The Journey of SCAPs (Stem Cells from Apical Papilla), from Their Native Tissue to Grafting: Impact of Oxygen Concentration

Tissue engineering strategies aim at characterizing and at optimizing the cellular component that is combined with biomaterials, for improved tissue regeneration. Here, we present the immunoMap of apical papilla, the native tissue from which SCAPs are derived. We characterized stem cell niches that correspond to a minority population of cells expressing Mesenchymal stromal/Stem Cell (CD90, CD105, CD146) and stemness (SSEA4 and CD49f) markers as well as endothelial cell markers (VWF, CD31). Based on the colocalization of TKS5 and cortactin markers, we detected migration-associated organelles, podosomes-like structures, in specific regions and, for the first time, in association with stem cell niches in normal tissue. From six healthy teenager volunteers, each with two teeth, we derived twelve cell banks, isolated and amplified under 21 or 3% O2. We confirmed a proliferative advantage of all banks when cultured under 3% versus 21% O2. Interestingly, telomerase activity was similar to that of the highly proliferative hiPSC cell line, but unrelated to O2 concentration. Finally, SCAPs embedded in a thixotropic hydrogel and implanted subcutaneously in immunodeficient mice were protected from cell death with a slightly greater advantage for cells preconditioned at 3% O2

Telomerase Activation in Hematological Malignancies

Telomerase expression and telomere maintenance are critical for cell proliferation and survival, and they play important roles in development and cancer, including hematological malignancies. Transcriptional regulation of the rate-limiting subunit of human telomerase reverse transcriptase gen (hTERT) is a complex process, and unveiling the mechanisms behind its reactivation is an important step for the development of diagnostic and therapeutic applications. Here, we review the main mechanisms of telomerase activation and the associated hematologic malignancies

L’effet du bruit de parole indésirable dans les open-space : expérience en laboratoire

National audienceLe bruit de parole est maintenant accepté comme la source principale de gêne pour les employées des open space. Ce travail poursuit une série d’études faites au sein de l’INRS et l’INSA de Lyon basées sur le modèle théorique d’Hongisto, qui relie un Décrément de Performance (DP) et l’indicateur de la transmission de la parole STI (Speech Transmission Index). Ce modèle prédit que pour des valeurs de STI de 0.7 à 1, ce qui traduit un signal de parole avec une intelligibilité presque de 100 %, le DP reste constant à 7 %. L’expérience que nous avons fait a pour but de collecter plus d’information sur la relation entre le DP et le STI, en faisant varié le STI jusqu’à 0.9. Cinquante-cinq sujets entre 25 et 59 ans ont passé l’expérience. Premièrement, quelques paramètres psychologiques ont été observés pour une meilleure caractérisation de la variabilité interindividuelle. Ensuite, les sujets ont passé une tâche de mémoire de travail (WM) en silence et en quatre conditions différentes de bruit (STI de 0.25 à 0.9). Cette tâche a été personnalisée par une mesure initiale de l’empan mnésique. Cela a permis de définir deux différentes charges cognitives (lourde / légère) autour de la valeur de l’empan de chaque sujet. Les sujets ont évalué subjectivement la charge mentale et la gêne à la fin de chaque tâche WM de chaque condition sonore. Les résultats ont montré un effet significatif entre le STI et le DP, la charge mentale et la gêne. De plus, une corrélation significative a été trouvée entre l’âge des sujets et leur performance pendant la tâche WM

IRRELEVANT SPEECH EFFECT IN OPEN PLAN OFFICES: A LABORATORY STUDY

International audienceIt seems now accepted that speech noise in open plan offices is the main source of discomfort for employees. This work follows a series of studies conducted at INRS France and INSA Lyon based on Hongisto's theoretical model (2005) linking the Decrease in Performance (DP) and the Speech Transmission Index (STI). This model predicts that for STI values between 0.7 and 1, which means a speech signal close to 100% of intelligibility, the DP remains constant at about 7%. The experiment that we carried out aimed to gather more information about the relation between DP and STI, varying the STI value up to 0.9. Fifty-five subjects between 25-59 years old participated in the experiment. First, some psychological parameters were observed in order to better characterize the inter-subjects variability. Then, subjects performed a Working-Memory (WM) task in silence and in four different sound conditions (STI from 0.25 to 0.9). This task was customized by an initial measure of mnemonic span so that two different cognitive loads (low/high) were equally defined for each subject around their span value. Subjects also subjectively evaluated their mental load and discomfort at the end of each WM task, for each noise condition. Results show a significant effect of the STI on the DP, the mental load and the discomfort. Furthermore, a significant correlation was found between the age of subjects and their performance during the WM task. This result was confirmed by a cluster analysis that enabled us to separate the subjects on two different groups, one group of younger and more efficient subjects and one group of older and less efficient subjects. General results did not show any increase of DP for the highest STI values, so the "plateau" hypothesis of Hongisto's model cannot be rejected on the basis of this experiment

hMZF-2, the Elusive Transcription Factor

International audienc

Cancer Gene Ther

Rnd3/RhoE is an atypical Rho GTPase family member, known to be deregulated in many types of cancer. Previously, we showed that RND3 expression is downregulated in hepatocellular carcinoma (HCC) cell lines and tissues. In cancer cells, Rnd3 is involved in the regulation of cell proliferation and cell invasion. The implication of Rnd3 in HCC invasion was importantly studied whereas its role in cell growth needs further investigation. Thus, in this work, we aimed to better understand the impact of Rnd3 on tumor hepatocyte proliferation. Our results indicate that the silencing of RND3 induces a cell growth arrest both in vitro in 2D and 3D culture conditions and in vivo in tumor xenografts. The growth alteration after RND3 silencing in HCC cells is not due to an increase of cell death but to the induction of senescence. This RND3 knockdown-mediated phenomenon is dependent on the decrease of hTERT expression. Interestingly, after re-expression of RND3, these cells are able to bypass senescence and regain the ability to proliferate, with a re-expression of hTERT. Given that a low expression of Rnd3 is linked to the presence of satellite nodules in HCC, the transient senescence state observed might play a role in cancer progression