scholarly journals UV Photocatalysis of Bone Marrow-Derived Macrophages on TiO2Nanotubes Mediates Intracellular Ca2+Influx via Voltage-Gated Ca2+Channels

2015 ◽  
Vol 2015 ◽  
pp. 1-7
Author(s):  
Seunghan Oh ◽  
Eun-Joo Choi ◽  
Munkhsoyol Erkhembaatar ◽  
Min Seuk Kim
Keyword(s):  
Bone Marrow ◽  
Bone Cells ◽  
Ros Generation ◽  
Voltage Gated ◽  
Dental Implantation ◽  
Intracellular Ros ◽  
Intracellular Ca ◽  
Intracellular Signal ◽  
Reactive Oxygen Species Concentration ◽  
Ca2 Channels

Titanium (Ti) possesses excellent properties for use in dental implants but has low osteogenic surface properties that result in limiting rapid osseointegration. The physiological interaction between the surface of the implant material and bone cells, especially osteoclasts, is a crucial factor in determining successful osseointegration. However, the details of such an interaction remain elusive. Here, we demonstrated that nanotopography on the Ti surface is a crucial factor for modulating intracellular signal transduction in bone marrow-derived macrophages (BMMs). To define this, intracellular Ca2+and ROS were simultaneously measured in BMMs that were seeded on polished Ti and TiO2nanotubes. We found that UV photocatalysis of TiO2immediately elicits intracellular calcium concentration ([Ca2+]i) increase and intracellular reactive oxygen species concentration ([ROS]i) reduction in cells on TiO2nanotubes. UV photocatalysis-mediated [Ca2+]iincrease is dependent on extracellular and intracellular ROS generation. Furthermore, extracellular Ca2+influx through voltage-gated calcium channels (VGCCs) is critical for the UV photocatalysis-mediated [Ca2+]iincrease, while phospholipase C (PLC) activation is not required. Considering the physiological roles of Ca2+signaling in BMMs and osteoclastogenesis, nanotopography on the Ti surface should be considered an important factor that can influence successful dental implantation.

Presenilin 1 Deficiency Alters the Activity of Voltage-Gated Ca2+ Channels in Cultured Cortical Neurons

2005 ◽  
Vol 94 (6) ◽  
pp. 4421-4429 ◽  
Author(s):  
David G. Cook ◽  
Xiaofan Li ◽  
Sheree D. Cherry ◽  
Angela R. Cantrell
Keyword(s):  
Cortical Neurons ◽  
Critical Role ◽  
Neuronal Firing ◽  
Voltage Gated ◽  
Voltage Dependent ◽  
Cultured Cortical Neurons ◽  
Intracellular Ca ◽  
Multiple Levels ◽  
P Type ◽  
Ca2 Channels

Presenilins 1 and 2 (PS1 and PS2, respectively) play a critical role in mediating γ-secretase cleavage of the amyloid precursor protein (APP). Numerous mutations in the presenilins are known to cause early-onset familial Alzheimer's disease (FAD). In addition, it is well established that PS1 deficiency leads to altered intracellular Ca2+ homeostasis involving endoplasmic reticulum Ca2+ stores. However, there has been little evidence suggesting Ca2+ signals from extracellular sources are influenced by PS1. Here we report that the Ca2+ currents carried by voltage-dependent Ca2+ channels are increased in PS1-deficient cortical neurons. This increase is mediated by a significant increase in the contributions of L- and P-type Ca2+ channels to the total voltage-mediated Ca2+ conductance in PS1 (−/−) neurons. In addition, chelating intracellular Ca2+ with 1,2-bis-( o-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid (BAPTA) produced an increase in Ca2+ current amplitude that was comparable to the increase caused by PS1 deficiency. In contrast to this, BAPTA had no effect on voltage-dependent Ca2+ conductances in PS1-deficient neurons. These data suggest that PS1 deficiency may influence voltage-gated Ca2+ channel function by means that involve intracellular Ca2+ signaling. These findings reveal that PS1 functions at multiple levels to regulate and stabilize intracellular Ca2+ levels that ultimately control neuronal firing behavior and influence synaptic transmission.

scholarly journals Concomitant genetic ablation of L-type Cav1.3 (α1D) and T-type Cav3.1 (α1G) Ca2+ channels disrupts heart automaticity

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Matthias Baudot ◽  
Eleonora Torre ◽  
Isabelle Bidaud ◽  
Julien Louradour ◽  
Angelo G. Torrente ◽  
...  
Keyword(s):  
Sinus Node ◽  
Atrioventricular Node ◽  
Pacemaker Activity ◽  
Genetic Ablation ◽  
Voltage Gated ◽  
Integral Role ◽  
Intracellular Ca ◽  
Cardiac Automaticity ◽  
Ca2 Channels

Abstract Cardiac automaticity is set by pacemaker activity of the sinus node (SAN). In addition to the ubiquitously expressed cardiac voltage-gated L-type Cav1.2 Ca2+ channel isoform, pacemaker cells within the SAN and the atrioventricular node co-express voltage-gated L-type Cav1.3 and T-type Cav3.1 Ca2+ channels (SAN-VGCCs). The role of SAN-VGCCs in automaticity is incompletely understood. We used knockout mice carrying individual genetic ablation of Cav1.3 (Cav1.3−/−) or Cav3.1 (Cav3.1−/−) channels and double mutant Cav1.3−/−/Cav3.1−/− mice expressing only Cav1.2 channels. We show that concomitant loss of SAN-VGCCs prevents physiological SAN automaticity, blocks impulse conduction and compromises ventricular rhythmicity. Coexpression of SAN-VGCCs is necessary for impulse formation in the central SAN. In mice lacking SAN-VGCCs, residual pacemaker activity is predominantly generated in peripheral nodal and extranodal sites by f-channels and TTX-sensitive Na+ channels. In beating SAN cells, ablation of SAN-VGCCs disrupted late diastolic local intracellular Ca2+ release, which demonstrates an important role for these channels in supporting the sarcoplasmic reticulum based “Ca2+clock” mechanism during normal pacemaking. These data implicate an underappreciated role for co-expression of SAN-VGCCs in heart automaticity and define an integral role for these channels in mechanisms that control the heartbeat.

scholarly journals Radiation Induces Apoptosis and Osteogenic Impairment through miR-22-Mediated Intracellular Oxidative Stress in Bone Marrow Mesenchymal Stem Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Zhonglong Liu ◽  
Tao Li ◽  
Si’nan Deng ◽  
Shuiting Fu ◽  
Xiaojun Zhou ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cell Injury ◽  
Ros Generation ◽  
Differentiation Potential ◽  
Fluorescent Intensity ◽  
Intracellular Ros ◽  
Marrow Mesenchymal Stem Cells ◽  
Cellular Apoptosis

Bone marrow mesenchymal stem cells (BMSCs) were characterized by their multilineage potential and were involved in both bony and soft tissue repair. Exposure of cells to ionizing radiation (IR) triggers numerous biological reactions, including reactive oxygen species (ROS), cellular apoptosis, and impaired differentiation capacity, while the mechanisms of IR-induced BMSC apoptosis and osteogenic impairment are still unclear. Through a recent study, we found that 6 Gy IR significantly increased the apoptotic ratio and ROS generation, characterized by ROS staining and mean fluorescent intensity. Intervention with antioxidant (NAC) indicated that IR-induced cellular apoptosis was partly due to the accumulation of intracellular ROS. Furthermore, we found that the upregulation of miR-22 in rBMSCs following 6 Gy IR played an important role on the ROS generation and subsequent apoptosis. In addition, we firstly demonstrated that miR-22-mediated ROS accumulation and cell injury had an important regulated role on the osteogenic capacity of BMSCs both in vitro and in vivo. In conclusion, IR-induced overexpression of miR-22 regulated the cell viability and differentiation potential through targeting the intracellular ROS.

Glucosamine Protects Rat Bone Marrow Cells Against Cisplatin-induced Genotoxicity and Cytotoxicity

2019 ◽  
Vol 19 (14) ◽  
pp. 1695-1702 ◽  
Author(s):  
Mohsen Cheki ◽  
Salman Jafari ◽  
Masoud Najafi ◽  
Aziz Mahmoudzadeh
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Micronucleus Assay ◽  
Ros Generation ◽  
Polychromatic Erythrocytes ◽  
Hematological Analysis ◽  
Antagonistic Potential ◽  
Harmful Effects ◽  
Rat Bone ◽  
Marrow Cells

Background and Objective: Glucosamine is a widely prescribed dietary supplement used in the treatment of osteoarthritis. In the present study, the chemoprotectant ability of glucosamine was evaluated against cisplatin-induced genotoxicity and cytotoxicity in rat bone marrow cells. Methods: Glucosamine was orally administrated to rats at doses of 75 and 150 mg/kg body weight for seven consecutive days. On the seventh day, the rats were treated with a single injection of cisplatin (5 mg/kg, i.p.) at 1h after the last oral administration. The cisplatin antagonistic potential of glucosamine was assessed by micronucleus assay, Reactive Oxygen Species (ROS) level analysis, hematological analysis, and flow cytometry. Results: Glucosamine administration to cisplatin-treated rats significantly decreased the frequencies of Micronucleated Polychromatic Erythrocytes (MnPCEs) and Micronucleated Normchromatic Erythrocytes (MnNCEs), and also increased PCE/(PCE+NCE) ratio in bone marrow cells. Furthermore, treatment of rats with glucosamine before cisplatin significantly inhibited apoptosis, necrosis and ROS generation in bone marrow cells, and also increased red blood cells count in peripheral blood. Conclusion: This study shows glucosamine to be a new effective chemoprotector against cisplatin-induced DNA damage and apoptosis in rat bone marrow cells. The results of this study may be helpful in reducing the harmful effects of cisplatin-based chemotherapy in the future.

scholarly journals Inhibition of glypican-1 expression induces an activated fibroblast phenotype in a human bone marrow-derived stromal cell-line

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sukhneeraj P. Kaur ◽  
Arti Verma ◽  
Hee. K. Lee ◽  
Lillie M. Barnett ◽  
Payaningal R. Somanath ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Marrow ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Stromal Cell ◽  
Prostate Cancer Cell ◽  
Bone Cells ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Prostate Cancer Cells

AbstractCancer-associated fibroblasts (CAFs) are the most abundant stromal cell type in the tumor microenvironment. CAFs orchestrate tumor-stromal interactions, and contribute to cancer cell growth, metastasis, extracellular matrix (ECM) remodeling, angiogenesis, immunomodulation, and chemoresistance. However, CAFs have not been successfully targeted for the treatment of cancer. The current study elucidates the significance of glypican-1 (GPC-1), a heparan sulfate proteoglycan, in regulating the activation of human bone marrow-derived stromal cells (BSCs) of fibroblast lineage (HS-5). GPC-1 inhibition changed HS-5 cellular and nuclear morphology, and increased cell migration and contractility. GPC-1 inhibition also increased pro-inflammatory signaling and CAF marker expression. GPC-1 induced an activated fibroblast phenotype when HS-5 cells were exposed to prostate cancer cell conditioned media (CCM). Further, treatment of human bone-derived prostate cancer cells (PC-3) with CCM from HS-5 cells exhibiting GPC-1 loss increased prostate cancer cell aggressiveness. Finally, GPC-1 was expressed in mouse tibia bone cells and present during bone loss induced by mouse prostate cancer cells in a murine prostate cancer bone model. These data demonstrate that GPC-1 partially regulates the intrinsic and extrinsic phenotype of human BSCs and transformation into activated fibroblasts, identify novel functions of GPC-1, and suggest that GPC-1 expression in BSCs exerts inhibitory paracrine effects on the prostate cancer cells. This supports the hypothesis that GPC-1 may be a novel pharmacological target for developing anti-CAF therapeutics to control cancer.

scholarly journals A novel phospho-modulatory mechanism contributes to the calcium-dependent regulation of T-type Ca2+ channels

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jean Chemin ◽  
Tamara Timic Stamenic ◽  
Magalie Cazade ◽  
Jodie Llinares ◽  
Iulia Blesneac ◽  
...  
Keyword(s):  
Calcium Dependent ◽  
Cell Functions ◽  
Medial Nucleus ◽  
Steady State Inactivation ◽  
Intracellular Ca ◽  
Phosphorylation Mechanism ◽  
Multiple Cell ◽  
Atp Analogs ◽  
Ca2 Channels ◽  
Endocytic Pathways

Abstract Cav3 / T-type Ca2+ channels are dynamically regulated by intracellular Ca2+ ions, which inhibit Cav3 availability. Here, we demonstrate that this inhibition becomes irreversible in the presence of non-hydrolysable ATP analogs, resulting in a strong hyperpolarizing shift in the steady-state inactivation of the residual Cav3 current. Importantly, the effect of these ATP analogs was prevented in the presence of intracellular BAPTA. Additional findings obtained using intracellular dialysis of inorganic phosphate and alkaline phosphatase or NaN3 treatment further support the involvement of a phosphorylation mechanism. Contrasting with Cav1 and Cav2 Ca2+ channels, the Ca2+-dependent modulation of Cav3 channels appears to be independent of calmodulin, calcineurin and endocytic pathways. Similar findings were obtained for the native T-type Ca2+ current recorded in rat thalamic neurons of the central medial nucleus. Overall, our data reveal a new Ca2+ sensitive phosphorylation-dependent mechanism regulating Cav3 channels, with potentially important physiological implications for the multiple cell functions controlled by T-type Ca2+ channels.

scholarly journals Role of a conserved glutamine in the function of voltage-gated Ca2+ channels revealed by a mutation in human CACNA1D

2018 ◽  
Vol 293 (37) ◽  
pp. 14444-14454 ◽  
Author(s):  
Edgar Garza-Lopez ◽  
Josue A. Lopez ◽  
Jussara Hagen ◽  
Ruth Sheffer ◽  
Vardiella Meiner ◽  
...  
Keyword(s):  
Voltage Gated ◽  
Ca2 Channels
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