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Difference between revisions of "Muntean 2017 MiP2017"

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{{Abstract
{{Abstract
|title=[[Image:MunteanDM.jpg|left|90px|Mitochondrial Physiology Society|MiPsociety]]
|title=[[Image:MunteanDM.jpg|left|90px|Danina Mundean]] Impairment of platelet mitochondrial respiration in metabolic syndrome: A pilot study.
|info=[[MiP2017]]
|info=[[MiP2017]]
|authors=Muntean DM, Petrus A, Ratiu C, Ionica M, Duicu O, Lighezan R
|year=2017
|year=2017
|event=MiP2017
|event=MiP2017
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]
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 - 4.23±0.16 vs 6.65±0.3. (p<0.001) and R/E - 0.42±0.04 vs 0.31±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.
|editor=[[Kandolf G]]
|editor=[[Kandolf G]]
|mipnetlab=RO Timisoara Muntean DM
}}
{{Labeling
|area=Respiration
|diseases=Other
|organism=Human
|tissues=Blood cells, Platelet
|pathways=N, S
|instruments=Oxygraph-2k
}}
}}
{{Labeling}}
== Affiliations and support ==
== Affiliations ==
::::Muntean DM(1,3), Petruș A(1), Rațiu C(1), Ionică 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]


== References ==
::::This work was supported by the research grant contract nr. 232/26.11.2015 -15819/9.12.2015 (R.L.).

Latest revision as of 15:10, 22 November 2017

Danina Mundean
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

COST Action MITOEAGLE

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 - 4.23±0.16 vs 6.65±0.3. (p<0.001) and R/E - 0.42±0.04 vs 0.31±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.


Bioblast editor: Kandolf G 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), Petruș A(1), Rațiu C(1), Ionică M(1), Duicu O(1,3), Lighezan R(2,3)
  1. 1Dept III-Pathophysiology
  2. Dept XIII - Parasitology
  3. Center for Transl Res & Syst Med; Univ Med Pharm, Timisoara, Romania. - [email protected]
This work was supported by the research grant contract nr. 232/26.11.2015 -15819/9.12.2015 (R.L.).