Differential Cell Replication within the Periosteum of the Pig Mandibular Ramus

AbstractThe unique apical hook in dicotyledonous plants protects the shoot apical meristem and cotyledons when seedlings emerge through the soil. Its formation involves differential cell growth under the coordinated control of plant hormones, especially ethylene and auxin. Microtubules are essential players in plant cell growth that are regulated by multiple microtubule-associated proteins (MAPs). However, the role and underlying mechanisms of MAP-microtubule modules in differential cell growth are poorly understood. In this study, we found that the previously uncharacterized Arabidopsis MAP WAVE-DAMPENED2-LIKE4 (WDL4) protein plays a positive role in apical hook opening. WDL4 exhibits a temporal expression pattern during hook development in dark-grown seedlings that is directly regulated by ethylene signaling. WDL4 mutants showed a delayed hook opening phenotype while overexpression of WDL4 resulted in enhanced hook opening. In particular, wdl4-1 mutants exhibited stronger auxin accumulation in the concave side of the apical hook. Furthermore, the regulation of the auxin maxima and trafficking of the auxin efflux carriers PIN-FORMED1 (PIN1) and PIN7 in the hook region is critical for WDL4-mediated hook opening. Together, our study demonstrates that WDL4 positively regulates apical hook opening by modulating auxin distribution, thus unraveling a mechanism for MAP-mediated differential plant cell growth.

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Weak Electromagnetic Fields Accelerate Fusion of Myoblasts

International Journal of Molecular Sciences ◽

10.3390/ijms22094407 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4407

Author(s):

Dana Adler ◽

Zehavit Shapira ◽

Shimon Weiss ◽

Asher Shainberg ◽

Abram Katz

Keyword(s):

Skeletal Muscle ◽

Cell Membrane ◽

Cell Fusion ◽

Electromagnetic Fields ◽

Muscle Development ◽

K Channel ◽

Gambogic Acid ◽

Cell Replication ◽

Myotube Formation ◽

Primary Myoblast

Weak electromagnetic fields (WEF) alter Ca2+ handling in skeletal muscle myotubes. Owing to the involvement of Ca2+ in muscle development, we investigated whether WEF affects fusion of myoblasts in culture. Rat primary myoblast cultures were exposed to WEF (1.75 µT, 16 Hz) for up to six days. Under control conditions, cell fusion and creatine kinase (CK) activity increased in parallel and peaked at 4–6 days. WEF enhanced the extent of fusion after one and two days (by ~40%) vs. control, but not thereafter. Exposure to WEF also enhanced CK activity after two days (almost four-fold), but not afterwards. Incorporation of 3H-thymidine into DNA was enhanced by one-day exposure to WEF (~40%), indicating increased cell replication. Using the potentiometric fluorescent dye di-8-ANEPPS, we found that exposure of cells to 150 mM KCl resulted in depolarization of the cell membrane. However, prior exposure of cells to WEF for one day followed by addition of KCl resulted in hyperpolarization of the cell membrane. Acute exposure of cells to WEF also resulted in hyperpolarization of the cell membrane. Twenty-four hour incubation of myoblasts with gambogic acid, an inhibitor of the inward rectifying K+ channel 2.1 (Kir2.1), did not affect cell fusion, WEF-mediated acceleration of fusion or hyperpolarization. These data demonstrate that WEF accelerates fusion of myoblasts, resulting in myotube formation. The WEF effect is associated with hyperpolarization but WEF does not appear to mediate its effects on fusion by activating Kir2.1 channels.

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STEM-09. INTRINSIC INTERFERON SIGNALING REGULATES THE CELL DEATH OF GLIOBLASTOMA STEM CELLS

Neuro-Oncology ◽

10.1093/neuonc/noaa215.826 ◽

2020 ◽

Vol 22 (Supplement_2) ◽

pp. ii198-ii198

Author(s):

Sabbi Khan Khan ◽

Emmanuel Martinez-Ledesma ◽

Sandeep Mittal ◽

Kaitlin Gandy ◽

Kristin Alfaro-Munoz ◽

...

Keyword(s):

Cell Death ◽

Treatment Resistance ◽

Primary Brain Tumor ◽

The Cancer Genome Atlas ◽

Cytokine Signaling ◽

Type I ◽

Type Ii ◽

Mechanistic Investigation ◽

Differential Cell ◽

Stat1 Signaling

Abstract Glioblastoma (GBM) is the most common, highly aggressive, and lethal primary brain tumor in adults. Interferon (IFN)-mediated signal transducer and activator of transcription 1 (STAT1) signaling contributes to various aspects of stemness, cell death, cytokine signaling in immune and non-immune cells. However, the role of IFN/STAT1 signaling in stemness, cell death and treatment resistance in GBM is unclear. This study aimed to investigate the cancer cell-intrinsic IFN/STAT1 signaling and its role in cell proliferation, stemness, and apoptosis. By using the metagene scores for type I and type II IFN-responsive genes, we evaluated basal IFN/STAT1 signaling in The Cancer Genome Atlas (TCGA) and in patient-derived cohorts of stem-like cells (GSCs) RNA expression datasets. In-silico analyses were further validated for the constitutive IFN signaling in a subset of GSCs using qPCR, WB and ELISA assays. We employed pharmacological activators and/or inhibitors of IFN/STAT1 signaling in GSCs to study its role in stemness and cell death. We found differential cell-intrinsic type I and type II IFN-signaling markers in GSCs and GBM tumors. High IFN-signaling is associated with mesenchymal phenotype and poor survival outcomes. Acute and chronic GSC exposure to recombinant IFNs reversibly activated both type I and II IFN-signaling in GSCs. IFN-β exposure induced apoptosis in intrinsically high IFN/STAT1-signaling GSCs, but not in the low IFN/STAT1-signaling GSCs. In summary, our findings demonstrate that GBM exhibit differential cell-intrinsic IFN-signaling, and basal IFN/STAT1 is a key factor for IFN-β-mediated cell death in GSCs. However, further mechanistic investigation of intrinsic IFN signaling in GBM, particularly in the stem cell compartment is needed.

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Modelling growth curves of the normal infant’s mandible: 3D measurements using computed tomography

Clinical Oral Investigations ◽

10.1007/s00784-021-03937-1 ◽

2021 ◽

Author(s):

Jan Aart M. Schipper ◽

Manouk J. S. van Lieshout ◽

Stefan Böhringer ◽

Bonnie L. Padwa ◽

Simon G. F. Robben ◽

...

Keyword(s):

Computed Tomography ◽

Growth Models ◽

Normal Growth ◽

Growth Patterns ◽

Ct Scans ◽

Mandibular Ramus ◽

Linear Measurements ◽

Mandibular Growth ◽

Gonial Angle ◽

Mandibular Body

Abstract Objectives Data on normal mandibular development in the infant is lacking though essential to understand normal growth patterns and to discriminate abnormal growth. The aim of this study was to provide normal linear measurements of the mandible using computed tomography performed in infants from 0 to 2 years of age. Material and methods 3D voxel software was used to calculate mandibular body length, mandibular ramus length, bicondylar width, bigonial width and the gonial angle. Intra- and inter-rater reliability was assessed for these measurements. They were found to be sufficient for all distances; intra-class correlation coefficients were all above 0.9. Regression analysis for growth modelling was performed. Results In this multi-centre retrospective study, 109 CT scans were found eligible that were performed for various reasons (e.g. trauma, craniosynostosis, craniofacial abscesses). Craniosynostosis patients had larger mandibular measurements compared to non-craniosynostosis patients and were therefore excluded. Fifty-one CT scans were analysed. Conclusions Analysis showed that the mandible increases more in size vertically (the mandibular ramus) than horizontally (the mandibular body). Most of the mandibular growth occurs in the first 6 months. Clinical relevance These growth models provide insight into normal mandibular development in the first 2 years of life. This reference data facilitates discrimination between normal and abnormal mandibular growth.

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A Morphometric Study of the Maxillary Artery and Lingula in Relation to Mandibular Ramus Osteotomies and TMJ Surgery

European Journal of Dentistry ◽

10.1055/s-0039-1697825 ◽

2010 ◽

Vol 04 (02) ◽

pp. 166-170 ◽

Cited By ~ 3

Author(s):

Huseyin Avni Balcioglu ◽

Cenk Kilic ◽

Altan Varol ◽

Hasan Ozan ◽

Necdet Kocabiyik ◽

...

Keyword(s):

Infratemporal Fossa ◽

Postoperative Hemorrhage ◽

Morphometric Study ◽

Maxillary Artery ◽

Mandibular Ramus ◽

Main Trunk ◽

Tmj Ankylosis ◽

Bony Landmarks ◽

Inferior Border ◽

Mandibular Notch

Objectives: Mandibular osteotomies and resection of the temporomandibular joint (TMJ) ankylosis are the mostly performed surgical procedures in the infratemporal fossa, which is in close proximity with the main trunk of the maxillary artery (MA). It is imperative to avoid the trunk or branches of the maxillary artery, otherwise, massive intraoperative or postoperative hemorrhage may develop. The goal of the study was to investigate the position of the maxillary artery in the infratemporal fossa and the lingula of the mandible.Methods: Significant landmarks were selected on the mandibles of formalin fixed cadavers, and the distances were measured between the maxillary artery and the bony landmarks with a digital caliper.Results: The average distances between the MA and the articular eminence, the medial cortex of the mandibular ramus, the inferior border of the pterygoid fovea and the mandibular notch were 1.67±0.48 mm, 5.38±2.47 mm, 16.84±1.74 mm, 2.94±0.52 mm, respectively. Course pattern of the MA at the subcondylar level was also mapped. In order to determine the position of the lingula, the average distances between the tip of the lingula and the mandibular notch, the inferior border of the ramus, the anterior margin of the ramus and posterior margin of the ramus were measured and found as 15.4±2.1 mm, 49.5±4.3 mm, 18.1±2.7 mm, 16.6±2.5 mm, respectively. No significant differences were found between the right and left sides, for all parameters.Conclusions: The studied parameters will assist and navigate clinicians to determine the anatomic proximity to the maxillary artery, and, minimize the risk of damaging the vessel. (Eur J Dent 2010;4:166-169)

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Insulin Stimulates Primary β-Cell Proliferation via Raf-1 Kinase

Endocrinology ◽

10.1210/en.2007-1557 ◽

2008 ◽

Vol 149 (5) ◽

pp. 2251-2260 ◽

Cited By ~ 56

Author(s):

Jennifer L. Beith ◽

Emilyn U. Alejandro ◽

James D. Johnson

Keyword(s):

Cell Proliferation ◽

Dominant Role ◽

Cell Mass ◽

Diabetes Type 2 ◽

Dominant Negative ◽

Cell Replication ◽

Β Cell ◽

Physiological Control ◽

Primary Mouse

A relative decrease in β-cell mass is key in the pathogenesis of type 1 diabetes, type 2 diabetes, and in the failure of transplanted islet grafts. It is now clear that β-cell duplication plays a dominant role in the regulation of adult β-cell mass. Therefore, knowledge of the endogenous regulators of β-cell replication is critical for understanding the physiological control of β-cell mass and for harnessing this process therapeutically. We have shown that concentrations of insulin known to exist in vivo act directly on β-cells to promote survival. Whether insulin stimulates adult β-cell proliferation remains unclear. We tested this hypothesis using dispersed primary mouse islet cells double labeled with 5-bromo-2-deoxyuridine and insulin antisera. Treating cells with 200-pm insulin significantly increased proliferation from a baseline rate of 0.15% per day. Elevating glucose from 5–15 mm did not significantly increase β-cell replication. β-Cell proliferation was inhibited by somatostatin as well as inhibitors of insulin signaling. Interestingly, inhibiting Raf-1 kinase blocked proliferation stimulated by low, but not high (superphysiological), insulin doses. Insulin-stimulated mouse insulinoma cell proliferation was dependent on both phosphatidylinositol 3-kinase/Akt and Raf-1/MAPK kinase pathways. Overexpression of Raf-1 was sufficient to increase proliferation in the absence of insulin, whereas a dominant-negative Raf-1 reduced proliferation in the presence of 200-pm insulin. Together, these results demonstrate for the first time that insulin, at levels that have been measured in vivo, can directly stimulate β-cell proliferation and that Raf-1 kinase is involved in this process. These findings have significant implications for the understanding of the regulation of β-cell mass in both the hyperinsulinemic and insulin-deficient states that occur in the various forms of diabetes.

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