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55 results for “Primary Cilia”
Confocal microscopy images (CZI files) of human chondrocytes of different resolutions and magnifications with stained nuclei and primary cilia
<p>This dataset is an addition of https://doi.org/10.5281/zenodo.7994589. Here, we have focused on the influence of the magnifications of microscope objectives and image resolution on the results of automated cilia length measurements.</p> <p>1. Methods</p> <p>1.1 Cell culture</p> <p>Human non-degenerative chondrocytes from a 30-year-old male donor (NHAC-kn, CC-2550; LONZA, Walkersville Inc., Walkersville, MD, USA) were used. These chondrocytes were seeded in passage four with a density of 28000 cells/cm<sup>2</sup> on collagen-coated glass coverslips (GG-15-Collagen; Neuvitro Corporation, Camas, WA, USA). The cells were cultivated in 12-well plates (Thermo Fisher Scientific Inc., Waltham, MA, USA) under hypoxic conditions at 37°C, 5% CO<sub>2</sub> and 5% O<sub>2</sub> with different media compositions for three days.<br> The basal medium consisted of Dulbecco’s Modified Eagle Medium (DMEM) (Gibco™) including high glucose (GlutaMAX™), sodium pyruvate supplements (Thermo Fisher Scientific Inc., Waltham, MA, USA), as well as 1% penicillin/streptomycin (Pen/Strep; Thermo Fisher Scientific Inc.), 1% Amphotericin B (Biochrom GmbH, Berlin, Germany), and 50 µg mL<sup>−1</sup> ascorbic acid (Sigma-Aldrich, Merck KGaA, Darmstadt, Germany). To this basal medium, the following supplements were added: ITS with Dexa + IGF-1 + TGF-β1: 1% Insulin-Transferrin-Selenium (ITS+™), 100 nM dexamethasone, 50 ng mL<sup>−1</sup> insulin-like growth factor (IGF)-1 (R&D Systems, Minneapolis, MN, USA) and 50 ng mL<sup>−1</sup> transforming growth factor (TGF)-β1 (Peprotec, Hamburg, Germany).</p> <p>1.2 Immunocytochemistry</p> <p>After three days of cultivation in the different media compositions, the chondrocytes were washed once with phosphate-buffered saline (PBS; Biochrom GmbH, Berlin, Germany) and fixed for 10 min at room temperature (RT) with 4% paraformaldehyde (ROTI ® Histofix, Carl Roth GmbH + Co. KG, Karlsruhe, Germany). After fixation, cells were washed again and permeabilized with 0.2% Triton-X100 (Merck, Darmstadt, Germany) for 10 min. For blocking the unspecific binding sites, cell-seeded coverslips were incubated with bovine serum albumin (BSA; Sigma-Aldrich) with a concentration of 5% in PBS for one hour at RT after another washing step with PBS. To stain the primary cilium, cells were incubated with anti-acetylated α-tubulin (6-11B-1) (RRID: AB 628409) labeled with Alexa Fluor 647 (sc-23950 AF647, Santa Cruz Biotechnology, Dallas, TX, USA) diluted 1:200 in PBS at 4°C overnight. Additionally, the Actin cytoskeleton was stained with Acti-stain 488 Fluorescent Phalloidin (Cytoskeleton, Inc., Denver, CO, USA) diluted 10 in PBS for 30 min at RT. Afterward, cells were washed three times with PBS, and the coverslips were fixed with Fluoroshield™ (Sigma-Aldrich) containing 4’,6-Diamidino-2-phenylindole (DAPI).</p> <p>1.3 Image acquisition</p> <p>Three-dimensional fluorescence images of stained cells were acquired with a ZEISS ELYRA LSM 780 confocal laser scanning microscope (CLSM) (Carl Zeiss AG, Oberkochen, Germany). To find optimal microscopy parameters for automated detection and length measurement of primary cilia, images were recorded using a Plan-Apochromat 63×/1.40 Oil DIC M27 objective (Carl Zeiss AG, Oberkochen, Germany) or an α Plan-Apochromat 100 × /1.46 Oil DIC M27 Elyra objective (Carl Zeiss AG, Oberkochen, Germany) as well as the following resolutions: 1024 × 1024, 2048 × 2048 and 4096 × 4096 pixels resulting in different voxel sizes (see metadata of files).</p>
Confocal microscopy images (CZI files) of human chondrocytes in different cell culture media with stained nuclei and primary cilia
<p>1. Methods</p> <p>1.1 Cell culture</p> <p>For investigating the influence of the cell culture medium composition on the lengths of primary cilia, human non-degenerative chondrocytes from a 30-year-old male donor (NHAC-kn, CC-2550; LONZA, Walkersville Inc., Walkersville, MD, USA) were used. These chondrocytes were seeded in passage four with a density of 28000 cells/cm<sup>2</sup> on collagen-coated glass coverslips (GG-15-Collagen; Neuvitro Corporation, Camas, WA, USA). The cells were cultivated in 12-well plates (Thermo Fisher Scientific Inc., Waltham, MA, USA) under hypoxic conditions at 37°C, 5% CO<sub>2</sub> and 5% O<sub>2</sub> with different media compositions for three days.<br> The basal medium consisted of Dulbecco’s Modified Eagle Medium (DMEM) (Gibco™) including high glucose (GlutaMAX™), sodium pyruvate supplements (Thermo Fisher Scientific Inc., Waltham, MA, USA), as well as 1% penicillin/streptomycin (Pen/Strep; Thermo Fisher Scientific Inc.), 1% Amphotericin B (Biochrom GmbH, Berlin, Germany), and 50 µg mL<sup>−1</sup> ascorbic acid (Sigma-Aldrich, Merck KGaA, Darmstadt, Germany). To this basal medium, different supplements were added, creating four groups:<br> 1) ITS: 1% Insulin-Transferrin-Selenium (ITS+™ Premix, BD Biosciences, Franklin Lakes, NJ, USA),<br> 2) ITS with Dexa: 1% Insulin-Transferrin-Selenium (ITS+™) and 100 nM dexamethasone (Sigma-Aldrich, Merck KGaA, Darmstadt, Germany),<br> 3) ITS with Dexa + IGF-1 + TGF-β1: 1% Insulin-Transferrin-Selenium (ITS+™), 100 nM dexamethasone, 50 ng mL<sup>−1</sup> insulin-like growth factor (IGF)-1 (R&D Systems, Minneapolis, MN, USA) and 50 ng mL<sup>−1</sup> transforming growth factor (TGF)-β1 (Peprotec, Hamburg, Germany),<br> 4) FBS: 10% fetal bovine serum (FBS, Pan Biotech, Aidenbach, Germany).</p> <p>1.2 Immunocytochemistry</p> <p>After three days of cultivation in the different media compositions, the chondrocytes were washed once with phosphate-buffered saline (PBS; Biochrom GmbH, Berlin, Germany) and fixed for 10 min at room temperature (RT) with 4% paraformaldehyde (ROTI ® Histofix, Carl Roth GmbH + Co. KG, Karlsruhe, Germany). After fixation, cells were washed again and permeabilized with 0.2% Triton-X100 (Merck, Darmstadt, Germany) for 10 min. For blocking the unspecific binding sites, cell-seeded coverslips were incubated with bovine serum albumin (BSA; Sigma-Aldrich) with a concentration of 5% in PBS for one hour at RT after another washing step with PBS. To stain the primary cilium, cells were incubated with anti-acetylated α-tubulin (6-11B-1) (RRID: AB 628409) labeled with Alexa Fluor 647 (sc-23950 AF647, Santa Cruz Biotechnology, Dallas, TX, USA) diluted 1:200 in PBS at 4°C overnight. Additionally, the Actin cytoskeleton was stained with Acti-stain 488 Fluorescent Phalloidin (Cytoskeleton, Inc., Denver, CO, USA) diluted 10 in PBS for 30 min at RT. Afterward, cells were washed three times with PBS, and the coverslips were fixed with Fluoroshield™ (Sigma-Aldrich) containing 4’,6-Diamidino-2-phenylindole (DAPI).</p> <p>1.3 Image acquisition</p> <p>Three-dimensional fluorescence images of stained cells were acquired with a ZEISS ELYRA LSM 780 confocal laser scanning microscope (CLSM) (Carl Zeiss AG, Oberkochen, Germany). Images were recorded using a Plan-Apochromat 63×/1.40 Oil DIC M27 objective (Carl Zeiss AG, Oberkochen, Germany). The distance of two layers was 0.2814 µm and the resolution 1024 × 1024 pixels (scan magnification: 0.6, pixel length: 0.2196 µm).</p>
Data from: Loss of primary cilia and dopaminergic neuroprotection in pathogenic LRRK2driven and idiopathic Parkinson’s disease
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Source Data files for: Primary cilia and SHH signaling impairments in human and mouse models of Parkinson's disease
<p>Parkinson’s disease (PD) as a progressive neurodegenerative disorder arises from multiple genetic and environmental factors. However, underlying pathological mechanisms remain poorly understood. Using multiplexed single-cell transcriptomics, we analyze human neural precursor cells (hNPCs) from sporadic PD (sPD) patients. Alterations in gene expression appear in pathways related to primary cilia (PC). Accordingly, in these hiPSC-derived hNPCs and neurons, we observe a shortening of PC. Additionally, we detect a shortening of PC in <em>PINK1</em>-deficient human cellular and mouse models of familial PD. Furthermore, in sPD models, the shortening of PC is accompanied by an increased SHH signal transduction. Inhibition of this pathway rescues the alterations in PC morphology and mitochondrial dysfunction. Thus, increased SHH activity due to ciliary dysfunction is needed for the development of pathoetiological phenotypes observed in sPD, like mitochondrial dysfunction. In sum, altered PC function is part of early PD pathoetiology and inhibiting the overactive SHH signaling is a potential neuroprotective therapy.</p>
Pathogenic LRRK2 mutations cause loss of primary cilia and Neurturin in striatal Parvalbumin interneurons (mice stereology and human brain tile-scan)
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Pathogenic LRRK2 control of primary cilia and Hedgehog signaling in neurons and astrocytes of mouse brain
<p>Previously, we showed that cholinergic interneurons of the dorsal striatum lose cilia in mice harboring the Parkinson's disease associated, kinase activating, R1441C LRRK2 mutation (<a href="https://www.biorxiv.org/content/10.1101/2021.03.02.433576v1#ref-8">Dhekne et al., 2018</a>). Here we show that this phenotype is also seen in two mouse strains carrying the most common human G2019S LRRK2 mutation. Heterozygous loss of the PPM1H phosphatase that is specific for LRRK2-phosphorylated Rab GTPases (<a href="https://www.biorxiv.org/content/10.1101/2021.03.02.433576v1#ref-3">Berndsen et al., 2019</a>) yields the same cilia loss phenotype, strongly supporting a connection between Rab GTPase phosphorylation and cilia loss. In addition, astrocytes throughout the striatum show a ciliation defect in LRRK2 and PPM1H<sup>-/+</sup> mutant models. Hedgehog signaling requires cilia, and loss of cilia correlates here with a loss in induction of Hedgehog signaling as monitored by in situ hybridization of <em>Gli1</em> transcripts. These data support a model in which LRRK2 and PPM1H mutant mice struggle to receive and respond to critical Hedgehog signals in the nigral-striatal pathway.</p>
Pathogenic LRRK2 control of primary cilia and Hedgehog signaling in neurons and astrocytes of mouse brain
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Data from: Stabilization of primary cilia reduces abortive cell cyle re-entry to protect injured adult CNS neurons from apoptosis
Abortive cell cycle (ACC) re-entry of apoptotic neurons is a recently characterized phenomenon that occurs after central nervous system (CNS) injury or over the course of CNS disease. Consequently, inhibiting cell cycle progression is neuroprotective in numerous CNS pathology models. Primary cilia are ubiquitous, centriole-based cellular organelles that prevent cell cycling, but their ability to modulate abortive cell cycle has not been described. Here, we show that neuronal cilia are ablated in-vitro and in-vivo following injury by hypoxia or optic nerve transection (ONT), respectively. Furthermore, forced cilia resorption sensitized neurons to these injuries and enhanced cell death. In contrast, pharmacological inhibition or shRNA knockdown of the proteins that disassemble the cilia increased neuron survival and decreased the phosphorylation of retinoblastoma (Rb), a master switch for cell cycle re-entry. Our findings show that the stabilization of neuronal primary cilia inhibits apoptotic cell cycling, which has implications for future therapeutic strategies that halt or slow the progression of neurodegenerative diseases and acute CNS injuries.
Data from: Stabilization of primary cilia reduces abortive cell cyle re-entry to protect injured adult CNS neurons from apoptosis
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Abnormal accumulation of extracellular vesicles in hippocampal dystrophic axons and regulation by the primary cilia gene intraflagellar transport homolog 88 in Alzheimer's disease
GEO Series GSE230240. Mus musculus. 8 samples. Type: Expression profiling by high throughput sequencing.
Cholangiocytes’ Primary Cilia Regulate DNA Damage Response and Repair
GEO Series GSE280249. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
Loss of colonic primary cilia promotes inflammation and carcinogenesis.
GEO Series GSE207877. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Primary cilia contribute to the aggressiveness of atypical teratoid/rhabdoid tumors
GEO Series GSE179668. Homo sapiens. 10 samples. Type: Expression profiling by high throughput sequencing.
The effects of primary cilia on endothelial gene expression exposed to flow
GEO Series GSE139580. Mus musculus. 18 samples. Type: Expression profiling by high throughput sequencing.
Primary cilia and SHH signaling impairments in human and mouse models of Parkinson’s disease
GEO Series GSE176160. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Primary cilia control Oligodendrocyte Precursor Cell proliferation in white matter injury via Hedgehog-independent CREB signaling.
GEO Series GSE243997. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Transcription factors SP5 and SP8 drive primary cilia formation in mammalian embryos
GEO Series GSE274844. Mus musculus. 2 samples. Type: Expression profiling by high throughput sequencing.
Primary cilia are required for the persistence of memory and stabilization of perineuronal nets
GEO Series GSE174076. Mus musculus. 25 samples. Type: Expression profiling by high throughput sequencing.
Changes in the primary cilia in Alzheimer’s disease early development is associated with alterations in the axon initial segment.
GEO Series GSE248779. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Single nuclei RNAseq datasets supporting the impact of primary cilia deficiency on astrocytes’ intercellular connectivity and neuronal transcriptomes in the brain.
GEO Series GSE253642. Mus musculus. 1 samples. Type: Expression profiling by high throughput sequencing.
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