Muntean 2017 MiP2017: Difference between revisions
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In the past years, respirometric profiling of peripheral blood cells has emerged as a minimally invasive approach allowing the assessment of mitochondrial dysfunction in various pathological conditions associated with metabolic stress. The present pilot study was purported to characterize the changes in platelet mitochondrial respiration in patients with metabolic syndrome. Β | In the past years, respirometric profiling of peripheral blood cells has emerged as a minimally invasive approach allowing the assessment of mitochondrial dysfunction in various pathological conditions associated with metabolic stress. The present pilot study was purported to characterize the changes in platelet mitochondrial respiration in patients with metabolic syndrome. Β | ||
To this aim blood samples were obtained from age-matched healthy adult donors and patients with metabolic syndrome and were subjected to two-step centrifugation in order to obtain | To this aim blood samples were obtained from age-matched healthy adult donors and patients with metabolic syndrome and were subjected to two-step centrifugation in order to obtain the platelet-rich plasma sample and the platelet pellet, respectively. Respiration of human platelets was assessed at 370C, after plasma membrane permeabilization with digitonin, using the Oxygraph-2k (Oroboros Ltd.), according to the Substrate-Uncoupler-Inhibitor-Titration (SUIT) protocol adapted to measure both complex I and complex II-dependent respiration. Β | ||
Both the respiratory control ratio (RCR, reflecting oxidative phosphorylation coupling efficiency) and the routine control ratio (R/E, as measure of mitochondrial dysfunction) were impaired in patients with metabolic syndrome vs. controls | Both the respiratory control ratio (RCR, reflecting oxidative phosphorylation coupling efficiency) and the routine control ratio (R/E, as measure of mitochondrial dysfunction) were impaired in patients with metabolic syndrome vs. controls as follows: RCR - 4.23Β±0.16 vs 6.65Β±0.3. (p<0.001) and R/E - 0.42Β±0.04 vs 0.31Β±0.01 (p<0.05), respectively. Β | ||
Our preliminary data suggest that metabolic syndrome is associated with the impairment of platelet mitochondrial respiration. Early detection of mitochondrial dysfunction in circulating cells as putative biomarker in cardiometabolic diseases is clearly warranted. | Our preliminary data suggest that metabolic syndrome is associated with the impairment of platelet mitochondrial respiration. Early detection of mitochondrial dysfunction in circulating cells as putative biomarker in cardiometabolic diseases is clearly warranted. |
Latest revision as of 15:10, 22 November 2017
Impairment of platelet mitochondrial respiration in metabolic syndrome: A pilot study. |
Link: MiP2017
Muntean DM, Petrus A, Ratiu C, Ionica M, Duicu O, Lighezan R (2017)
Event: MiP2017
In the past years, respirometric profiling of peripheral blood cells has emerged as a minimally invasive approach allowing the assessment of mitochondrial dysfunction in various pathological conditions associated with metabolic stress. The present pilot study was purported to characterize the changes in platelet mitochondrial respiration in patients with metabolic syndrome.
To this aim blood samples were obtained from age-matched healthy adult donors and patients with metabolic syndrome and were subjected to two-step centrifugation in order to obtain the platelet-rich plasma sample and the platelet pellet, respectively. Respiration of human platelets was assessed at 370C, after plasma membrane permeabilization with digitonin, using the Oxygraph-2k (Oroboros Ltd.), according to the Substrate-Uncoupler-Inhibitor-Titration (SUIT) protocol adapted to measure both complex I and complex II-dependent respiration.
Both the respiratory control ratio (RCR, reflecting oxidative phosphorylation coupling efficiency) and the routine control ratio (R/E, as measure of mitochondrial dysfunction) were impaired in patients with metabolic syndrome vs. controls as follows: RCR - 4.23Β±0.16 vs 6.65Β±0.3. (p<0.001) and R/E - 0.42Β±0.04 vs 0.31Β±0.01 (p<0.05), respectively.
Our preliminary data suggest that metabolic syndrome is associated with the impairment of platelet mitochondrial respiration. Early detection of mitochondrial dysfunction in circulating cells as putative biomarker in cardiometabolic diseases is clearly warranted.
β’ Bioblast editor: Kandolf G
β’ O2k-Network Lab: RO Timisoara Muntean DM
Labels: MiParea: Respiration Pathology: Other
Organism: Human Tissue;cell: Blood cells, Platelet
Pathway: N, S
HRR: Oxygraph-2k
Affiliations and support
- Muntean DM(1,3), PetruΘ A(1), RaΘiu C(1), IonicΔ M(1), Duicu O(1,3), Lighezan R(2,3)
- 1Dept III-Pathophysiology
- Dept XIII - Parasitology
- Center for Transl Res & Syst Med; Univ Med Pharm, Timisoara, Romania. - [email protected]
- Muntean DM(1,3), PetruΘ A(1), RaΘiu C(1), IonicΔ M(1), Duicu O(1,3), Lighezan R(2,3)
- This work was supported by the research grant contract nr. 232/26.11.2015 -15819/9.12.2015 (R.L.).