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Palacka 2021 Int J Mol Sci

From Bioblast
Publications in the MiPMap
Palacka P, Gvozdjáková A, Rausová Z, Kucharská J, Slopovský J, Obertová J, Furka D, Furka S, Singh KK, Sumbalová Z (2021) Platelet mitochondrial bioenergetics reprogramming in patients with urothelial carcinoma.

» Int J Mol Sci 23:388. PMID: 35008814 Open Access

Palacka Patrik, Gvozdjakova Anna,  Rausova Zuzana,  Kucharska Jarmila,  Slopovsky Jan,  Obertova Jana,  Furka Daniel,  Furka Samuel,  Singh Keshav K, Sumbalova Zuzana (2021) Int J Mol Sci

Abstract: Mitochondrial bioenergetics reprogramming is an essential response of cells to stress. Platelets, an accessible source of mitochondria, have a crucial role in cancer development; however, the platelet mitochondrial function has not been studied in urothelial carcinoma (UC) patients. A total of 15 patients with UC and 15 healthy controls were included in the study. Parameters of platelet mitochondrial respiration were evaluated using the high-resolution respirometry method, and the selected antioxidant levels were determined by HPLC. In addition, oxidative stress was evaluated by the thiobarbituric acid reactive substances (TBARS) concentration in plasma. We demonstrated deficient platelet mitochondrial respiratory chain functions, oxidative phosphorylation (OXPHOS), and electron transfer (ET) capacity with complex I (CI)-linked substrates, and reduced the endogenous platelet coenzyme Q10 (CoQ10) concentration in UC patients. The activity of citrate synthase was decreased in UC patients vs. controls (p = 0.0191). γ-tocopherol, α-tocopherol in platelets, and β-carotene in plasma were significantly lower in UC patients (p = 0.0019; p = 0.02; p = 0.0387, respectively), whereas the plasma concentration of TBARS was increased (p = 0.0022) vs. controls. The changes in platelet mitochondrial bioenergetics are consistent with cell metabolism reprogramming in UC patients. We suppose that increased oxidative stress, decreased OXPHOS, and a reduced platelet endogenous CoQ10 level can contribute to the reprogramming of platelet mitochondrial OXPHOS toward the activation of glycolysis. The impaired mitochondrial function can contribute to increased oxidative stress by triggering the reverse electron transport from the CoQ10 cycle (Q-junction) to CI. Keywords: Mitochondrial bioenergetics, Oxidative stress, Platelets, Reprogramming, Urothelial carcinoma Bioblast editor: Plangger M O2k-Network Lab: SK Bratislava Sumbalova Z

Selected quotations

  • In line with current knowledge, platelets in the blood circulation activate and encase the malignant cells detached from the primary tumor due to the secretion of growth factors and chemokines, such as vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), or transforming growth factor β (TGF-β). Platelet-derived growth factors also instigate tumor cell proliferation and angiogenesis to establish metastatic foci [6].
  • The O2 flow after Gp addition is 20–30% lower than the respiratory capacity, as additional uncoupler titration is necessary to reach the maximum O2 flow at this state.

Labels: MiParea: Respiration, Patients  Pathology: Cancer 

Organism: Human  Tissue;cell: Platelet  Preparation: Permeabilized cells, Intact cells 

Coupling state: LEAK, ROUTINE, OXPHOS, ET  Pathway: F, N, S, Gp, NS, ROX  HRR: Oxygraph-2k