Biomedical subjects

Chantal Remy

Publications and source records attributed to Chantal Remy.

3 recordsLinked to original sources

PubMed2006

Measuring hemoglobin oxygen saturation during graded hypoxic hypoxia in rat striatum.

We evaluated in vivo reflectance spectroscopy of visible light as a method to assess brain tissue hemoglobin oxygen saturation in rat striatum (SstrO2). Seven anesthetized and mechanically ventilated rats were subjected to incremental reduction in the fraction of inspired oxygen (Fio2): 0.35, 0.25, 0.15, 0.12, and 0.10, followed by a reoxygenation period (Group 1). At each episode, local changes in SstrO2 and in cerebral blood flow (LCBF) were simultaneously determined in the two striatal regions, using reflectance spectroscopy and laser Doppler flowmetry, respectively. Another group of rats (Group 2, n = 6) was also studied to measure sagittal sinus blood hemoglobin saturation (SssO2) during graded hypoxic hypoxia. Corpus striatum exhibited a significant graded decrease in SstrO2, from 38% +/- 17% at Fio2 of 0.35 (control) to 16% +/- 10% at Fio2 of 0.12 and to 13% +/- 7% at Fio2 of 0.10 (P < 0.05), with no difference between the two hemispheres. These local changes in SstrO2 were associated with a significant graded increase in LCBF: 161% +/- 26% of control values and 197% +/- 34% during these 2 hypoxic episodes, respectively (P < 0.05). All local changes were fully reversed during the reoxygenation period. In Group 2, SssO2 decreased from 38% +/- 8% at Fio2 of 0.35 (control) to 10% +/- 3% at Fio2 of 0.10, closely related to SstrO2 decreasing in hypoxia. This study shows that reflectance spectroscopy of the visible light in rat striatum could be a possible measure of continuous changes in SstrO2. SssO2 and LCBF measurements during graded hypoxic hypoxia indicate that changes in SstrO2 reflect primarily those in brain venous oxygenation.

Animals↗

PubMed2005

Specific AHNAK expression in brain endothelial cells with barrier properties.

The blood-brain barrier (BBB) is essential for maintaining brain homeostasis and low permeability. Because disruption of the BBB may contribute to many brain disorders, they are of considerable interests in the identification of the molecular mechanisms of BBB development and integrity. We here report that the giant protein AHNAK is expressed at the plasma membrane of endothelial cells (ECs) forming specific blood-tissue barriers, but is absent from the endothelium of capillaries characterized by extensive molecular exchanges between blood and extracellular fluid. In the brain, AHNAK is widely distributed in ECs with BBB properties, where it co-localizes with the tight junction protein ZO-1. AHNAK is absent from the permeable brain ECs of the choroid plexus and is down-regulated in permeable angiogenic ECs of brain tumors. In the choroid plexus, AHNAK accumulates at the tight junctions of the choroid epithelial cells that form the blood-cerebrospinal fluid (CSF) barrier. In EC cultures, the regulation of AHNAK expression and its localization corresponds to general criteria of a protein involved in barrier organization. AHNAK is up-regulated by angiopoietin-1 (Ang-1), a morphogenic factor that regulates brain EC permeability. In bovine cerebral ECs co-cultured with glial cells, AHNAK relocates from the cytosol to the plasma membrane when endothelial cells acquire BBB properties. Our results identify AHNAK as a protein marker of endothelial cells with barrier properties.

Angiopoietin-1↗

PubMed2005

Cellular disorders induced by high magnetic fields.

PURPOSE: To evaluate whether static high magnetic fields (HMFs), in the range of 10-17 T, affect the cytoskeleton and cell organization in different types of mammalian cells, including fibroblasts, epithelial cells, and differentiating neurons. MATERIALS AND METHODS: Cells were exposed to HMF for 30 or 60 minutes and subsequently assessed for viability. Cytoskeleton arrays and focal adhesions were visualized using immunofluorescence microscopy. RESULTS: Cell exposure to HMF over 10 T in the case of cycling cells, and over 15 T in the case of neurons, affected cell viability, apparently because of cell detachment from culture dishes. In the remaining adherent cells, the organization of actin assemblies was perturbed, and both cell adhesion and spreading were impaired. Moreover, in the case of neurons, exposure to HMF induced growth cone retraction and delayed cell differentiation. CONCLUSION: Cell exposure to HMF (over 10T and 15 T in the case of cycling cells and neurons, respectively) affects the cell cytoskeleton, with deleterious effects on cell viability, organization, and differentiation. Further studies are needed to determine whether such perturbations, as observed here in cultured cells, have consequences in whole animals.

Animals↗