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G Fauconnier

Publications and source records attributed to G Fauconnier.

4 recordsLinked to original sources
PubMed2002

Localization of alpha-endosulphine in pancreatic somatostatin delta cells and expression during rat pancreas development.

AIMS/HYPOTHESIS: alpha-Endosulphine, a protein that belongs to the cAMP-regulated-phosphoprotein family, has been reported to modulate insulin secretion in vitro through interaction with the pancreatic beta-cell ATP-sensitive potassium (K(ATP)) channel. In this study, we analysed the tissue distribution of alpha-endosulphine and determined its pancreatic cellular localization. METHODS: Quantitative tissue distribution of alpha-endosulphine was studied by RIA on tissue extracts and cellular/subcellular localization was done using immunocytochemistry, morphometry and western blot analysis. alpha-Endosulphine and somatostatin release from RINT-3 somatostatin-secreting cells was quantified by RIA. RESULTS: alpha-Endosulphine, concentrated particularly in the central nervous system, was also detected in a wide variety of tissues including the pancreas. Immunohistochemistry analysis of adult rat pancreatic sections showed that alpha-endosulphine localized in somatostatin delta cells, where its expression increased during post-natal development. Immunoreactive cells were detected from foetal age E19, and the number of somatostatin cells co-expressing alpha-endosulphine increased with developmental age from E19 until adult. alpha-Endosulphine, highly expressed in the cytoplasm of RINT3 somatostatin-secreting cell line, was recovered in the particulate fraction of RINT3 cell extracts but was not co-secreted with somatostatin. CONCLUSION/INTERPRETATION: alpha-Endosulphine is expressed in all tissues tested including pancreas and is also detected in plasma. Pancreatic alpha-endosulphine is specifically localized in somatostatin delta cells. This cytosolic protein is not co-secreted with somatostatin and could be physically associated with particulate components of the cells. These findings are not in favour of an endocrine/paracrine effect of alpha-endosulphine on the beta-cell K(ATP) channel.

Aging↗
PubMed1997

[Detection of renal artery stenoses by MRI with surface reconstruction. Value in patients with chronic renal failure].

Forty-three patients with renal artery stenoses were examined with time of flight MR angiography using maximum intensity projection and surface shaded rendering, and with digital substraction angiography. Sensitivity and specificity were 0.83 and 0.78 for main and secondary arteries, 0.87 and 0.84 for main arteries. In azotemic patients, the positive predictive value was estimated at 40%-70% and the negative predictive value at 95%-98%, while the prevalence of renal artery stenoses varied from 10% to 30%. These results validate MRI for the detection of renal artery stenoses in this population. Surface shaded display was more accurate than maximum intensity projection to reconstruct time of flight sequences and to grade renal artery stenoses.

Adult↗
PubMed1994

cis-Acting elements controlling transcription from rat serine protease inhibitor 2.1 gene promoter. Characterization of two growth hormone response sites and a dominant purine-rich element.

The cis-acting elements that are functionally important for the basal, the growth hormone (GH), and the glucocorticoid hormone (GC) regulation of expression of the rat serine protease inhibitor 2.1 gene (spi 2.1) were mapped. Normal rat hepatocytes were transiently transfected with constructs harboring deleted or mutated versions of the spi 2.1 proximal promoter region fused to the chloramphenicol acetyltransferase gene. A purine-rich sequence (GAGA box, nucleotides -57 to -45), whose mutation or deletion almost completely knocks out both basal and hormone-stimulated promoter activities, plays the role of a key control element. A positive GC response element, spanning nucleotides -88 to -74, confers GC responsiveness to a heterologous promoter. Two structurally unrelated GH-response elements (GHRE) were identified. GHRE-II (nucleotides -136 to -104) contains a CCAAT enhancer binding protein binding site whose mutation completely abolishes its GH-dependent enhancer function. GHRE-I, which spans nucleotides -61 to +8, is not an enhancer element. Its GH-dependent activity depends on the preservation of the distance separating the GAGA box and elements of the basic transcriptional machinery. Taken together, these results have revealed the existence of an apparently new type of promoter functioning that strictly depends on the integrity of a key regulatory (G + A) motif.

Animals↗