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Your search keyword '"Weronika Baszanowska"' showing total 4 results
Start Over Author "Weronika Baszanowska" Publisher mdpi ag
4 results on '"Weronika Baszanowska"'

1. Recombinant Human Prolidase (rhPEPD) Induces Wound Healing in Experimental Model of Inflammation through Activation of EGFR Signalling in Fibroblasts

Author

Weronika Baszanowska, Magdalena Niziol, Ilona Oscilowska, Justyna Czyrko-Horczak, Wojciech Miltyk, and Jerzy Palka

Subjects
prolidase, epidermal growth factor receptor, fibroblasts, interleukin 1β, wound healing, β1-integrin, Organic chemistry, QD241-441
Abstract

The potential of recombinant human prolidase (rhPEPD) to induce wound healing in an experimental model of IL-1β-induced inflammation in human fibroblasts was studied. It was found that rhPEPD significantly increased cell proliferation and viability, as well as the expression of the epidermal growth factor receptor (EGFR) and downstream signaling proteins, such as phosphorylated PI3K, AKT, and mTOR, in the studied model. Moreover, rhPEPD upregulated the expression of the β1 integrin receptor and its downstream signaling proteins, such as p-FAK, Grb2 and p-ERK 1/2. The inhibition of EGFR signaling by gefitinib abolished rhPEPD-dependent functions in an experimental model of inflammation. Subsequent studies showed that rhPEPD augmented collagen biosynthesis in IL-1β-treated fibroblasts as well as in a wound healing model (wound closure/scratch test). Although IL-1β treatment of fibroblasts increased cell migration, rhPEPD significantly enhanced this process. This effect was accompanied by an increase in the activity of MMP-2 and MMP-9, suggesting extracellular matrix (ECM) remodeling during the inflammatory process. The data suggest that rhPEPD may play an important role in EGFR-dependent cell growth in an experimental model of inflammation in human fibroblasts, and this knowledge may be useful for further approaches to the treatment of abnormalities of wound healing and other skin diseases.

Published
2023
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2. Metformin Treatment or PRODH/POX-Knock out Similarly Induces Apoptosis by Reprograming of Amino Acid Metabolism, TCA, Urea Cycle and Pentose Phosphate Pathway in MCF-7 Breast Cancer Cells

Author

Thi Yen Ly Huynh, Ilona Oscilowska, Jorge Sáiz, Magdalena Nizioł, Weronika Baszanowska, Coral Barbas, and Jerzy Palka

Subjects
PRODH/POX, metformin, MCF-7crPOX cells, proline, glutamine, lactic acid, Microbiology, QR1-502
Abstract

It has been considered that proline dehydrogenase/proline oxidase (PRODH/POX) is involved in antineoplastic activity of metformin (MET). The aim of this study is identification of key metabolites of glycolysis, pentose phosphate pathway (PPP), tricarboxylic acids (TCA), urea cycles (UC) and some amino acids in MET-treated MCF-7 cells and PRODH/POX-knocked out MCF-7 (MCF-7crPOX) cells. MCF-7crPOX cells were generated by using CRISPR-Cas9. Targeted metabolomics was performed by LC-MS/MS/QqQ. Expression of pro-apoptotic proteins was evaluated by Western blot. In the absence of glutamine, MET treatment or PRODH/POX-knock out of MCF-7 cells contributed to similar inhibition of glycolysis (drastic increase in intracellular glucose and pyruvate) and increase in the utilization of phospho-enol-pyruvic acid, glucose-6-phosphate and some metabolites of TCA and UC, contributing to apoptosis. However, in the presence of glutamine, MET treatment or PRODH/POX-knock out of MCF-7 cells contributed to utilization of some studied metabolites (except glucose), facilitating pro-survival phenotype of MCF-7 cells in these conditions. It suggests that MET treatment or PRODH/POX-knock out induce similar metabolic effects (glucose starvation) and glycolysis is tightly linked to glutamine metabolism in MCF-7 breast cancer cells. The data provide insight into mechanism of anticancer activity of MET as an approach to further studies on experimental breast cancer therapy.

Published
2021
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3. Troglitazone-Induced PRODH/POX-Dependent Apoptosis Occurs in the Absence of Estradiol or ERβ in ER-Negative Breast Cancer Cells

Author

Jerzy Pałka, Sylwia Lewoniewska, Izabela Prokop, Weronika Baszanowska, Katarzyna Bielawska, Ilona Oscilowska, and Thi Yen Ly Huynh

Subjects
collagen, medicine.drug_class, viruses, Estrogen receptor, PRODH/POX, Article, 03 medical and health sciences, 0302 clinical medicine, Proline dehydrogenase, estrogen, Medicine, Proline, 030304 developmental biology, chemistry.chemical_classification, 0303 health sciences, Reactive oxygen species, Proline oxidase, business.industry, apoptosis, Troglitazone, virus diseases, General Medicine, Molecular biology, chemistry, Apoptosis, Estrogen, 030220 oncology & carcinogenesis, business, breast cancer cells, medicine.drug
Abstract

Simple Summary PRODH/POX (proline dehydrogenase/proline oxidase) is a mitochondrial enzyme that catalyzes proline degradation generating reactive oxygen species (ROS). Estrogens limit proline availability for PRODH/POX by stimulating collagen biosynthesis. It has been considered that estrogens determine efficiency of troglitazone (TGZ)-induced PRODH/POX-dependent apoptosis in breast cancer cells. The studies were performed in wild-type and PRODH/POX-silenced estrogen-dependent MCF-7 cells and estrogen-independent MDA-MB-231 cells. DNA and collagen biosynthesis were determined by radiometric method, ROS production was measured by fluorescence assay, protein expression was determined by Western blot and proline concentration by LC/MS analysis. We found that: i/TGZ-induced apoptosis in MDA-MB-231 occurs only in the absence of estradiol or ERβ, ii/the process is mediated by PRODH/POX, iii/and is facilitated by proline availability for PRODH/POX by TGZ-dependent inhibition of collagen biosynthesis (proline utilizing process). The data suggest that combined TGZ and anti-estrogen treatment could be considered in experimental therapy of ER negative breast cancers. Abstract The impact of estradiol on troglitazone (TGZ)-induced proline dehydrogenase/proline oxidase (PRODH/POX)-dependent apoptosis was studied in wild-type and PRODH/POX-silenced estrogen receptor (ER) dependent MCF-7 cells and ER-independent MDA-MB-231 cells. DNA and collagen biosynthesis were determined by radiometric method, prolidase activity evaluated by colorimetric method, ROS production was measured by fluorescence assay. Protein expression was determined by Western blot and proline concentration by LC/MS analysis. PRODH/POX degrades proline yielding reactive oxygen species (ROS). Estrogens stimulate collagen biosynthesis utilizing free proline and limiting its availability for PRODH/POX-dependent apoptosis. TGZ cytotoxicity was highly pronounced in wild-type MDA-MB-231 cells cultured in medium without estradiol or in the cells cultured in medium with estradiol but deprived of ERβ (by ICI-dependent degradation), while in PRODH/POX-silenced cells the process was not affected. The TGZ cytotoxicity was accompanied by increase in PRODH/POX expression, ROS production, expression of cleaved caspase-3, caspase-9 and PARP, inhibition of collagen biosynthesis, prolidase activity and decrease in intracellular proline concentration. The phenomena were not observed in PRODH/POX-silenced cells. The data suggest that TGZ-induced apoptosis in MDA-MB-231 cells cultured in medium without estradiol or deprived of ERβ is mediated by PRODH/POX and the process is facilitated by proline availability for PRODH/POX by TGZ-dependent inhibition of collagen biosynthesis. It suggests that combined TGZ and antiestrogen treatment could be considered in experimental therapy of estrogen receptor negative breast cancers.

Published
2021

4. Prolidase Stimulates Proliferation and Migration Through Activation of the PI3K/Akt/mTOR Signaling Pathway in Human Keratinocytes

Author

Jerzy Pałka, Magdalena Misiura, Ilona Ościłowska, Weronika Baszanowska, and Wojciech Miltyk

Subjects
0301 basic medicine, Dipeptidases, medicine.medical_treatment, PEPD, wound healing, Ligands, Receptor, IGF Type 1, lcsh:Chemistry, Phosphatidylinositol 3-Kinases, 0302 clinical medicine, Cell Movement, Epidermal growth factor receptor, lcsh:QH301-705.5, Spectroscopy, biology, Chemistry, Integrin beta1, TOR Serine-Threonine Kinases, General Medicine, Computer Science Applications, Cell biology, prolidase, ErbB Receptors, 030220 oncology & carcinogenesis, Signal transduction, Protein Binding, Signal Transduction, keratinocytes, EGFR, Models, Biological, Article, Catalysis, Inorganic Chemistry, 03 medical and health sciences, Cell Line, Tumor, medicine, Humans, Physical and Theoretical Chemistry, Molecular Biology, Protein kinase B, PI3K/AKT/mTOR pathway, Cell Proliferation, Cell growth, Growth factor, Organic Chemistry, 030104 developmental biology, lcsh:Biology (General), lcsh:QD1-999, biology.protein, Proto-Oncogene Proteins c-akt, Transforming growth factor
Abstract

Recent reports have indicated prolidase (PEPD) as a ligand of the epidermal growth factor receptor (EGFR). Since this receptor is involved in the promotion of cell proliferation, growth, and migration, we aimed to investigate whether prolidase may participate in wound healing in vitro. All experiments were performed in prolidase-treated human keratinocytes assessing cell vitality, proliferation, and migration. The expression of downstream signaling proteins induced by EGFR, insulin-like growth factor 1 (IGF-1), transforming growth factor &beta, 1 (TGF-&beta, 1), and &beta, 1-integrin receptors were evaluated by Western immunoblotting and immunocytochemical staining. To determine collagen biosynthesis and prolidase activity radiometric and colorimetric methods were used, respectively. Proline content was determined by applying the liquid chromatography coupled with mass spectrometry. We found that prolidase promoted the proliferation and migration of keratinocytes through stimulation of EGFR-downstream signaling pathways in which the PI3K/Akt/mTOR axis was involved. Moreover, PEPD upregulated the expression of &beta, 1-integrin and IGF-1 receptors and their downstream proteins. Proline concentration and collagen biosynthesis were increased in HaCaT cells under prolidase treatment. Since extracellular prolidase as a ligand of EGFR induced cell growth, migration, and collagen biosynthesis in keratinocytes, it may represent a potential therapeutic approach for the treatment of skin wounds.

Published
2020

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