotocin induced type 1 diabetes model in rats. However, a feature common to both systems was the upregulation of the GRP78 protein. Moreover, in vivo studies showed the disruption of the antioxidant system and an escalation of mitophagy against the background of a depletion of the level of ATP in pancreatic cells. In conclusion, we suggest that glucotoxic conditions induced GRP78 upregulation, and next cause depletion of the antioxidant pool and disruption of the functioning of antioxidant defense enzymes and in consequence promote mitophagy in pancreatic cells. Therefore, GRP78 may be considered as a potential therapeutic factor in patients with diabetes.
Item
Glucotoxicity is mediated by cytoplasmic distribution of RAP1 in pancreatic β-cells
(Elsevier, 2024-03-28) Deręgowska, Anna; Tomaszek, Natalia; Cuch, Patrycja; Kozioł, Katarzyna; Kaniuka, Olga; Sabadashka, Mariya; Bandura, Yurii; Sybirna, Nataliia
Diabetes mellitus (DM) is a group of chronic metabolic disorders characterized by persistent hyperglycemia. In our study, we analyzed the level and location of RAP1 changes in the development of β-cell dysfunction induced by glucotoxicity. We employed three pancreatic β-cell lines, namely INS-1, 1.2B4, and NIT-1, as well as a streptozotocin-induced diabetes rat model. We demonstrate that after high glucose treatment, RAP1 is increased, probably through induction by AKT, allowing RAP1 to shuttle from the nucleus to the cytoplasm and activate NF-κB signaling. Furthermore, non-enzymatic post-translational modifications of RAP1, such as advanced glycation end products and carbonylation may affect the function of RAP1, such as activation of the NF-κB signaling. Taken together, we showed that RAP1 is a new player in the mechanism of glucotoxicity in pancreatic β-cells.
Item
Dataset used in research paper entitled “New Mitochondria-Targeted Fisetin Derivative Compromises Mitophagy and Limits Survival of Drug-Induced Senescent Breast Cancer Cells”
(Journal of Medicinal Chemistry (ACS), 2024-09-25) Rzeszutek, Iwona; Cybularczyk-Cecotka, Martyna; Deręgowska, Anna; Stec, Paulina; Wnuk, Maciej; Kołodziej, Olga; Kałafut, Joanna; Wawruszak, Anna; Witkowski, Wojciech; Litwinienko, Grzegorz; Lewińska, Anna
Mitochondria are considered as promising targets for cancer treatment. In the present study, triphenyl phosphonium cationic group-conjugated fisetin (mito-fisetin) was synthesized, and its anticancer activity was investigated in several cellular models of estrogen receptor (ER)-positive breast cancer in vitro and in vivo in proliferating and tamoxifen-promoted senescent states. Mito-fisetin, when used at low micromolar concentrations, stimulated the dissipation of mitochondrial membrane potential and oxidative stress, and affected mitochondrial function, resulting in apoptosis induction in senescent breast cancer cells. Mito-fisetin-mediated cytotoxicity was due to increased levels of phosphorylated AMPK, decreased levels of AKT and HSP90, and impaired mitophagic response, as judged by the analysis of the markers of mitophagosome formation. Senescent breast cancer cells were found to be more sensitive to mito-fisetin treatment than proliferating ones. We postulate that mitochondrial targeting in the case of fisetin may be considered as a promising anticancer and senotherapeutic strategy to eliminate drug-resistant senescent breast cancer cells.