Effects of Thyroid Hormone on mRNAs of Phosphoglycerate Mutase Subunits in Rat Muscle during Development

González-Cinca, Nuria; Gonzálo, Sergio; Ascaso, Carlos; Carreras, José; Climent, F.

doi:10.1159/000057947

Cited by 16 publications

(2 citation statements)

References 36 publications

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“…We previously showed that both T 3 and hypoxia increased PGAM expression and activity levels in different rabbit tissues in vivo [6, 18], although not all tissues respond in the same manner. In both erythroblasts and reticulocytes, T 3 and hypoxia increase PGAM activity and mRNA levels.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Thyroid Hormone and Hypoxia on 2,3-Bisphosphoglycerate, Bisphosphoglycerate Synthase and Phosphoglycerate Mutase in Rabbit Erythroblasts and Reticulocytes in vivo

González-Cinca

Ossa²,

Carreras³

et al. 2004

Horm Res Paediatr

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Objectives: The effects of triiodothyronine (T₃) and hypoxia on 2,3-bisphosphoglycerate (2,3-BPG) studied in vitro are unclear. To clarify these effects we selected a more physiologic approach: the in vivo study in rabbits. We also present the changes produced by T₃ and hypoxia on phosphoglycerate mutase (PGAM), which requires 2,3-BPG as a cofactor, and 2,3-BPG synthase (BPGS), the enzyme responsible for 2,3-BPG synthesis in erythroblasts and reticulocytes. Methods: Hyperthyroidism was induced by daily T₃ injection (250 µg/kg), hypoxia by a mixture of 90% nitrogen and 10% oxygen and hypothyroidism by propylthiouracil (PTU) added to drinking water. Results: Both T₃ administration and hypoxic conditions increased 2,3-BPG levels and BPGS mRNA levels and activity in erythroblasts but not in reticulocytes. Unlike BPGS, both PGAM mRNA levels and activity were increased in erythroblasts and reticulocytes under hyperthyrodism and hypoxia. The antihormone PTU produced opposite effects to T₃. Conclusion: The results presented here suggest that both hyperthyroidism and hypoxia modulate in vivo red cell 2,3-BPG content by changes in the expression of BPGS. Similarly, the changes in PGAM activity are also explained by changes in its expression.

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Section: Discussionmentioning

confidence: 99%

“…T 3 plasma levels were determined using the ‘Immunolite’ (Diagnostic Products Co, Los Angeles, Calif., USA). Hyperthyroidism was induced by daily T 3 injection (250 µg/kg), and rabbits were euthanized at 10 treatment days, as previously reported [18]. Control animals were similarly injected with 0.1% saline.…”

Section: Methodsmentioning

confidence: 99%

Effects of Thyroid Hormone and Hypoxia on 2,3-Bisphosphoglycerate, Bisphosphoglycerate Synthase and Phosphoglycerate Mutase in Rabbit Erythroblasts and Reticulocytes in vivo

González-Cinca

Ossa²,

Carreras³

et al. 2004

Horm Res Paediatr

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Kwon

Kim

et al. 2003

Molecular Biology Reports

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Although Hox genes are known to mediate developmental decisions involved in pattern formation during embryogenesis, it is still not well understood what Hox regulates. In order to analyze Hoxc8 downstream target genes, a stable cell line overexpressing Hoxc8 was established using F9 murine teratocarcinoma cells, proteom samples were analyzed by 2-DE, and compared with controls. The protein spots having differences more than 4 fold in intensity were selected, analyzed by MALDI-TOF, and grouped in terms of putative function; cytoskeleton and motility (vimentin, gamma-actin, tropomyosin, and tubulin beta-5 chain); folding, modification and degradation of protein (GRP78, proteasome subunit alpha type 5, 26S proteasome regulatory subunit p27 protein, and PDIR); metabolism (ATP synthase beta subunit, Pgam1, and CAII); transcription/translation factors and general nucleic acid binding proteins (RbAp46, PCNA, eEF-1-beta, and nucleophosmin). Although it may not be significant, 50% of the genes were located on chromosomes 2 and 3, suggesting the possibility of a non-random distribution of Hox downstream genes. Almost 50% of the genes analyzed showed some relation with Hox protein directly or indirectly; i.e., tubulin beta 5, EF-1 beta and PCNA have been reported to contain putative Hox binding regulatory sites and genes like vimentin, pgam1 and nucleophosmin to be regulated by RA, a potent modulator of Hox expression. These results altogether imply that proteom analysis could be a possible tool for the analysis of the potent Hox realizator genes, which provides a new insight into the function of Hox on pattern formation during embryogenesis.

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Loss of white matter integrity is associated with gait disorders in cerebral small vessel disease

Laat

Tuladhar

Norden

et al. 2010

Brain

246

215

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Gait disturbances are common in the elderly. Cerebral small vessel disease, including white matter lesions and lacunars infarcts, is thought to disrupt white matter tracts that connect important motor regions, hence resulting in gait disturbances. Pathological studies have demonstrated abnormalities in white matter that may appear normal on brain imaging. The loss of integrity in such normal-appearing white matter may partly be due to small vessel disease and may play a role in causing gait disturbances. The white matter regions involved in these gait disturbances, both in white matter lesions and normal-appearing white matter, remain unclear. We, therefore, aimed to investigate the relation between the location of white matter lesions and gait using voxel-based morphometry analysis, as well as between white matter integrity and gait by applying tract-based spatial statistics to diffusion tensor imaging parameters. Magnetic resonance imaging was carried out on 429 individuals in the age range of 50 and 85 years, with cerebral small vessel disease without dementia or parkinsonism. Gait was assessed quantitatively. White matter lesions, especially in the centrum semiovale and periventricular frontal lobe, were related to a lower gait velocity, shorter stride length and broader stride width. Loss of white matter integrity, as indicated by a lower fractional anisotropy and higher mean diffusivity, in numerous regions was related to a lower gait performance. Most of these regions were located in the normal-appearing white matter. The strongest significant association was found in the corpus callosum, particularly the genu. Most of the associations in the normal-appearing white matter disappeared after controlling for white matter lesions and lacunar infarcts, except for some in the corpus callosum. In conclusion, our study showed that using a combination of voxel-based morphometry analysis of the white matter lesions and diffusion tensor imaging is of added value in investigating the pathophysiology of gait disturbances in subjects with small vessel disease. Our data demonstrate that, in elderly subjects with small vessel disease, widespread disruption of white matter integrity, predominantly in the normal-appearing white matter, is involved in gait disturbances. In particular, loss of fibres interconnecting bilateral cortical regions, especially the prefrontal cortex that is involved in cognitive control on motor performance, may be important. The most important mechanisms underlying affected normal-appearing white matter are probably a direct effect of small vessel disease or, indirectly, remote effects of white matter lesions and lacunar infarcts.

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Effects of Thyroid Hormone on mRNAs of Phosphoglycerate Mutase Subunits in Rat Muscle during Development

Cited by 16 publications

References 36 publications

Effects of Thyroid Hormone and Hypoxia on 2,3-Bisphosphoglycerate, Bisphosphoglycerate Synthase and Phosphoglycerate Mutase in Rabbit Erythroblasts and Reticulocytes in vivo

Effects of Thyroid Hormone and Hypoxia on 2,3-Bisphosphoglycerate, Bisphosphoglycerate Synthase and Phosphoglycerate Mutase in Rabbit Erythroblasts and Reticulocytes in vivo

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Loss of white matter integrity is associated with gait disorders in cerebral small vessel disease

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