Journal articles on the topic 'Stimulation cellulaire'
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1
Carmen Martínez, Maria, Corinne Kunzelmann, and Jean-Marie Freyssinet. "Remodelage de la membrane plasmique et stimulation cellulaire." médecine/sciences 20, no. 2 (February 2004): 189–95. http://dx.doi.org/10.1051/medsci/2004202189.
2
Vallée, Alexandre. "Activation de la glycolyse aérobie par la voie canonique WNT/β-caténine." médecine/sciences 34, no. 4 (April 2018): 326–30. http://dx.doi.org/10.1051/medsci/20183404013.
Abstract:
L’énergie est le principal facteur déterminant de la viabilité neuronale. Dans cette synthèse, nous proposons l’hypothèse d’une activation anormale de la glycolyse aérobie par la stimulation de la voie de signalisation canonique WNT/β-caténine dans la sclérose latérale amyotrophique (SLA). La stimulation de la voie canonique WNT induit en effet l’activation de la glycolyse aérobie, appelée aussi effet Warburg, via la stimulation des enzymes glycolytiques comme PKM2, PDK1, LDH-A et MCT-1 et les transporteurs de glucose Glut. La glycolyse aérobie consiste en la conversion de la majeure partie du glucose en lactate quelle que soit la teneur en oxygène. Une dérégulation du métabolisme énergétique cellulaire qui favorise la mort cellulaire participerait à la progression de la SLA. Contrôler l’expression de la voie de signalisation canonique WNT/β-caténine pourrait ainsi apparaître comme une cible intéressante pour moduler la glycolyse aérobie et donc la progression de la SLA.
3
Mollard, Patrice. "L’hypophyse dévoilée : du couplage stimulation-sécrétion aux réseaux cellulaires câblant la glande." Biologie Aujourd’hui 216, no. 3-4 (2022): 83–87. http://dx.doi.org/10.1051/jbio/2022021.
Abstract:
L’année 2021 s’est terminée par un événement de grande tristesse : le décès d’Andrée Tixier-Vidal. Elle fut non seulement une pionnière en biologie cellulaire mais également la promotrice charismatique de fédérations collaboratives multidisciplinaires particulièrement stimulantes et fructueuses. Cette note en retrace les succès en termes de découvertes à la fois sur le couplage stimulation-sécrétion des cellules endocrines de l’hypophyse et sur l’organisation de ces cellules hypophysaires en réseaux 3D multicellulaires à l’origine des sécrétions pulsées des hormones hypophysaires qui contrôlent des fonctions de base de l’organisme comme la croissance corporelle et la reproduction.
4
SEYER, P., S. GRANDEMANGE, L. PESSEMESSE, F. CASAS, G. CABELLO, and C. WRUTNIAK-CABELLO. "L’activité mitochondriale est un régulateur majeur de la différenciation des myoblastes et de l’expression des isoformes de myosine." INRAE Productions Animales 19, no. 4 (September 13, 2006): 279–86. http://dx.doi.org/10.20870/productions-animales.2006.19.4.3495.
Abstract:
Parallèlement à son rôle dans le métabolisme énergétique, l’activité mitochondriale intervient également dans l’induction de l’apoptose, ainsi que dans la régulation de la prolifération et de la différenciation cellulaires. Il existe en particulier une véritable régulation de la différenciation des myoblastes par l’activité mitochondriale, indépendante de la production d’ATP. Elle implique notamment le contrôle de l’expression de myogénine et de l’activité des facteurs myogéniques.
Dans cette étude, nous démontrons que l’expression du proto-oncogène c-Myc est respectivement stimulée ou diminuée par une inhibition ou une stimulation de l’activité mitochondriale. Cette régulation s’effectue en grande partie au niveau de la stabilité du messager, et au niveau de la localisation cellulaire de la protéine dans les myoblastes aviaires. De plus, la surexpression de c-Myc reproduit très exactement les effets d’une inhibition de l’activité mitochondriale : i) abrogation de la différenciation terminale ; ii) inhibition de l’expression de Myogénine, sans altération de celle de MyoD ; iii) blocage de l’aptitude des facteurs myogéniques à induire la différenciation ; iv) inhibition de la sortie des myoblastes du cycle cellulaire. Ces résultats démontrent que c-Myc est une cible importante de l’activité mitochondriale, impliquée dans l’influence de l’organite sur la différenciation des myoblastes.
Nous avons également mis en évidence l’existence d’un autre gène cible de l’organite qui code la phosphatase calcium dépendante Calcineurine. Son expression est respectivement inhibée ou stimulée par l’inhibition ou la stimulation de l’activité mitochondriale. De plus, l’expression d’une forme constitutivement active de Calcineurine stimule la différenciation des myoblastes et l’expression de Myogénine, alors que ces deux événements sont bloqués par l’expression d’un ARN antisens Calcineurine. Enfin, la stimulation de l’activité mitochondriale, comme l’expression d’une forme constitutivement active de Calcineurine stimule spécifiquement l’expression de l’isoforme lente des chaînes lourdes de myosine.
Ces données démontrent donc que, notamment via l’expression de Calcineurine, l’activité mitochondriale régule non seulement la différenciation des myoblastes, mais détermine également le type contractile des fibres musculaires
5
Gruffat, Henri, and Evelyne Manet. "Co-infection EBV/KSHV." médecine/sciences 34, no. 1 (January 2018): 79–82. http://dx.doi.org/10.1051/medsci/20183401017.
Abstract:
Le virus herpétique humain associé au sarcome de Kaposi (KSHV) est l’agent étiologique du lymphome primitif des séreuses (PEL) dans lequel le virus d’Epstein-Barr (EBV) est aussi très souvent présent. Jusqu’à présent, seuls des modèles cellulaires permettaient d’explorer l’interaction des deux virus conduisant à la transformation des cellules. Un modèle de co-infection de souris humanisées, développé récemment permet désormais d’explorer ce phénomène in vivo. Il démontre que la co-infection par EBV et par KSHV augmente la persistance de KSHV et favorise la transformation cellulaire via la stimulation de la réplication de l’EBV par KSHV. Il s’agit du premier modèle de PEL chez le petit animal. Cette avancée ouvre ainsi des perspectives intéressantes pour de futures études de ce lymphome.
6
Kahn, A. "MAP-kinase, un intégrateur possible des différentes voies de stimulation de la division cellulaire." médecine/sciences 6, no. 4 (1990): 392. http://dx.doi.org/10.4267/10608/4154.
7
Dumond, Aurore, Luc Demange, and Gilles Pagès. "Les neuropilines." médecine/sciences 36, no. 5 (May 2020): 487–96. http://dx.doi.org/10.1051/medsci/2020080.
Abstract:
Une angiogenèse exacerbée est une des caractéristiques (« hallmarks ») du cancer, définies par Hanahan et Weinberg1. Cependant, le ciblage de la voie de signalisation du VEGF (vascular endothelial growth factor) ou de ses récepteurs a montré ses limites thérapeutiques. Après un bénéfice thérapeutique indéniable pour les patients, les tumeurs récidivent après quelques mois, et deviennent généralement métastatiques et incurables. Les neuropilines 1 et 2 (NRP1, 2) dont l’activité a été décrite initialement dans le système nerveux, stimulent de nombreuses fonctions impliquées dans l’agressivité tumorale, notamment la prolifération cellulaire, l’angiogenèse et la lymphangiogenèse, ainsi que la tolérance immunitaire. Ainsi, une surexpression de NRP1 ou 2 dans de nombreuses tumeurs, est corrélée à une survie courte des patients. Cette revue a pour objectif de décrire les mécanismes d’action impliqués dans la stimulation de NRP1 et NRP2 et de faire le point sur les stratégies thérapeutiques en études précliniques ou en essais de phase précoces chez des patients atteints de différents cancers.
8
Gur, Serap, and Wayne J. G. Hellstrom. "Activation of P2Y1 and P2Y2 nucleotide receptors by adenosine 5′-triphosphate analogues augmented nerve-mediated relaxation of human corpus cavernosum." Canadian Urological Association Journal 3, no. 4 (May 1, 2013): 314. http://dx.doi.org/10.5489/cuaj.1127.
Abstract:
Introduction: Adenosine 5′-triphosphate (ATP) is a ubiquitous cellularenergy source. We evaluated the effect of ATP and its analogueson nonadrenergic and noncholinergic relaxation in precontractedhuman corpus cavernosal smooth muscle (HCCSM).Methods: We obtained specimens of human corpus cavernosum(HCC) from patients undergoing penile prosthesis surgery (patientage 46–70 yr, n = 17) with prior approval from the local institutionalreview board. Isolated HCC strips were placed in organbaths containing Krebs solution and functional experiments wereconducted. Immunohistochemical localization studies were performedto establish the presence of purinergic P2X1, P2Y1 andP2Y2 receptors in HCC.Results: The amplitude of relaxation induced by electrical-fieldstimulation (EFS) on HCC was significantly increased after exposureto ATP (P2X and P2Y agonists), 2-MeSATP (P2Y1 agonist), and uridine5’ triphosphate (P2Y2 agonist), but not α,β-methylene ATP(P2X1 agonist). The P2X1 antagonist pyridoxal-5’-phosphate-6-azophenyl-2’, 4’-disulfonate, and the nonspecific P2Y antagonist,reactive blue 2, did not inhibit the potentiated response of EFS onHCC. Although immunoreactivity for both P2Y1 and P2Y2 receptorswas localized abundantly in HCC, there was only low-levelimmunostaining for the P2X1 receptor.Conclusion: These data demonstrate that nerve-mediated relaxation ofHCCSM strips precontracted with phenylephrine in organ bath preparationsis amplified by stimulating purinergic P2Y1 and P2Y2 receptors.Although nucleotides are important regulators of HCCSM tone, theseobservations suggest an independent purinergic relaxing mechanismin the HCC, separate from the better known nitrergic system.Introduction : L’adénosine 5’-triphosphate (ATP) est une sourced’énergie cellulaire générale. L’effet de l’ATP et de ses analoguessur le relâchement non adrénergique et non cholinergique du musclelisse précontracté du corps caverneux a été évalué.Méthode : Des échantillons de corps caverneux humains (CCH)ont été obtenus à partir de patients porteurs d’une prothèse pénienne(âgés de 46 à 70 ans, n = 17) avec l’approbation préalabledu comité d’éthique de l’établissement. Des bandes isolées deCCH ont été placées dans des bains organiques contenant unesolution de Krebs et des expériences fonctionnelles ont ensuite étéréalisées. On a eu recours à des tests de localisation immunohistochimiquepour déceler la présence des récepteurs purinergiquesP2X1, P2Y1 et P2Y2 dans les échantillons de CCH.Résultats : L’ampleur du relâchement produit par stimulation électriquedes échantillons de CCH a été significativement accrue aprèsexposition à l’ATP (agoniste des récepteurs P2X et P2Y),à la 2-MeSATP (agoniste du récepteur P2Y1) et à l’UTP (agonistedu récepteur P2Y2), mais pas à la α,β-MeATP (agoniste du récepteurP2X1). L’antagoniste du récepteur P2X1, le pyridoxal-5'-phosphate-6-azophényl-2’, 4’-disulfonate, et l’agoniste nonspécifique du récepteur P2Y, le bleu chimiquement réactif, n’ontpas inhibé la réponse potentialisée par stimulation électriquedes bandes de CCH. Même si une immunoréactivité des récep teursP2Y1 et P2Y2 a été grandement notée dans les bandes de CCH, onn’a obtenu qu’une faible immunocoloration pour le récepteur P2X1.Conclusion : Ces données montrent que le relâchement par voienerveuse des bandes de CCH précontractées par phényléphrinedans des bains organiques est amplifié par la stimulation des récepteurspurinergiques P2Y1 et P2Y2. Bien que les nucléotides constituentdes facteurs importants de régulation du tonus des CCH,ces observations portent à croire à l’existence d’un mécanismeindépendant de relâchement purinergique distinct du système nitrergiquemieux connu.
9
Lucas, P. J., C. V. Bare, and R. E. Gress. "The human anti-murine xenogeneic cytotoxic response. II. Activated murine antigen-presenting cells directly stimulate human T helper cells." Journal of Immunology 154, no. 8 (April 15, 1995): 3761–70. http://dx.doi.org/10.4049/jimmunol.154.8.3761.
Abstract:
Abstract Generation of a human T cell anti-murine xenogeneic response has previously been shown to be dependent on presentation of murine Ag by human APC. We have undertaken a series of experiments to better delineate the cellular defects that prevent effective production of IL-2 by human T cells upon direct exposure to murine stimulator populations. It was found that although resting human T cells cannot respond effectively to resting murine APC, they can respond to activated murine stimulator populations. Such APC activation could be mediated by murine granulocyte-macrophage-CSF or LPS that were associated with increased expression of B7-2 on the xenogeneic stimulating cell populations. Blocking studies with Ab provided further evidence that costimulation through CD28 played a critical role in the stimulation of human T cells by activated murine-stimulator cells in the production of IL-2. These results demonstrate the usefulness of this xenogeneic system in understanding human T cell-APC interactions and defining minimally sufficient T cell activation requirements. They further delineate the cellular level of deficient activation in the xenogeneic stimulation of human T cells by murine cell populations, and identify the potential importance of CD28/CTLA4 and its ligands in xenogeneic responses. These observations and concepts have implications for clinical efforts in xenografting.
10
Lin, James C. A., Jimmy K. Li, and Walter H. Chang. "Signal Transduction Pathway of Ultrasound Stimulation on Osteoblasts(Cellular & Tissue Engineering)." Proceedings of the Asian Pacific Conference on Biomechanics : emerging science and technology in biomechanics 2004.1 (2004): 87–88. http://dx.doi.org/10.1299/jsmeapbio.2004.1.87.
11
Crémoux, P., F. Calvo, C. Gauville, G. Lagier, and JP Abila. "STIMULATION PAR LA 1, 25 DIHYDROXYVITAMINE D3 (1, 25 (OH) 2 D3) DE L'ACTIVITE ADENYLATE CYCLASE DES CELLULES DE CANCER DU SEIN HUMAIN (T47D): MODE D'ACTION ET EFFET SUR LA PROLIFERATION CELLULAIRE." Reproduction Nutrition Développement 29, Suppl. 1 (1989): 9. http://dx.doi.org/10.1051/rnd:19890710.
12
Chang, Walter H., Jimmy K. Li, and James C. A. Lin. "Biological Response of Low Intensity Ultrasound Stimulation on Osteoblasts(Cellular & Tissue Engineering)." Proceedings of the Asian Pacific Conference on Biomechanics : emerging science and technology in biomechanics 2004.1 (2004): 89–90. http://dx.doi.org/10.1299/jsmeapbio.2004.1.89.
13
Nowak, Karl, Eilhard Mix, Jan Gimsa, Ulf Strauss, Kiran Kumar Sriperumbudur, Reiner Benecke, and Ulrike Gimsa. "Optimizing a Rodent Model of Parkinson's Disease for Exploring the Effects and Mechanisms of Deep Brain Stimulation." Parkinson's Disease 2011 (2011): 1–19. http://dx.doi.org/10.4061/2011/414682.
Abstract:
Deep brain stimulation (DBS) has become a treatment for a growing number of neurological and psychiatric disorders, especially for therapy-refractory Parkinson's disease (PD). However, not all of the symptoms of PD are sufficiently improved in all patients, and side effects may occur. Further progress depends on a deeper insight into the mechanisms of action of DBS in the context of disturbed brain circuits. For this, optimized animal models have to be developed. We review not only charge transfer mechanisms at the electrode/tissue interface and strategies to increase the stimulation's energy-efficiency but also the electrochemical, electrophysiological, biochemical and functional effects of DBS. We introduce a hemi-Parkinsonian rat model for long-term experiments with chronically instrumented rats carrying a backpack stimulator and implanted platinum/iridium electrodes. This model is suitable for (1) elucidating the electrochemical processes at the electrode/tissue interface, (2) analyzing the molecular, cellular and behavioral stimulation effects, (3) testing new target regions for DBS, (4) screening for potential neuroprotective DBS effects, and (5) improving the efficacy and safety of the method. An outlook is given on further developments of experimental DBS, including the use of transgenic animals and the testing of closed-loop systems for the direct on-demand application of electric stimulation.
14
Di, Ya-Li, Xiao-Ming Lu, Zu-Qing Zhu, and Fu-Xing Zhu. "Time Course of Carbendazim Stimulation on Pathogenicity of Sclerotinia sclerotiorum Indicates a Direct Stimulation Mechanism." Plant Disease 100, no. 7 (July 2016): 1454–59. http://dx.doi.org/10.1094/pdis-11-15-1349-re.
Abstract:
Previous studies have demonstrated that subtoxic doses of carbendazim have a stimulatory effect on pathogenicity of Sclerotinia sclerotiorum on rapeseed plants. The present study focused on the time-course profile of the stimulatory effect and its relevance to stimulation mechanisms. At 12 h postinoculation (HPI), initial necrotic lesions were visible only for rapeseed leaves treated with carbendazim at 0.2 and 1 μg/ml, whereas no disease symptoms were observed for the nontreated control. At 18 HPI, carbendazim stimulation on pathogenicity was more obvious than at 12 HPI. Study with scanning electron microscopy demonstrated that no discernable differences in the development of disease symptoms could be detected at 8 HPI. However, at 12 HPI, necrotic symptoms of the epidermal cells were apparent only for leaves sprayed with carbendazim. These results indicated that stimulations on pathogenicity occurred in the first 12 h, implying that direct stimulation rather than overcompensation to the disruption of homeostasis was likely to be the underlying mechanism for pathogenicity stimulation. Greenhouse experiments showed that spraying carbendazim at 400 μg/ml on potted rapeseed plants had statistically significant (P < 0.05) stimulations on pathogenicity for inoculations at 1, 3, 5, and 7 days after application (DAA). The stimulation action eventually disappeared for inoculations at 14 DAA. Mycelia grown on potato dextrose agar (PDA) supplemented with carbendazim at 400 μg/ml were more pathogenic than the nontreated control. However, after additional growth of the mycelia on fungicide-free PDA for 2 days, the stimulatory effect disappeared completely, indicating that carbendazim was indispensable for pathogenicity stimulations. Studies on biochemical mechanisms indicated that cell-wall-degrading enzymes such as cellulase, pectinase, and polygalacturonase were not involved in pathogenicity stimulations. These results will advance our understanding of the nature and mechanisms of fungicide stimulation on fungal pathogenicity and, thus, are valuable for judicious applications of fungicides.
15
Vilkhu, Ramandeep S., Sasidhar S. Madugula, Lauren E. Grosberg, Alex R. Gogliettino, Pawel Hottowy, Wladyslaw Dabrowski, Alexander Sher, Alan M. Litke, Subhasish Mitra, and E. J. Chichilnisky. "Spatially patterned bi-electrode epiretinal stimulation for axon avoidance at cellular resolution." Journal of Neural Engineering 18, no. 6 (November 15, 2021): 066007. http://dx.doi.org/10.1088/1741-2552/ac3450.
Abstract:
Abstract Objective. Epiretinal prostheses are designed to restore vision to people blinded by photoreceptor degenerative diseases by stimulating surviving retinal ganglion cells (RGCs), which carry visual signals to the brain. However, inadvertent stimulation of RGCs at their axons can result in non-focal visual percepts, limiting the quality of artificial vision. Theoretical work has suggested that axon activation can be avoided with current stimulation designed to minimize the second spatial derivative of the induced extracellular voltage along the axon. However, this approach has not been verified experimentally at the resolution of single cells. Approach. In this work, a custom multi-electrode array (512 electrodes, 10 μm diameter, 60 μm pitch) was used to stimulate and record RGCs in macaque retina ex vivo at single-cell, single-spike resolution. RGC activation thresholds resulting from bi-electrode stimulation, which consisted of bipolar currents simultaneously delivered through two electrodes straddling an axon, were compared to activation thresholds from traditional single-electrode stimulation. Main results. On average, across three retinal preparations, the bi-electrode stimulation strategy reduced somatic activation thresholds (∼21%) while increasing axonal activation thresholds (∼14%), thus favoring selective somatic activation. Furthermore, individual examples revealed rescued selective activation of somas that was not possible with any individual electrode. Significance. This work suggests that a bi-electrode epiretinal stimulation strategy can reduce inadvertent axonal activation at cellular resolution, for high-fidelity artificial vision.
16
Prebet, Thomas, Quoc-Hung Le, Jean-Michel Boiron, Didier Blaise, Anne Huynh, Ibrahim Yakoub-Agha, Hélène Esperou, Fréderic Garban, Jean Henri Bourhis, and Mauricette Michallet. "Impact of Hematopoietic Stem Cell (HSC) Recruitment and Graft Composition on Transplant Outcome after Reduced Intensity Allogeneic Peripheral Blood Stem Cell Transplantation (PBSCT): A Study of the Société Française de Greffe de Moelle Osseuse et de Thérapie Cellulaire (SFGM-TC) Registry." Blood 106, no. 11 (November 16, 2005): 1146. http://dx.doi.org/10.1182/blood.v106.11.1146.1146.
Abstract:
Abstract Evidence of an impact of graft product on transplant outcome after PBSCT is actually rising. Here, we investigated retrospectively the potential impact of HSC recruitment procedure (i.e. G-CSF stimulation schedule and apheresis number) and graft composition (CD34+ and CD3+ cell number) on transplant outcome (GVHD, OS, EFS). Our analysis concerned 488 HLA matched sibling allogeneic reduced intensity conditioning (RIC) PBSCT for hematological malignancies (116 MM, 110 AML, 109 NHL, 41 CLL, 41 MDS, 24 CML, 19 HD, 17 ALL and 11 MPS) reported on the SFGM-TC registry between 1998 and 2004. Follow-up was updated in April 2005. RIC-PBSCT was performed during first line treatment in 225 (49%) patients and a previous HSCT was recorded in 55% of the cases. Before RICT, 161 patients were in Complete Response, 161 in Partial Response, 34 in Stable Disease and 132 in Progressive Disease. Regarding donors, median age was 49 years, sex mismatching and ABO incompatibility were seen in 222 and 162 patients respectively. CMV status was positive either in donor or recipient in 152 cases. G-CSF median duration was 5 days (3–7days) at a median dose of 10μg/kg/day (4.6–16). G-CSF was given bid in 40% of the stimulations. Filgrastim was used in 59% of the donors and Lenograstim in 41% of the donors. A single apheresis was performed in 107 donors, 2 in 298 donors, more than 2 in 93 donors. The median number of CD34+ cells infused was 5.6x106 CD34+/kg (1–26) and the median CD3+ cells was 302x106 CD3+/kg (63–996). Conditioning regimen was most frequently an association of Fludarabine Busulfan and Anti Thymocyte Globuline (246 cases, duration of ATG 1 day: 18%, 2 days: 20%, 3 days: 20%, 4 days: 8% 5 days: 33%) or Fludarabine + TBI 2 Gy (123 patients). GVHD prophylaxis was a cyclosporine based treatment in 478 patients [95% of the cases (+ Methotrexate: 29%, + Mycophenolate Mofetil: 26%)]. Median follow-up after transplantation was 35 months (range: 0–86). Acute GVHD (grade II-IV) and cGVHD incidences were 35% (n=163 on 488 patients) and 50% (n=217 on 430 patients) respectively. The 3-year OS was 40% and the 3-year EFS was 34%. Treatment related mortality was 12% at 1 year and 15% at 3 years. In multivariate analysis studying pre and post transplant factors, a significant impact was shown of G-CSF duration (HR: 0.79 (0.62–1) p=0,05), G-CSF daily dose (HR: 1.13 (1–1.28) p=0,04) on OS. Other variables also influenced OS (NHL vs AML, aGVHD grade II vs 0-I and III-IV vs 0-I and cGVHD: yes vs no) and EFS (Sex mismatch, ABO incompatibility, NHL vs AML, FBS ATG duration: 5 days vs 2 days, aGVHD grade II vs 0-I and III-IV vs 0-I and cGVHD: yes vs no). No influence of graft composition or stem cell recruitment was demonstrated on aGVHD and cGVHD incidences although we found a significant impact of conditioning (FBS ATG 1 day vs 2days and 5days vs 2days). In conclusion, this study demonstrates that, surprisingly, graft composition has no impact on transplant outcome. Prolonged administration of moderate dose of G-CSF seems to be the best schedule for PBSC recruitment.
17
Zalkhani, Raha, Ahmad Ali Moazedi, Zohreh Ghotbeddin, and Mahdi Pourmahdi Borujeni. "Interaction of Sodium Valproate With Low-Frequency Electrical Stimulation During Kindlingn." Basic and Clinical Neuroscience Journal 11, no. 6 (November 1, 2020): 831–40. http://dx.doi.org/10.32598/bcn.11.6.1392.2.
Abstract:
Introduction: The interaction between antiepileptic drugs and brain electrical stimulation is a potential therapy to control seizures in patients with pharmacoresistance to drugs. So, the present study aimed to design to determine the effect of a subeffective dose of sodium valproate combined with low-frequency electrical stimulation during kindling. Methods: One tripolar electrode was implanted stereotactically in the CA1 hippocampus of male Wistar rats. One week after surgery, the rats were kindled by electrical stimulation of hippocampus in a rapid manner (12 stimulations/day) for 6 days with sodium valproate alone or combined with low-frequency electrical stimulation (four packages contained 200 monophasic square wave pulses of 0.1-ms duration at 1 Hz, immediately after kindling stimulations). The duration of afterdischarge, maximum latency to stages 4 and 5, and the maximum duration of these stages were recorded by electromadule during kindling. Results: Application of sodium valproate with low-frequency electrical stimulation caused a reduction in cumulative afterdischarge duration. The maximum latency to the onset of stage 5 seizure increased after sodium valproate application alone, without having a significant effect on the fourth stage. Our findings showed reductions in the seizures duration and increasing in the latency times of both stages after the application of sodium valproate with low-frequency electrical stimulation. Conclusion: It seems that usage of sodium valproate with low-frequency electrical stimulation during kindling was more effective to suppress the epileptic activity than its administration alone and may have a critical role on the antiepileptic effects of sodium valproate.
18
Whisenant, N., B. X. Zhang, M. Khademazad, P. Loessberg, and S. Muallem. "Regulation of Na-K-2Cl cotransport in osteoblasts." American Journal of Physiology-Cell Physiology 261, no. 3 (September 1, 1991): C433—C440. http://dx.doi.org/10.1152/ajpcell.1991.261.3.c433.
Abstract:
Uptake of 86Rb was used to follow the activity of Na-K-2Cl cotransport in the osteosarcoma cell line UMR-106-01. The ouabain-resistant fraction of 86Rb uptake was sensitive to bumetanide and furosemide. Furosemide-sensitive 86Rb uptake required the presence of Na+, K+, and Cl- in the incubation medium. These observations indicate the presence of a Na-K-2Cl cotransport system in osteoblasts. Cotransporter activity was stimulated by agonists which increase adenosine 3',5'-cyclic monophosphate (cAMP), cytosolic free Ca2+ ([Ca2+]i), and protein kinase C (PKC) activity such as parathyroid hormone (PTH) and prostaglandin E2 (PGE2). However, endothelin, which increases [Ca2+]i and PKC activity without affecting cellular levels of cAMP, was ineffective in stimulating the cotransporter. Accordingly, increasing cellular cAMP with forskolin was as effective as PTH and PGE2 in stimulating the cotransporter. Stimulation of PKC with TPA inhibited the cotransporter in a time- and concentration-dependent manner. No stimulation of cotransport could be demonstrated at any 12-O-tetradecanoyl-phorbol-13-acetate (TPA) concentration or incubation time. The Na-K-2Cl cotransporter was stimulated by cell shrinkage. Maximal stimulation was observed after swelling the cells in hypotonic medium and subsequent shrinkage in isotonic medium. Stimulation by cell shrinkage can be demonstrated in control, agonist-, cAMP-, and TPA-treated cells. These observations suggest that 1) the osteoblastic Na-K-2Cl cotransporter is activated by calciotropic hormones predominantly through an increase in cellular cAMP, and 2) in osteoblasts, the cotransporter is independently regulated by different biochemical pathways.
19
SCANTLEBURY, Thea, Allan D. SNIDERMAN, and Katherine CIANFLONE. "Regulation by retinoic acid of acylation-stimulating protein and complement C3 in human adipocytes." Biochemical Journal 356, no. 2 (May 24, 2001): 445–52. http://dx.doi.org/10.1042/bj3560445.
Abstract:
Acylation-stimulating protein (ASP), a product of complement C3, stimulates triacylglycerol synthesis in adipocytes. Previous studies have identified transthyretin, associated with chylomicrons, as a stimulator of C3 and ASP production. Since both transthyretin and chylomicrons transport retinyl ester/retinol, our goal was to investigate whether retinoic acid (RA) could be a potential hormonal mediator of the effect. Inhibitors of protein synthesis and protein secretion eliminated the stimulatory effects of chylomicrons on both C3 and ASP production in human differentiated adipocytes, suggesting that de novo protein synthesis and secretion are both required. Incubation with chylomicrons increased C3 mRNA levels (37±1.5%). RA alone or with chylomicrons had a stimulatory effect on C3 production (29-fold at 16.6nM RA) and ASP production. An RA receptor antagonist blocked stimulation of C3 mRNA and C3 secretion by both RA and chylomicrons. Finally, RA and chylomicrons activated a 1.8kb C3-promoter–luciferase construct transfected into 3T3-F442 and 3T3-L1 cells (by 41±0.2% and 69±0.3% respectively), possibly via RA receptor half-sites identified by sequence analysis. This is the first evidence documenting stimulation by RA of the C3 gene. Thus we propose RA as a novel cellular trigger in chylomicrons that subsequently results in increased ASP production by adipocytes after a meal.
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Jia, Ying, Junmei Zhang, Bo Chen, Minghong Luo, Weiyin Cheng, Yalin Wang, Juan Liu, and Hua Yang. "Strain Stimulations with Different Intensities on Fibroblast Viability and Protein Expression." Open Life Sciences 12, no. 1 (October 23, 2017): 285–93. http://dx.doi.org/10.1515/biol-2017-0033.
Abstract:
AbstractBackgroundMechanical stimulation via acupuncture and tuina massage triggers various cell responses. This study aims to understand these cellular bio-physical mechanisms by investigating the effect of different stimulation intensities on cell viability and protein expression.MethodologyConnective tissue fibroblasts were cultured in vitro. Three varying intensities of mechanical strain stimulation were applied to the cells, either once or three times and compared with non-stimulated controls. Changes in fibroblast viability and fibroblast protein expression were observed.ResultsStrain stimulation intensity significantly increased fibroblast cell survival rate (p<0.01) to effectively improve cell viability. Moreover, the combined influence of both the strain stimulation intensity and number of stimulations on the fibroblast survival rate significantly differed (p<0.05). Strain intensity also significantly altered fibroblast protein expression between the three groups (p<0.0001). Cluster analysis showed that the medium-intensity strain stimulation posed the maximum influence on protein expression.ConclusionThe difference in cell viability and protein expression of the connective tissue fibroblast during the in vitro strain process reveals the cytobiological mechanism of basic medicinal mechanical stimulation.
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Xiao, Guihua, Yilin Song, Yu Zhang, Yu Xing, Shengwei Xu, Mixia Wang, Junbo Wang, Deyong Chen, Jian Chen, and Xinxia Cai. "Dopamine and Striatal Neuron Firing Respond to Frequency-Dependent DBS Detected by Microelectrode Arrays in the Rat Model of Parkinson’s Disease." Biosensors 10, no. 10 (September 28, 2020): 136. http://dx.doi.org/10.3390/bios10100136.
Abstract:
(1) Background: Deep brain stimulation (DBS) is considered as an efficient treatment method for alleviating motor symptoms in Parkinson’s disease (PD), while different stimulation frequency effects on the specific neuron patterns at the cellular level remain unknown. (2) Methods: In this work, nanocomposites-modified implantable microelectrode arrays (MEAs) were fabricated to synchronously record changes of dopamine (DA) concentration and striatal neuron firing in the striatum during subthalamic nucleus DBS, and different responses of medium spiny projecting neurons (MSNs) and fast spiking interneurons (FSIs) to DBS were analyzed. (3) Results: DA concentration and striatal neuron spike firing rate showed a similar change as DBS frequency changed from 10 to 350 Hz. Note that the increases in DA concentration (3.11 ± 0.67 μM) and neural spike firing rate (15.24 ± 2.71 Hz) were maximal after the stimulation at 100 Hz. The MSNs firing response to DBS was significant, especially at 100 Hz, while the FSIs remained stable after various stimulations. (4) Conclusions: DBS shows the greatest regulatory effect on DA concentration and MSNs firing rate at 100 Hz stimulation. This implantable MEA in the recording of the neurotransmitter and neural spike pattern response to DBS provides a new insight to understand the mechanism of PD at the cellular level.
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Lee, YY, I. Kurtz, K. Yamato, Z. el-Hajjoui, and HP Koeffler. "Tumor necrosis factor stimulates Na+/H+ antiporter in human fibroblasts: dissociation between intracellular alkalinization and cytokine mRNA accumulation." Blood 79, no. 9 (May 1, 1992): 2262–66. http://dx.doi.org/10.1182/blood.v79.9.2262.2262.
Abstract:
Abstract Several hormones and cytokines stimulate the cellular Na+/H+ antiporter and this stimulation may be a signal transduction mechanism to mediate gene expression. We find that tumor necrosis factor rapidly stimulates both the Na+/H+ antiporter and the accumulation of mRNA coding for granulocyte-macrophage colony-stimulating factor and interleukin-6 in fibroblasts. Further experiments show that these phenomena occur independent of each other.
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Lee, YY, I. Kurtz, K. Yamato, Z. el-Hajjoui, and HP Koeffler. "Tumor necrosis factor stimulates Na+/H+ antiporter in human fibroblasts: dissociation between intracellular alkalinization and cytokine mRNA accumulation." Blood 79, no. 9 (May 1, 1992): 2262–66. http://dx.doi.org/10.1182/blood.v79.9.2262.bloodjournal7992262.
Abstract:
Several hormones and cytokines stimulate the cellular Na+/H+ antiporter and this stimulation may be a signal transduction mechanism to mediate gene expression. We find that tumor necrosis factor rapidly stimulates both the Na+/H+ antiporter and the accumulation of mRNA coding for granulocyte-macrophage colony-stimulating factor and interleukin-6 in fibroblasts. Further experiments show that these phenomena occur independent of each other.
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Kachadorian, W. A., J. Muller, and V. A. DiScala. "Variability of cellular responsiveness to ADH stimulation in toad urinary bladder." American Journal of Physiology-Renal Physiology 256, no. 4 (April 1, 1989): F590—F595. http://dx.doi.org/10.1152/ajprenal.1989.256.4.f590.
Abstract:
The hydrosmotic response of toad bladder to antidiuretic hormone (ADH) is quantitatively linked to the induced fusion of aggrephores with, and the appearance of aggregates of tightly packed intramembrane particles in the luminal membrane of granular cells. We used these morphological indexes of hormonally induced cell activation 1) to assess the variability of individual cell responsiveness to a maximally stimulating concentration of ADH and 2) to compare cell response patterns in paired tissues where the extent of whole tissue stimulation, as evidenced by transtissue water flow, was either maximal or submaximal. The results indicate that individual cell responsiveness within the same tissue to standardized maximal ADH treatment varies between two- and sevenfold, depending on the morphological endpoint measured. Furthermore, based on skewness in endpoint distribution, this variability appears to reflect inherent heterogeneity of granular cell reactivity to hormone. In relation to proportional tissue responses elicited by different stimulating concentrations of ADH, our observations of luminal membrane aggregate incidence suggest that the responding cells, whatever their sensitivity, participate in a graded, rather than "all-or-none," "on-off" manner.
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Song, Shijie, Shuojing Song, Chuanhai Cao, Xiaoyang Lin, Kunyu Li, Vasyl Sava, and Juan Sanchez-Ramos. "Hippocampal Neurogenesis and the Brain Repair Response to Brief Stereotaxic Insertion of a Microneedle." Stem Cells International 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/205878.
Abstract:
We tested the hypothesis that transient microinjury to the brain elicits cellular and humoral responses that stimulate hippocampal neurogenesis. Brief stereotaxic insertion and removal of a microneedle into the right hippocampus resulted in (a) significantly increased expression of granulocyte-colony stimulating factor (G-CSF), the chemokine MIP-1a, and the proinflammatory cytokine IL12p40; (b) pronounced activation of microglia and astrocytes; and (c) increase in hippocampal neurogenesis. This study describes immediate and early humoral and cellular mechanisms of the brain’s response to microinjury that will be useful for the investigation of potential neuroprotective and deleterious effects of deep brain stimulation in various neuropsychiatric disorders.
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Takanezawa, Sota, Shin-ichi Morita, Yukihiro Ozaki, and Yasushi Sako. "2P199 Raman Micro-spectroscopy of the Dynamics of Cellular Chemical State upon Stimulation with Growth Factors(12. Cell biology,Poster)." Seibutsu Butsuri 54, supplement1-2 (2014): S228. http://dx.doi.org/10.2142/biophys.54.s228_1.
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Huang, Xin, Zhengxiang Huang, Weidong Gao, Wendong Gao, Ruiying He, Yulin Li, Ross Crawford, Yinghong Zhou, Lan Xiao, and Yin Xiao. "Current Advances in 3D Dynamic Cell Culture Systems." Gels 8, no. 12 (December 16, 2022): 829. http://dx.doi.org/10.3390/gels8120829.
Abstract:
The traditional two-dimensional (2D) cell culture methods have a long history of mimicking in vivo cell growth. However, these methods cannot fully represent physiological conditions, which lack two major indexes of the in vivo environment; one is a three-dimensional 3D cell environment, and the other is mechanical stimulation; therefore, they are incapable of replicating the essential cellular communications between cell to cell, cell to the extracellular matrix, and cellular responses to dynamic mechanical stimulation in a physiological condition of body movement and blood flow. To solve these problems and challenges, 3D cell carriers have been gradually developed to provide a 3D matrix-like structure for cell attachment, proliferation, differentiation, and communication in static and dynamic culture conditions. 3D cell carriers in dynamic culture systems could primarily provide different mechanical stimulations which further mimic the real in vivo microenvironment. In this review, the current advances in 3D dynamic cell culture approaches have been introduced, with their advantages and disadvantages being discussed in comparison to traditional 2D cell culture in static conditions.
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Zhu, Ercheng, Alain S. Comtois, Liwei Fang, Norman R. Comtois, and Alejandro E. Grassino. "Influence of tension time on muscle fiber sarcolemmal injury in rat diaphragm." Journal of Applied Physiology 88, no. 1 (January 1, 2000): 135–41. http://dx.doi.org/10.1152/jappl.2000.88.1.135.
Abstract:
We hypothesized that the amount of sarcolemmal injury is directly related to the total tension time (TTtot), calculated as mean tension × total stimulation time. Diaphragm strips from Sprague-Dawley rats were superfused at optimal muscle length with Krebs containing procion orange to identify sarcolemmal injury. TTtot was induced by stimulation with 100 Hz for 3 min at duty cycles of 0.02, 0.15, 0.3, and 0.6, or with continuous contractions at 0.2, 0.4, 0.6, and 1.0 of maximal tension. A significant positive correlation between TTtot and the percentage of fibers with injured sarcolemma ( r 2 = 0.63, P < 0.05) is seen. Stimulation (at 100 Hz, duty cycle = 1) resulted in fast fatigue with low injury, likely caused by altered membrane conductivity. Stimulations inducing the largest injury are those showing progressive force loss and high TTtot, where injury may be due to activation of membrane degradative enzymes. The maximal tension measured at 20 min poststimulation was inversely related to the number of fibers injured, suggesting loss of force is caused by cellular injury.
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Chen, Yafen, Yoon-Hee Cha, Diamond Gleghorn, Benjamin C. Doudican, Guofa Shou, Lei Ding, and Han Yuan. "Brain network effects by continuous theta burst stimulation in mal de débarquement syndrome: simultaneous EEG and fMRI study." Journal of Neural Engineering 18, no. 6 (November 30, 2021): 066025. http://dx.doi.org/10.1088/1741-2552/ac314b.
Abstract:
Abstract Objective. Heterogeneous clinical responses to treatment with non-invasive brain stimulation are commonly observed, making it necessary to determine personally optimized stimulation parameters. We investigated neuroimaging markers of effective brain targets of treatment with continuous theta burst stimulation (cTBS) in mal de débarquement syndrome (MdDS), a balance disorder of persistent oscillating vertigo previously shown to exhibit abnormal intrinsic functional connectivity. Approach. Twenty-four right-handed, cTBS-naive individuals with MdDS received single administrations of cTBS over one of three stimulation targets in randomized order. The optimal target was determined based on the assessment of acute changes after the administration of cTBS over each target. Repetitive cTBS sessions were delivered on three consecutive days with the optimal target chosen by the participant. Electroencephalography (EEG) was recorded at single-administration test sessions of cTBS. Simultaneous EEG and functional MRI data were acquired at baseline and after completion of 10–12 sessions. Network connectivity changes after single and repetitive stimulations of cTBS were analyzed. Main results. Using electrophysiological source imaging and a data-driven method, we identified network-level connectivity changes in EEG that correlated with symptom responses after completion of multiple sessions of cTBS. We further determined that connectivity changes demonstrated by EEG during test sessions of single administrations of cTBS were signatures that could predict optimal targets. Significance. Our findings demonstrate the effect of cTBS on resting state brain networks and suggest an imaging-based, closed-loop stimulation paradigm that can identify optimal targets during short-term test sessions of stimulation. ClinicalTrials.gov Identifier: NCT02470377.
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Whitlock, D. M., and R. L. Terjung. "ATP depletion in slow-twitch red muscle of rat." American Journal of Physiology-Cell Physiology 253, no. 3 (September 1, 1987): C426—C432. http://dx.doi.org/10.1152/ajpcell.1987.253.3.c426.
Abstract:
Rat slow-twitch muscle, in contrast to fast-twitch muscle, maintains its ATP content near normal during intense stimulation conditions that produce rapid fatigue. An extensive depletion of adenine nucleotide content by the deamination of AMP to IMP + NH3, typical of fast-twitch muscle, does not occur. We evaluated whether this response of slow-twitch muscle could be simply due to failure of synaptic transmission or related to cellular conditions influencing enzyme activity. Stimulation of soleus muscles in situ via the nerve or directly in the presence of curare at 120 tetani/min for 3 min resulted in extensive fatigue but normal ATP contents. Thus the lack of ATP depletion must be related to cellular events distal to neuromuscular transmission. Even nerve and direct muscle stimulation (with curare) during ischemia did not cause a large depletion of ATP or a large elevation of lactate content (12.0 +/- 0.7 mumol/g), even though the decline in tension was essentially complete. However, if the same tension decline during ischemia was prolonged by stimulating for 10 min at 12 tetani/min a large decrease in ATP (2.24 +/- 0.09 mumol/g) and increase in IMP (2.47 +/- 0.16 mumol/g) and lactate (30.4 +/- 2.0 mumol/g) content occurred. Thus adenine nucleotide deamination to IMP can occur in slow-twitch muscle during specific contraction conditions. The cellular events leading to the activation of AMP deaminase require an intense contraction condition and may be related to acidosis caused by a high lactate content.
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Umashankar, Abishek, and Prashanth Prabhu. "The application of vagus nerve stimulation in individuals with misophonia." Neuroscience Research Notes 3, no. 5 (October 11, 2021): 36–43. http://dx.doi.org/10.31117/neuroscirn.v3i5.105.
Abstract:
Stimulating the Vagus nerve helps maintain the autonomic tone, indicating stabilising any hyperactivity in the nervous system. The vagus nerve stimulation is applied in individuals with seizures, depression, sepsis, pain, obesity, cardiovascular disease, lung disease, diabetes, stroke, and traumatic brain injury. Auditory neuroscience has been widely applied in individuals with tinnitus and has been demonstrated as a successful neuromodulation technique. Individuals with peripheral lesions of the hair cells induce a maladaptive change in the plasticity resulting in hyperactivity in the auditory and non-auditory structures. In order to reduce this hyperactivity, neuromodulation techniques such as; transcranial magnetic stimulation, transcranial direct current stimulation, transcranial alternating current stimulation, transcranial random noise stimulation, neurofeedback, epidural and subdural cortical and deep brain stimulation. The vagus nerve stimulation is also one form of neuromodulation technique considered to reduce the symptoms of tinnitus. It is believed that the ramus Auricularis Nervi vagi, an afferent sensory branch of the vagus nerve, innervates the afferent sensory branch of the vagus nerve, the ramus auricularis nervi vagi also innervate the outer ear canal and parts of the auricle. This auricular branch of the vagus nerve also called Arnold's nerve, which gives a projection to the nucleus of the solitary tract. The vagus nerve stimulation in individuals with tinnitus works to activate the auricular branch of the vagus nerve to reduce its symptoms. A similar principle of vagus nerve stimulation can be tried upon in individuals with misophonia. Literatures states that individuals with misophonia have hyperactivity in their non-classical auditory pathway that can be suppressed with the help of vagus nerve stimulation. The article discusses the possible effects of vagus nerve stimulation in individuals with misophonia.
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Yang, Hong, Gerry Shaw, and Mohan K. Raizada. "ANG II stimulation of neuritogenesis involves protein kinase B in brain neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 1 (July 1, 2002): R107—R114. http://dx.doi.org/10.1152/ajpregu.00611.2001.
Abstract:
Stimulation of the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (PKB) signal transduction pathway has been linked to the neuromodulatory action of ANG II in the brain neurons of the spontaneously hypertensive rat (Yang H and Raizada MK. J Neurosci 19: 2413–2423, 1999). The cellular consequences of this signaling pathway, however, remain unknown in the brain neurons from the normotensive rat. The present study was designed to test the hypothesis that the PI3K-PKB signaling cascade activates an ANG II-mediated neuritogenic action by stimulating cellular growth-associated protein-43 (GAP-43) and neurite extension in Wistar-Kyoto rat brain neurons. ANG II activation of the ANG II type 1 receptor caused increases in PKB activity, cellular GAP-43 levels, and neurite extension in a time- and dose-dependent manner. Depletion of PKB by specific antisense oligonucleotides attenuated ANG II stimulation of both GAP-43 and neurite extension. PKB involvement in neuritogenic action is further supported by the observation that neurons that overexpress PKB develop extensive neuronal processes in the absence of ANG II. These observations demonstrate that PKB is directly involved in ANG II-mediated effects and may recruit both nuclear and cytoplasmic signaling systems for this action.
33
Downing, J. R., C. W. Rettenmier, and C. J. Sherr. "Ligand-induced tyrosine kinase activity of the colony-stimulating factor 1 receptor in a murine macrophage cell line." Molecular and Cellular Biology 8, no. 4 (April 1988): 1795–99. http://dx.doi.org/10.1128/mcb.8.4.1795-1799.1988.
Abstract:
Metabolic labeling of simian virus 40-immortalized murine macrophages with 32Pi and immunoblotting with antibodies to phosphotyrosine demonstrated that the c-fms proto-oncogene product (colony-stimulating factor 1 [CSF-1] receptor) was phosphorylated on tyrosine in vivo and rapidly degraded in response to CSF-1. Stimulation of the CSF-1 receptor also induced immediate phosphorylation of several other cellular proteins on tyrosine. By contrast, the mature cell surface glycoprotein encoded by the v-fms oncogene was phosphorylated on tyrosine in the absence of CSF-1, suggesting that it functions as a ligand-independent kinase.
34
Downing, J. R., C. W. Rettenmier, and C. J. Sherr. "Ligand-induced tyrosine kinase activity of the colony-stimulating factor 1 receptor in a murine macrophage cell line." Molecular and Cellular Biology 8, no. 4 (April 1988): 1795–99. http://dx.doi.org/10.1128/mcb.8.4.1795.
Abstract:
Metabolic labeling of simian virus 40-immortalized murine macrophages with 32Pi and immunoblotting with antibodies to phosphotyrosine demonstrated that the c-fms proto-oncogene product (colony-stimulating factor 1 [CSF-1] receptor) was phosphorylated on tyrosine in vivo and rapidly degraded in response to CSF-1. Stimulation of the CSF-1 receptor also induced immediate phosphorylation of several other cellular proteins on tyrosine. By contrast, the mature cell surface glycoprotein encoded by the v-fms oncogene was phosphorylated on tyrosine in the absence of CSF-1, suggesting that it functions as a ligand-independent kinase.
35
Huston, D. P., R. N. Jenkins, S. E. Gresens, R. Smith, and R. R. Rich. "Cellular requirements for the generation of primary cell-mediated lympholysis responses to Qa-1 antigens." Journal of Immunology 134, no. 4 (April 1, 1985): 2198–204. http://dx.doi.org/10.4049/jimmunol.134.4.2198.
Abstract:
Abstract Mixed leukocyte cultures (MLC) between NZB responder spleen cells and Qa-1-disparate stimulator spleen cells were employed to determine the cellular requirements for the generation of primary anti-Qa-1 cell-mediated lympholysis (CML) responses. Although primary anti-Qa-1 cytotoxic lymphocytes (CTL) were generated during H-2-homologous stimulation, anti-Qa-1 CTL were not detectable from MLC in which the stimulators were H-2 allogeneic. Anti-Qa-1 CTL also were not generated from MLC in which the stimulators were semiallogeneic. Thus, H-2 identity between responder and stimulator cells was not sufficient to permit the generation of primary anti-Qa-1 CTL when H-2 disparity was also present. The capacity for H-2 disparity to prevent anti-Qa-1 CML responses was further demonstrated in MLC containing both H-2-allogeneic and H-2-homologous stimulator cells. Therefore, in subsequent studies we employed NZB responders and H-2-homologous, Qa-1-disparate stimulators. When various subpopulations of stimulator cells were studied for their ability to induce anti-Qa-1 CTL, nylon wool-adherent cells were found to be potent stimulators, but nylon wool-nonadherent cells were not. Furthermore, depletion of macrophages from the stimulator population abrogated the generation of anti-Qa-1 CML responses, despite the presence of responder macrophages in the culture. In contrast, all fractionated subpopulations stimulated anti-H-2 CML responses. When macrophage-enriched cells were used as stimulators, anti-Qa-1 CTL could be generated with approximately 80-fold fewer stimulator cells than when unfractionated splenocytes were used as stimulators. These findings indicated that stimulator macrophages were essential for the generation of primary anti-Qa-1 CTL. Direct evidence for macrophage expression of Qa-1-antigens was obtained by using a Qa-1b-specific CTL clone. These studies provide i) the first evidence for Qa-1 expression on macrophages, ii) a basis for comparison of the cellular interactions necessary to generate CTL against H-2K/D-encoded vs Qa-1-encoded class 1 antigens, and iii) a model for investigating the mechanisms responsible for the immunodominance of H-2K/D alloantigens.
36
Rosenberg, Nahum. "The role of the cytoskeleton in mechanotransduction in human osteoblastlike cells." Human & Experimental Toxicology 22, no. 5 (May 2003): 271–74. http://dx.doi.org/10.1191/0960327103ht362oa.
Abstract:
The regulation of osteoblast proliferation is a key factor in maintaining bone mass. The enhancement of this process can be achieved by stimulating the proliferation of these cells. Mechanical stimulation is one of the important enhancing factors, but the exact cellular mechanisms of mechanical stimulation, i.e., mechanotransduction, are unknown. In order to investigate the role of the cytoskeleton components in mechanotransduction for cell proliferation, I compared the total DNA content in cultured replicates of osteoblast-like cells derived from three human donors following their exposure to enhancing mechanical stimulation, with and without added specific microtubular and microfilament polymerization blockers (Colchicin and Cytochalasin D, respectively). The results revealed the essential and unique role of the microtubular component of the cytoskeleton in mechanotransduction for proliferation by showing that Colchicin blocked the expected increase in the DNA content after mechanical stimulation of the cultured replicates without altering the total DNA content in replicates at static conditions. Conversely, a specific blockage of the microfilament polymerization presented uniform cytotoxic effect in both static and biomechanically active environments. Since previous reports indicated the essential role of microfilament polymerization for the osteoblast metabolic activity, the results of this study further support the hypothesis that the mechanotransduction mechanisms for proliferation and metabolic activity are mediated by different intracellular pathways.
37
Woller, Michael J., Gary T. Campbell, and Charles A. Blake. "Induction of Cellular Follicle-Stimulating Hormone in the Hamster Adenohypophysis Requires Intermittent Stimulation by Luteinizing Hormone Releasing Hormone." Journal of Neuroendocrinology 7, no. 5 (May 1995): 393–400. http://dx.doi.org/10.1111/j.1365-2826.1995.tb00774.x.
38
Westerblad, H., J. A. Lee, J. Lannergren, and D. G. Allen. "Cellular mechanisms of fatigue in skeletal muscle." American Journal of Physiology-Cell Physiology 261, no. 2 (August 1, 1991): C195—C209. http://dx.doi.org/10.1152/ajpcell.1991.261.2.c195.
Abstract:
Prolonged activation of skeletal muscle leads to a decline of force production known as fatigue. In this review we outline the ionic and metabolic changes that occur in muscle during prolonged activity and focus on how these changes might lead to reduced force. We discuss two distinct types of fatigue: fatigue due to continuous high-frequency stimulation and fatigue due to repeated tetanic stimulation. The causes of force decline are considered under three categories: 1) reduced Ca2+ release from the sarcoplasmic reticulum, 2) reduced myofibrillar Ca2+ sensitivity, and 3) reduced maximum Ca(2+)-activated tension. Reduced Ca2+ release can be due to impaired action potential propagation in the T tubules, and this is a principal cause of the tension decline with continuous tetanic stimulation. Another type of failing Ca2+ release, which is homogeneous across the fibers, is prominent with repeated tetanic stimulation; the underlying mechanisms of this reduction are not fully understood, although several possibilities emerge. Changes in intracellular metabolites, particularly increased concentration of Pi and reduced pH, lead to reduced Ca2+ sensitivity and reduced maximum tension, which make an important contribution to the force decline, especially with repeated tetanic stimulation.
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Funke, Klaus, and Alia Benali. "Cortical cellular actions of transcranial magnetic stimulation." Restorative Neurology and Neuroscience 28, no. 4 (2010): 399–417. http://dx.doi.org/10.3233/rnn-2010-0566.
40
Levy, Estrella Mariel, María Paula Roberti, and José Mordoh. "Natural Killer Cells in Human Cancer: From Biological Functions to Clinical Applications." Journal of Biomedicine and Biotechnology 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/676198.
Abstract:
Natural killer (NK) cells are central components of the innate immunity. In murine models, it has been shown that NK cells can control both local tumor growth and metastasis due to their ability to exert direct cellular cytotoxicity without prior sensitization and to secrete immunostimulatory cytokines like IFN-γ. The latter participates in cancer elimination by inhibiting cellular proliferation and angiogenesis, promoting apoptosis, and stimulating the adaptive immune system, and it is instrumental for enhancing Ag processing and presentation. Nevertheless, NK cells display impaired functionality and capability to infiltrate tumors in cancer patients. Also, NK cells are feasible targets of stimulation to participate in immunotherapeutic approaches like antibody-based strategies and adoptive cell transfer. Thus, multiple attempts currently aim to manipulate NK for utilization in the immunotherapy of cancer.
41
Hooper, S. L., and M. Moulins. "Cellular and synaptic mechanisms responsible for a long-lasting restructuring of the lobster pyloric network." Journal of Neurophysiology 64, no. 5 (November 1, 1990): 1574–89. http://dx.doi.org/10.1152/jn.1990.64.5.1574.
Abstract:
1. In the lobster Palinurus vulgaris a sensory input in the lateral posterolateral nerve (lpln) of the stomatogastric nervous system (STS) is able to turn on the cardiac sac (CS) network and to induce dramatic long-lasting alterations in the output of the pyloric network. This long-lasting alteration of pyloric network output consists primarily of changes in the activity of the two neurons that innervate the muscles of the cardiopyloric valve of the stomach, with the dilator neuron (the ventricular dilator, VD) transferring from the pyloric network to the CS network and the constrictor neuron (the inferior cardiac, IC) shifting to fire earlier in the pyloric pattern. 2. The inferior ventricular (IV) neurons of the CS network make complex multiaction synaptic connections onto several pyloric neurons in a related species, Panulirus interruptus. We show that many of the short-term alterations in pyloric activity observed during CS network bursts in Palinurus are due to similar IV neuron synaptic connections. However, the long-lasting effects of lpln stimulation on pyloric output are not due to this synaptic input, because 1) direct activation of the IV neurons does not induce long-lasting changes in pyloric activity and 2) pharmacologic disconnection of this synaptic input does not abolish lpln stimulation's long-lasting effects. Lpln stimulation therefore activates two different neuronal inputs to the pyloric network. 3. The transfer of the VD neuron from the pyloric to the CS network is the result of the concerted actions of these two inputs. Lpln stimulation turns on the CS network, and the IV neurons of the CS network excite the VD neuron and ensure it fires with the CS network. The second neuronal input (that not involving known CS network neurons) abolishes in a long-lasting fashion the VD neuron regenerative (plateau) properties, and thus suppresses the ability of the VD neuron to participate in the pyloric rhythmic pattern between CS network bursts. 4. Experimental manipulation of VD neuron activity can both mimic and reverse the effects of lpln stimulation on the IC neuron. The changes in IC neuron activity are therefore not due to direct lpln-activated synaptic input onto the IC neuron, but instead are indirect "network" effects arising from the changes in VD neuron activity.
42
Puissant, C., M. Bayat-Sarmadi, E. Devinoy, and L.-M. Houdebine. "Variation of transferrin mRNA concentration in the rabbit mammary gland during the pregnancy–lactation–weaning cycle and in cultured mammary cells. A comparison with the other major milk protein mRNAs." European Journal of Endocrinology 130, no. 5 (May 1994): 522–29. http://dx.doi.org/10.1530/eje.0.1300522.
Abstract:
Puissant C, Bayat-Sarmadi M, Devinoy E, Houdebine L-M. Variation of transferrin mRNA concentration in the rabbit mammary gland during the pregnancy–lactation–weaning cycle and in cultured mammary cells. A comparison with the other major milk protein mRNAs. Eur J Endocrinol 1994;130:522–9. ISSN 0804–4643 The concentration of transferrin mRNA was evaluated during pregnancy and lactation in rabbit mammary gland and liver using northern blot and dot blot assays. Transferrin mRNA was present in the virgin rabbit mammary gland and its concentration increased as pregnancy proceeded, with a major enhancement after day 15. A high concentration was reached 3 days after parturition, with no additional increase during lactation and with a marked decline after weaning. During the same period, the concentration of transferrin mRNA showed only a very weak variation in liver. This mRNA was six times more abundant in mammary gland than in liver of lactating rabbit. The accumulation of transferrin mRNA in the mammary gland was concomitant with the accumulation of αs1-, β-, kcasein and WAP (whey acidic protein) mRNAs. The concentration of glyceraldehyde 3-phosphate dehydrogenase mRNA, taken as a non-inducible control mRNA, declined progressively during pregnancy to reach its lower level in lactation. These observations suggest that casein, WAP and transferrin mRNAs are subjected to a similar control mechanism in vivo, at least in the second half of pregnancy and during lactation. Experiments carried out in vitro using isolated rabbit epithelial mammary cells cultured on collagen I gel indicated that transferrin mRNA was abundant and only weakly inducible by the lactogenic hormones insulin, cortisol and prolactin, as opposed to caseins and WAP mRNAs. R5020, an analogue of progesterone, inhibited at most very slightly the accumulation of αs1-casein mRNA in the presence of prolactin and it did not reduce the expression of transferrin gene. The mammary cells cultured on a plastic support contained much less transferrin mRNA than those maintained on collagen gel or on EHS (Engelbreth–Holm–Swarm) extracellular matrix independently of any hormonal stimulation. These data suggest that although caseins, WAP and transferrin mRNAs have parallel variations during the pregnancy–lactation–weaning cycle, they are subjected to different mechanisms of regulation at the molecular level. The accumulation of the mRNAs for caseins and WAP is positively regulated by lactogenic hormones and by the presence of the extracellular matrix, whereas the accumulation of transferrin mRNA is positively regulated essentially by the presence of the matrix. The fact that the levels of all the mRNAs studied here are increased simultaneously as progesterone starts declining suggests that the steroid controls the action of a factor, possibly the presence of the extracellular matrix, that regulates the expression of all the milk protein genes. L-M Houdebine, Unité de Differenciation Cellulaire, Institut National de la Recherche Agronomique, 78352 Jouy-en-Josas Cédex, France
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Marks, J. D., D. F. Donnelly, and G. G. Haddad. "Adenosine-induced inhibition of vagal motoneuron excitability: receptor subtype and mechanisms." American Journal of Physiology-Lung Cellular and Molecular Physiology 264, no. 2 (February 1, 1993): L124—L132. http://dx.doi.org/10.1152/ajplung.1993.264.2.l124.
Abstract:
With the use of intracellular techniques and a medullary slice preparation, we examined the changes in cellular and membrane properties of single adult rat vagal motoneurons during exposure to potent and specific agonists and antagonists of adenosine A1 and A2 receptors. A1 receptor stimulation increased input resistance, but markedly reduced spontaneous neuronal firing and increased rheobase. A1 agonists also increased the amplitude of the action potential afterhyperpolarization (AHP) in a dose-dependent manner. Prior treatment with A1 antagonists blocked these electrophysiological effects. Blockade of Ca2+ entry with Co2+ abolished the AHP increase. Synaptic blockade with both tetrodotoxin and high Mg2+, low Ca2+ solutions prevented the increase in input resistance. A2 receptor stimulation was without effect. Perfusion with adenosine in the presence of dipyridamole caused effects similar to A1 agonist stimulation, but no effect in the absence of dipyridamole. These results show that adenosine decreases vagal motoneuron excitability by stimulating A1 receptors. Our data also support the idea that the adenosine-induced decrease in excitability is presynaptic in nature. In addition, the AHP increase may be mediated by enhanced Ca2+ entry into the postsynaptic neuron.
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Borsuk, Daria, Maryna Bondarenko, and Olga Zaytseva. "TRANSCRANIAL NEAR-INFRARED THERAPY FOR COGNITIVE PERFORMANCE AND NEUROLOGICAL STATUS ENHANCEMENT." Grail of Science, no. 36 (February 26, 2024): 447–52. http://dx.doi.org/10.36074/grail-of-science.16.02.2024.078.
Abstract:
There is a growing interest in non-invasive treatment options in the field of neurotherapy with transcranial near-infrared (tNIR) light demonstrating promising results across a broad spectrum of neurological disorders. This paper explores the therapeutic potential of tNIR and its efficacy in stimulating cellular functions to improve outcomes in neurodegenerative diseases such as dementia, Parkinson’s disease, Alzheimer’s disease as well as traumatic brain injury, stroke recovery, neuroinflammatory conditions, depression, and BDNF stimulation. Through the direct transcranial application of low-level wavelengths of red or near-infrared light, tNIR stimulation activates neural tissue metabolism, modulates brain function, enhances cognitive performance, and alleviates chronic brain inflammation. This study synthesizes current research findings to illustrate the mechanisms underlying tNIR's action, evaluates its potential across various neurotherapeutic applications, and presents an overview of its current therapeutic implementations. Studies demonstrate the tNIR's capacity to penetrate the skull, stimulate neural tissues, enhance mitochondrial function, and increase ATP production. tNIR has been shown to improve cognitive functions and reduce neuroinflammation, offering a novel approach to treating neurodegenerative conditions. tNIR’s application extends to stroke recovery, where it has been shown to reduce infarct zones as well as nerve regeneration through promoting synaptogenesis and BDNF stimulation.
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Chalisova, N. I., and A. E. Korovin. "PROTECTIVE EFFECT OF AMINO ACIDS IN THE ORGANOTYPIC CULTURE OF THE ECTODERMAL GENESIS TISSUES AT THE CYCLOPHOSPHANE PRESENCE." Bulletin of the Russian Military Medical Academy 19, no. 4 (December 15, 2017): 47–52. http://dx.doi.org/10.17816/brmma12431.
Abstract:
The effect of the 20 coded amino acids was investigated on the development of the processes of the proliferation in the organotypic tissue culture of rat skin and brain cortex. Some amino acids at 0.05 ng/ml concentration stimulated the cellular proliferation in the growth zone of explants. The other inhibited it. The combination of the stimulating and inhibiting amino acids - Leucine with Proline or Tyrosine-, lead to the proliferation stimulation by 24-32%. The mustard-like agent cyclophosphane at 1 mg/ml concentration inhibited the cellular proliferation. However, the delay of this inhibiting effect of cyclophosphane was observed by the using of combination of amino acids with cyclophosphane. Thus, the amino acids can be protectors of the cellular proliferation by the toxic effect of the cyclophosphane on the tissues of the ectodermal genesis. This effect can be used for the treatment of the mustard injury of skin, brain cortex and for the delay of the adverse effect of cytostatic in oncology
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Ariel, M., and T. X. Fan. "Electrophysiological evidence for a bisynaptic retinocerebellar pathway." Journal of Neurophysiology 69, no. 4 (April 1, 1993): 1323–30. http://dx.doi.org/10.1152/jn.1993.69.4.1323.
Abstract:
1. Electrical microstimulation was applied to an in vitro turtle brain preparation while recording extracellular activity from the cerebellar cortex. A visual input to the cerebellum was investigated by measuring spike responses evoked by stimulation of drifting visual patterns imaged onto the contralateral retinal eyecup. A vestibular input was assessed by extracellular field potentials following brief current pulses through monopolar suction electrodes holding the eighth cranial nerve (nVIII). 2. The cortical topography of visual and vestibular inputs was first examined. Visual units and vestibular fields show considerable topographic overlap in the rostrolateral quadrant of the cerebellum. In addition, granule layer units were isolated that responded to current stimulation of nVIII (60-150 microA monopolar). In some cases, spikes occurred at short and fixed latency after each current pulse for stimulus frequencies of 100 Hz. The responses of these units suggest a direct path between the stimulating and recording electrodes without intervening synapses. Alternatively, extracellular units were also encountered that responded with longer, more variable latencies but only for low stimulation frequencies (< or = 20 Hz). Of the units that responded to nVIII stimulation, three units also responded to visual stimuli, yet those units all failed to follow high-frequency stimulation of nVIII. This cortical area may then be a site for convergence of visual and vestibular signals on postsynaptic cells. 3. The cellular identity of the visual units in the granule layer and the visual pathways leading there were next investigated.(ABSTRACT TRUNCATED AT 250 WORDS)
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Zhang, Jianwei, Wenjin Zhu, Jingyi Liang, Limei Li, Longhui Zheng, Xiaowen Shi, Chao Wang, Youming Dong, Cheng Li, and Xiuhong Zhu. "In Situ Synthesis of Gold Nanoparticles from Chitin Nanogels and Their Drug Release Response to Stimulation." Polymers 16, no. 3 (January 31, 2024): 390. http://dx.doi.org/10.3390/polym16030390.
Abstract:
In this study, gold nanoparticles (AuNPs) were synthesized in situ using chitin nanogels (CNGs) as templates to prepare composites (CNGs@AuNPs) with good photothermal properties, wherein their drug release properties in response to stimulation by near-infrared (NIR) light were investigated. AuNPs with particle sizes ranging from 2.5 nm to 90 nm were prepared by varying the reaction temperature and chloroauric acid concentration. The photothermal effect of different materials was probed by near-infrared light. Under 1 mg/mL of chloroauric acid at 120 °C, the prepared CNGs@AuNPs could increase the temperature by 32 °C within 10 min at a power of 2 W/cm2. The Adriamycin hydrochloride (DOX) was loaded into the CNGs@AuNPs to investigate their release behaviors under different pH values, temperatures, and near-infrared light stimulations. The results showed that CNGs@AuNPs were pH- and temperature-responsive, suggesting that low pH and high temperature could promote drug release. In addition, NIR light stimulation accelerated the drug release. Cellular experiments confirmed the synergistic effect of DOX-loaded CNGs@AuNPs on chemotherapy and photothermal therapy under NIR radiation.
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Zhao, Yangbing, David Boczkowski, Smita K. Nair, and Eli Gilboa. "Inhibition of invariant chain expression in dendritic cells presenting endogenous antigens stimulates CD4+ T-cell responses and tumor immunity." Blood 102, no. 12 (December 1, 2003): 4137–42. http://dx.doi.org/10.1182/blood-2003-06-1867.
Abstract:
Abstract Induction of potent and sustained antiviral or antitumor immunity is dependent on the efficient activation of CD8+ and CD4+ T cells. While dendritic cells constitute a powerful platform for stimulating cellular immunity, presentation of endogenous antigens by dendritic cells transfected with nucleic acid-encoded antigens favors the stimulation of CD8+ T cells over that of CD4+ T cells. A short incubation of mRNA-transfected dendritic cells with antisense oligonucleotides directed against the invariant chain enhances the presentation of mRNA-encoded class II epitopes and activation of CD4+ T-cell responses in vitro and in vivo. Immunization of mice with the antisense oligonucleotide-treated dendritic cells stimulates a more potent and longer lasting CD8+ cytotoxic T-cell (CTL) response and enhances the antitumor efficacy of dendritic cell-based tumor vaccination protocols. Transient inhibition of invariant chain expression represents a simple and general method to enhance the stimulation of CD4+ T-cell responses from endogenous antigens. (Blood. 2003;102:4137-4142)
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Toka, Felix Ngosa, Kiera Dunaway, Felicia Smaltz, Lidia Szulc-Dabrowska, Jenny Drnevich, Matylda Barbara Mielcarska, Magdalena Bossowska-Nowicka, and Matthias Schweizer. "Bacterial and viral pathogen associated molecular patterns create different early transcriptomic landscapes in bovine macrophages." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 59.19. http://dx.doi.org/10.4049/jimmunol.200.supp.59.19.
Abstract:
Abstract Pathogens stimulate immune functions of dendritic cells and macrophages (MΦ). There is no clear understanding of the nature of transcriptomic changes caused in cells upon stimulation through pattern recognition receptors by various pathogens. Our study investigated the early transcriptomic changes of bovine MΦ in response to stimulation with CpG or poly I:C. BMΦ were incubated with CpG or pI:C for 6 h and RNA isolated for transcriptomic analysis by RNAseq. Bioinformatics tools were used to analyze differentially expressed genes (DE). Results showed that, of the 13740 genes mapped to the bovine genome, 2245 had p-value ≤0.05, deemed as DE. At 6 h post stimulation, pI:C induced a different transcriptomic profile from that induced by CpG. CpG upregulated 347 and downregulated 210 genes. pI:C upregulated 761 and downregulated 414 genes. The highest expressed genes in both stimulations belonged to the TNF superfamily, TNFSF18 (CpG) and TNFSF10 (pI:C) and in both cases the lowest downregulated gene was CYP1A1. CpG induced canonical pathways that are unrelated to immune response in BMΦ in contrast to pI:C which induced canonical pathways directly related to antiviral immune functions dominated by IFN signalling genes. The transcriptomic profile after pI:C stimulation was consistent with TLR3 signalling. CpG influenced expression of genes involved in molecular and cellular functions in free radical scavenging. We conclude that CpG and pI:C induce different early transcriptional landscapes in BMΦ line, but each suited to a specific function of BMΦ during interaction with pathogens.
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DESSAUGE, Frédéric, Cindy SCHLEDER, Marie-Héléne PERRUCHOT, and Karl ROUGER. "Développement des modèles de culture cellulaire de muscle en 3D : de nouvelles opportunités pour les productions animales." INRAE Productions Animales 36, no. 2 (September 13, 2023). http://dx.doi.org/10.20870/productions-animales.2023.36.2.7626.
Abstract:
Le muscle squelettique est organisé en faisceau de fibres musculaires de différentes tailles et parcouru par des réseaux vasculaires et nerveux. Les cellules satellites sont des cellules souches logées le long des fibres musculaires et sont à la base des progéniteurs myogéniques (myoblastes). Les cellules satellites peuvent être aisément extraites du muscle et cultivées. Les modèles typiques de culture en deux dimensions (2D) de cellules dérivées du muscle squelettique ne peuvent pas recréer complètement l'organisation et la fonction des tissus musculaires vivants, ce qui limite leurs utilités dans les études physiologiques approfondies. Le développement de modèles de culture 3D fonctionnels offre une opportunité unique pour mimer les tissus vivants et modéliser les maladies musculaires. A cet égard, ce nouveau type de modèles in vitro augmente significativement notre compréhension de l'implication des différentes populations cellulaires dans la formation du muscle squelettique et de leurs interactions, ainsi que les modalités de réponse d'un muscle pathologique à de nouvelles thérapies. Ce deuxième point pourrait conduire à l'identification de traitements efficaces. Dans cette synthèse, nous traitons des progrès significatifs qui ont été réalisés ces dernières années pour concevoir des structures ressemblant à des tissus musculaires, fournissant des outils utiles pour étudier le comportement des cellules souches résidentes. Nous nous intéressons plus particulièrement au développement de systèmes basés sur des « myosphères » et des faisceaux de fibres ou « myobundles » ainsi que sur les systèmes de bio-impression. Les protocoles de stimulation électrique/mécanique et les systèmes de co-culture développés pour améliorer le processus et les fonctionnalités de maturation des tissus seront également présentés. La formation de tissus musculaires biomimétiques représente une nouvelle technologie pour étudier la fonction et l'organisation spatiale des muscles squelettiques dans un grand nombre de contextes physiologiques, pathologiques et agronomiques.