Difference between revisions of "Chakraborty 2014 J Cardiovasc Dis"
Beno Marija (talk | contribs) |
|||
| (11 intermediate revisions by 5 users not shown) | |||
| Line 1: | Line 1: | ||
{{Publication | {{Publication | ||
|title=Chakraborty M, Phillips ARJ, Macdonald J, Windsor JA, Hickey AJR ( | |title=Chakraborty M, Phillips ARJ, Macdonald J, Windsor JA, Hickey AJR (2014) Mitochondrial respiration in mononuclear cells and heart fibers in spontaneously hypertensive rats. J Cardiovasc Dis ISSN:2330-459. | ||
|info=[http://researchpub.org/journal/jcvd/number/vol2-no1/vol2-no1-3.pdf vol2-no1-3] | |info=[http://researchpub.org/journal/jcvd/number/vol2-no1/vol2-no1-3.pdf vol2-no1-3] | ||
|authors=Chakraborty M, Phillips ARJ, Macdonald J, Windsor JA, Hickey AJR | |authors=Chakraborty M, Phillips ARJ, Macdonald J, Windsor JA, Hickey AJR | ||
|year= | |year=2014 | ||
|journal=J Cardiovasc Dis | |journal=J Cardiovasc Dis | ||
|abstract=Mitochondrial function is altered | |abstract=Mitochondrial function is altered in organs in hypertension and may be implicated in subclinical organ damage. Therefore measuring mitochondrial function may be clinically useful but, a biopsy of organ/tissue is required to measure mitochondrial function and that is invasive in the clinical setting. The aim of this study was to measure mitochondrial function from easily obtainable circulating mononuclear cells (MC) and the heart tissue of spontaneous hypertensive rats (SHR) at an early hypertensive and a compensated hypertrophic stage. Six and 14 months age SHR and Wistar control rats were divided into four groups and mitochondrial function was measured in MC and permeabilized heart fibers. MC showed decreased respiratory control ratios and decreased electron transfer-pathway capacity attributable to Complex I in SHR. These findings suggest that MC were less efficient at producing adenine triphosphate (ATP) and were less dependent on CI substrates. In contrast, heart tissue from SHR and Wistars showed similar mitochondrial function at both ages. Altered mitochondrial function was present in MC at a stage in the disease when it was not detectable in the heart. This study provides a protocol to study mitochondrial function from MC which may be correlated with subclinical organ damage in patients with hypertension. | ||
in organs in hypertension and | |keywords=Hypertension, Mitochondria, Oxidative phosphorylation, Electron transport system, Subclinical organ damage, Spontaneous hypertensive rat, Mononuclear cells | ||
may be implicated in subclinical organ damage. Therefore | |||
measuring mitochondrial function may be clinically useful but, a | |||
biopsy of organ/tissue is required to measure mitochondrial function | |||
and that is invasive in the | |||
to measure mitochondrial function from easily obtainable | |||
circulating mononuclear cells (MC) and the heart tissue of | |||
spontaneous hypertensive rats (SHR) at an early hypertensive and a | |||
compensated hypertrophic stage. Six | |||
and 14 months age SHR and | |||
Wistar control rats were divided into four groups and mitochondrial | |||
function was measured in MC and permeabilized heart fibers. MC | |||
showed decreased respiratory control ratios and decreased electron | |||
findings suggest that MC were less efficient at producing adenine | |||
triphosphate (ATP) and were less dependent on CI substrates. | |||
In | |||
contrast, heart tissue from SHR and Wistars showed similar | |||
mitochondrial function at both | |||
Altered mitochondrial function | |||
was present in MC at a stage in the disease when it was not | |||
detectable in the heart. This study provides a protocol to study | |||
mitochondrial function from MC which may be correlated with | |||
subclinical organ damage in | |||
|keywords= | |||
|mipnetlab=NZ Auckland Hickey AJ | |mipnetlab=NZ Auckland Hickey AJ | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration, Instruments;methods | |area=Respiration, Instruments;methods | ||
|diseases=Cardiovascular | |||
|organism=Rat | |organism=Rat | ||
|tissues=Heart, Blood cells | |tissues=Heart, Blood cells | ||
|preparations=Permeabilized cells, Permeabilized tissue | |preparations=Permeabilized cells, Permeabilized tissue | ||
|couplingstates=LEAK, ROUTINE, OXPHOS, ET | |||
|couplingstates=LEAK, OXPHOS, | |pathways=N, S, Gp, CIV, NS, ROX | ||
| | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
== Correction == | |||
An Oroboros Oxygraph-2k was used in this publication, whereas the Anton Paar/Oroboros Oxygraph was the first-generation instrument for high-resolution respirometry, which was replaced by the Oxygraph-2k in 2002. | |||
* ''Further details'': [[Gnaiger 2012 Abstract Bioblast-Gentle Science]] | |||
Latest revision as of 12:19, 23 January 2019
| Chakraborty M, Phillips ARJ, Macdonald J, Windsor JA, Hickey AJR (2014) Mitochondrial respiration in mononuclear cells and heart fibers in spontaneously hypertensive rats. J Cardiovasc Dis ISSN:2330-459. |
Chakraborty M, Phillips ARJ, Macdonald J, Windsor JA, Hickey AJR (2014) J Cardiovasc Dis
Abstract: Mitochondrial function is altered in organs in hypertension and may be implicated in subclinical organ damage. Therefore measuring mitochondrial function may be clinically useful but, a biopsy of organ/tissue is required to measure mitochondrial function and that is invasive in the clinical setting. The aim of this study was to measure mitochondrial function from easily obtainable circulating mononuclear cells (MC) and the heart tissue of spontaneous hypertensive rats (SHR) at an early hypertensive and a compensated hypertrophic stage. Six and 14 months age SHR and Wistar control rats were divided into four groups and mitochondrial function was measured in MC and permeabilized heart fibers. MC showed decreased respiratory control ratios and decreased electron transfer-pathway capacity attributable to Complex I in SHR. These findings suggest that MC were less efficient at producing adenine triphosphate (ATP) and were less dependent on CI substrates. In contrast, heart tissue from SHR and Wistars showed similar mitochondrial function at both ages. Altered mitochondrial function was present in MC at a stage in the disease when it was not detectable in the heart. This study provides a protocol to study mitochondrial function from MC which may be correlated with subclinical organ damage in patients with hypertension. • Keywords: Hypertension, Mitochondria, Oxidative phosphorylation, Electron transport system, Subclinical organ damage, Spontaneous hypertensive rat, Mononuclear cells
• O2k-Network Lab: NZ Auckland Hickey AJ
Labels: MiParea: Respiration, Instruments;methods
Pathology: Cardiovascular
Organism: Rat Tissue;cell: Heart, Blood cells Preparation: Permeabilized cells, Permeabilized tissue
Coupling state: LEAK, ROUTINE, OXPHOS, ET
Pathway: N, S, Gp, CIV, NS, ROX
HRR: Oxygraph-2k
Correction
An Oroboros Oxygraph-2k was used in this publication, whereas the Anton Paar/Oroboros Oxygraph was the first-generation instrument for high-resolution respirometry, which was replaced by the Oxygraph-2k in 2002.
- Further details: Gnaiger 2012 Abstract Bioblast-Gentle Science
