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Journal articles on the topic 'Modulating aggregation'

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Author: Grafiati

Published: 6 September 2023

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1

Huang, Yaliang, Yong Chang, Lin Liu, and Jianxiu Wang. "Nanomaterials for Modulating the Aggregation of β-Amyloid Peptides." Molecules 26, no. 14 (July 15, 2021): 4301. http://dx.doi.org/10.3390/molecules26144301.

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The aberrant aggregation of amyloid-β (Aβ) peptides in the brain has been recognized as the major hallmark of Alzheimer’s disease (AD). Thus, the inhibition and dissociation of Aβ aggregation are believed to be effective therapeutic strategiesforthe prevention and treatment of AD. When integrated with traditional agents and biomolecules, nanomaterials can overcome their intrinsic shortcomings and boost their efficiency via synergistic effects. This article provides an overview of recent efforts to utilize nanomaterials with superior properties to propose effective platforms for AD treatment. The underlying mechanismsthat are involved in modulating Aβ aggregation are discussed. The summary of nanomaterials-based modulation of Aβ aggregation may help researchers to understand the critical roles in therapeutic agents and provide new insight into the exploration of more promising anti-amyloid agents and tactics in AD theranostics.

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Wang, Bo, Emily H. Pilkington, Yunxiang Sun, Thomas P. Davis, Pu Chun Ke, and Feng Ding. "Modulating protein amyloid aggregation with nanomaterials." Environmental Science: Nano 4, no. 9 (2017): 1772–83. http://dx.doi.org/10.1039/c7en00436b.

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3

Ringertz, BO. "NEUTROPHIL AGGREGATION - FACTORS MODULATING STIMULUS-SPECIFIC RESPONSES." Acta Pathologica Microbiologica Scandinavica Series C: Immunology 94C, no. 1-6 (August 15, 2009): 1–9. http://dx.doi.org/10.1111/j.1699-0463.1986.tb02082.x.

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4

Polumuri, Swamy kumar, Lydia Haile, Roshni Rao, and Daniela Verthelyi. "Aggregation and innate immune response modulating impurities." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 129.2. http://dx.doi.org/10.4049/jimmunol.198.supp.129.2.

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Abstract Therapeutic proteins can induce immune responses that affect the safety and efficacy even if derived from human sequences. The factors that contribute to the immunogenicity of this therapeutics are poorly understood, but protein aggregation is thought to facilitate it. Previously, our lab showed that trace levels of product or process derived innate immune response modulating impurities (IIRMIs) can also increase product immunogenicity. In this study we hypothesized that protein aggregates and IIRMIs may synergize to facilitate product immunogenicity and explored it using clinical grade Human Serum Albumin (HSA) and Intravenous Immunoglobulin (IVIG) proteins as model. Protein aggregations formed by mechanical stress (shaking and stirring) were characterized by SDS-PAGE, turbidity, MFI and FlowCAM. Cellular responses to aggregated proteins with trace levels of IIRMs were tested in human PBMC. We show that stirring and shaking resulted in the formation of stable aggregates with size ranges of 2 – 50 μm for stirred HSA; and 2–100 μm for IVIG. Despite the similarity in size, the functional assays showed that aggregates of IVIG result in increased mRNA expression of IL-8, IL-6, IL-1β and CCL-2 whereas HSA aggregates did not. Further, we analyzed how the aggregated product changed the transcriptome using Nanostring and showed that aggregated IVIG (shaken or stirred) significantly increased the mRNA of CCL2, CCL7, CCL3, CCL24, CSF1, CXCL2, IRAK1, EGR2, CEBPβ, PPARg, TNFSF15 and whereas HSA aggregates did not. Similarly MAPKs (pp38, pERK and pJNK) and pAKT were activated when PBMC were stimulated with IVIG aggregates but not HSA aggregates. Lastly, we examined whether the effect was mediated by Toll like receptors.

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Kreiser, Ryan P., Aidan K. Wright, Natalie R. Block, Jared E. Hollows, Lam T. Nguyen, Kathleen LeForte, Benedetta Mannini, Michele Vendruscolo, and Ryan Limbocker. "Therapeutic Strategies to Reduce the Toxicity of Misfolded Protein Oligomers." International Journal of Molecular Sciences 21, no. 22 (November 17, 2020): 8651. http://dx.doi.org/10.3390/ijms21228651.

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The aberrant aggregation of proteins is implicated in the onset and pathogenesis of a wide range of neurodegenerative disorders, including Alzheimer’s and Parkinson’s diseases. Mounting evidence indicates that misfolded protein oligomers produced as intermediates in the aggregation process are potent neurotoxic agents in these diseases. Because of the transient and heterogeneous nature of these elusive aggregates, however, it has proven challenging to develop therapeutics that can effectively target them. Here, we review approaches aimed at reducing oligomer toxicity, including (1) modulating the oligomer populations (e.g., by altering the kinetics of aggregation by inhibiting, enhancing, or redirecting the process), (2) modulating the oligomer properties (e.g., through the size–hydrophobicity–toxicity relationship), (3) modulating the oligomer interactions (e.g., by protecting cell membranes by displacing oligomers), and (4) reducing oligomer toxicity by potentiating the protein homeostasis system. We analyze examples of these complementary approaches, which may lead to the development of compounds capable of preventing or treating neurodegenerative disorders associated with protein aggregation.

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6

Baum, Jean. "Modulating Alpha-Synuclein Aggregation through IDP-IDP Interactions." Biophysical Journal 116, no. 3 (February 2019): 4a. http://dx.doi.org/10.1016/j.bpj.2018.11.049.

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7

Lo Cascio, Filippa, Stephanie Garcia, Mauro Montalbano, Nicha Puangmalai, Salome McAllen, Andrea Pace, Antonio Palumbo Piccionello, and Rakez Kayed. "Modulating disease-relevant tau oligomeric strains by small molecules." Journal of Biological Chemistry 295, no. 44 (July 31, 2020): 14807–25. http://dx.doi.org/10.1074/jbc.ra120.014630.

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The pathological aggregation of tau plays an important role in Alzheimer's disease and many other related neurodegenerative diseases, collectively referred to as tauopathies. Recent evidence has demonstrated that tau oligomers, small and soluble prefibrillar aggregates, are highly toxic due to their strong ability to seed tau misfolding and propagate the pathology seen across different neurodegenerative diseases. We previously showed that novel curcumin derivatives affect preformed tau oligomer aggregation pathways by promoting the formation of more aggregated and nontoxic tau aggregates. To further investigate their therapeutic potential, we have extended our studies o disease-relevant brain-derived tau oligomers (BDTOs). Herein, using well-characterized BDTOs, isolated from brain tissues of different tauopathies, including Alzheimer's disease, progressive supranuclear palsy, and dementia with Lewy bodies, we found that curcumin derivatives modulate the aggregation state of BDTOs by reshaping them and rescue neurons from BDTO-associated toxicity. Interestingly, compound CL3 showed an effect on the aggregation pattern of BDTOs from different tauopathies, resulting in the formation of less neurotoxic larger tau aggregates with decreased hydrophobicity and seeding propensity. Our results lay the groundwork for potential investigations of the efficacy and beneficial effects of CL3 and other promising compounds for the treatment of tauopathies. Furthermore, CL3 may aid in the development of tau imaging agent for the detection of tau oligomeric strains and differential diagnosis of the tauopathies, thus enabling earlier interventions.

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8

Liu, Jing, Ziang Chen, Jia Hu, Hongxia Sun, Yan Liu, Zhongyi Liu, and Jinpeng Li. "Time-resolved color-changing long-afterglow for security systems based on metal–organic hybrids." Inorganic Chemistry Frontiers 9, no. 3 (2022): 584–91. http://dx.doi.org/10.1039/d1qi01435h.

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9

Bai, Yulong, Yanan Huang, Wang Wan, Wenhan Jin, Di Shen, Haochen Lyu, Lianggang Zeng, and Yu Liu. "Derivatizing merocyanine dyes to balance their polarity and viscosity sensitivities for protein aggregation detection." Chemical Communications 57, no. 98 (2021): 13313–16. http://dx.doi.org/10.1039/d1cc05200d.

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10

Qi, Yu, Wenshan Chen, Fangfei Liu, Jing Liu, Tong Zhang, and Wei Chen. "Aggregation morphology is a key factor determining protein adsorption on graphene oxide and reduced graphene oxide nanomaterials." Environmental Science: Nano 6, no. 5 (2019): 1303–9. http://dx.doi.org/10.1039/c8en01408f.

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11

Du, Zhi, Meng Li, Jinsong Ren, and Xiaogang Qu. "Current Strategies for Modulating Aβ Aggregation with Multifunctional Agents." Accounts of Chemical Research 54, no. 9 (April 21, 2021): 2172–84. http://dx.doi.org/10.1021/acs.accounts.1c00055.

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12

Fontaine, Sarah N., Jonathan J. Sabbagh, Jeremy Baker, Carlos R. Martinez-Licha, April Darling, and Chad A. Dickey. "Cellular factors modulating the mechanism of tau protein aggregation." Cellular and Molecular Life Sciences 72, no. 10 (February 11, 2015): 1863–79. http://dx.doi.org/10.1007/s00018-015-1839-9.

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13

Karch, Celeste M., and David R. Borchelt. "Aggregation modulating elements in mutant human superoxide dismutase 1." Archives of Biochemistry and Biophysics 503, no. 2 (November 2010): 175–82. http://dx.doi.org/10.1016/j.abb.2010.07.027.

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14

Martínez-Martínez, Virginia, Raquel García, Luis Gómez-Hortigüela, Joaquín Pérez-Pariente, and Iñigo López-Arbeloa. "Modulating Dye Aggregation by Incorporation into 1D-MgAPO Nanochannels." Chemistry - A European Journal 19, no. 30 (June 18, 2013): 9859–65. http://dx.doi.org/10.1002/chem.201301285.

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15

Kulig, Melissa, and Heath Ecroyd. "The small heat-shock protein αB-crystallin uses different mechanisms of chaperone action to prevent the amorphous versus fibrillar aggregation of α-lactalbumin." Biochemical Journal 448, no. 3 (November 21, 2012): 343–52. http://dx.doi.org/10.1042/bj20121187.

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Stress conditions can destabilize proteins, promoting them to unfold and adopt intermediately folded states. Partially folded protein intermediates are unstable and prone to aggregation down off-folding pathways leading to the formation of either amorphous or amyloid fibril aggregates. The sHsp (small heat-shock protein) αB-crystallin acts as a molecular chaperone to prevent both amorphous and fibrillar protein aggregation; however, the precise molecular mechanisms behind its chaperone action are incompletely understood. To investigate whether the chaperone activity of αB-crystallin is dependent upon the form of aggregation (amorphous compared with fibrillar), bovine α-lactalbumin was developed as a model target protein that could be induced to aggregate down either off-folding pathway using comparable buffer conditions. Thus when α-lactalbumin was reduced it aggregated amorphously, whereas a reduced and carboxymethylated form aggregated to form amyloid fibrils. Using this model, αB-crystallin was shown to be a more efficient chaperone against amorphously aggregating α-lactalbumin than when it aggregated to form fibrils. Moreover, αB-crystallin forms high molecular mass complexes with α-lactalbumin to prevent its amorphous aggregation, but prevents fibril formation via weak transient interactions. Thus, the conformational stability of the protein intermediate, which is a precursor to aggregation, plays a critical role in modulating the chaperone mechanism of αB-crystallin.

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16

Pandey, Gaurav, Sudhir Morla, Harshal B. Nemade, Sachin Kumar, and Vibin Ramakrishnan. "Modulation of aggregation with an electric field; scientific roadmap for a potential non-invasive therapy against tauopathies." RSC Advances 9, no. 9 (2019): 4744–50. http://dx.doi.org/10.1039/c8ra09993f.

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17

Perrault, Christelle, Nadine Ajzenberg, Paulette Legendre, Ghassem Rastegar-Lari, Dominique Meyer, Jose A. Lopez, and Dominique Baruch. "Modulation by Heparin of the Interaction of the A1 Domain of von Willebrand Factor With Glycoprotein Ib." Blood 94, no. 12 (December 15, 1999): 4186–94. http://dx.doi.org/10.1182/blood.v94.12.4186.

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Abstract The conformation of the A1 domain of von Willebrand factor (vWF) is a critical determinant of its interaction with the glycoprotein (GP) Ib/V/IX complex. To better define the regulatory mechanisms of vWF A1 domain binding to the GPIb/V/IX complex, we studied vWF-dependent aggregation properties of a cell line overexpressing the GPIb, GPIbβ, and GPIX subunits (CHO-GPIbβ/IX cells). We found that CHO-GPIbβ/IX cell aggregation required the presence of both soluble vWF and ristocetin. Ristocetin-induced CHO-GPIbβ/IX cell aggregation was completely inhibited by the recombinant VCL fragment of vWF that contains the A1 domain. Surprisingly, the substitution of heparin for ristocetin resulted in the formation of CHO-GPIbβ/IX cell aggregates. Using monoclonal antibodies blocking vWF interaction with GPIb/V/IX or mocarhagin, a venom metalloproteinase that removes the amino-terminal fragment of GPIb extending from aa 1 to 282, we demonstrated that both ristocetin- and heparin-induced aggregations involved an interaction between the A1 domain of vWF and the GPIb subunit of the GPIb/V/IX complex. The involvement of heparin in cell aggregation was also demonstrated after treatment of heparin with heparinase that abolished CHO-GPIbβ/IX cell aggregation. These results indicated that heparin was able to induce vWF-dependent CHO-GPIbβ/IX cell aggregation. In conclusion, we demonstrated that heparin is capable of positively modulating the vWF interaction with the GPIb/V/IX complex.

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18

Perrault, Christelle, Nadine Ajzenberg, Paulette Legendre, Ghassem Rastegar-Lari, Dominique Meyer, Jose A. Lopez, and Dominique Baruch. "Modulation by Heparin of the Interaction of the A1 Domain of von Willebrand Factor With Glycoprotein Ib." Blood 94, no. 12 (December 15, 1999): 4186–94. http://dx.doi.org/10.1182/blood.v94.12.4186.424k24_4186_4194.

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The conformation of the A1 domain of von Willebrand factor (vWF) is a critical determinant of its interaction with the glycoprotein (GP) Ib/V/IX complex. To better define the regulatory mechanisms of vWF A1 domain binding to the GPIb/V/IX complex, we studied vWF-dependent aggregation properties of a cell line overexpressing the GPIb, GPIbβ, and GPIX subunits (CHO-GPIbβ/IX cells). We found that CHO-GPIbβ/IX cell aggregation required the presence of both soluble vWF and ristocetin. Ristocetin-induced CHO-GPIbβ/IX cell aggregation was completely inhibited by the recombinant VCL fragment of vWF that contains the A1 domain. Surprisingly, the substitution of heparin for ristocetin resulted in the formation of CHO-GPIbβ/IX cell aggregates. Using monoclonal antibodies blocking vWF interaction with GPIb/V/IX or mocarhagin, a venom metalloproteinase that removes the amino-terminal fragment of GPIb extending from aa 1 to 282, we demonstrated that both ristocetin- and heparin-induced aggregations involved an interaction between the A1 domain of vWF and the GPIb subunit of the GPIb/V/IX complex. The involvement of heparin in cell aggregation was also demonstrated after treatment of heparin with heparinase that abolished CHO-GPIbβ/IX cell aggregation. These results indicated that heparin was able to induce vWF-dependent CHO-GPIbβ/IX cell aggregation. In conclusion, we demonstrated that heparin is capable of positively modulating the vWF interaction with the GPIb/V/IX complex.

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19

Du, Xiaoyang, Juewen Zhao, Hao Zhang, Xi Lu, Lei Zhou, Zhenhua Chen, Hui Lin, Caijun Zheng, and Silu Tao. "Modulating the molecular packing and distribution enables fullerene-free ternary organic solar cells with high efficiency and long shelf-life." Journal of Materials Chemistry A 7, no. 35 (2019): 20139–50. http://dx.doi.org/10.1039/c9ta07542a.

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20

Miller, Jessica J., Anaïs Blanchet, Christophe Orvain, Lucienne Nouchikian, Yasmin Reviriot, Ryan M. Clarke, Diego Martelino, Derek Wilson, Christian Gaiddon, and Tim Storr. "Bifunctional ligand design for modulating mutant p53 aggregation in cancer." Chemical Science 10, no. 46 (2019): 10802–14. http://dx.doi.org/10.1039/c9sc04151f.

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21

Márquez, Maripaz, Luis M. Blancas-Mejía, Adriana Campos, Luis Rojas, Gilberto Castañeda-Hernández, and Liliana Quintanar. "A bifunctional non-natural tetrapeptide modulates amyloid-beta peptide aggregation in the presence of Cu(ii)." Metallomics 6, no. 12 (2014): 2189–92. http://dx.doi.org/10.1039/c4mt00257a.

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A novel bifunctional non-natural tetrapeptide, Met-Asp-d-Trp-Aib, is capable of binding copper, competing with amyloid-beta peptide (Aβ) for Cu(ii), and modulating Aβ aggregation. The study of this tetrapeptide provides further insights into the role of Cu(ii) in the Aβ aggregation pathway, and into the design of compounds with therapeutic potential for Alzheimer's disease.

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22

Bera, Avisek, Subhasish Sahoo, Kalyan Goswami, Subir Kumar Das, Pooja Ghosh, and Priyadarsi De. "Modulating Insulin Aggregation with Charge Variable Cholic Acid-Derived Polymers." Biomacromolecules 22, no. 11 (October 22, 2021): 4833–45. http://dx.doi.org/10.1021/acs.biomac.1c01107.

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23

Douglas, Peter M., Daniel W. Summers, and Douglas M. Cyr. "Molecular chaperones antagonize proteotoxicity by differentially modulating protein aggregation pathways." Prion 3, no. 2 (April 2009): 51–58. http://dx.doi.org/10.4161/pri.3.2.8587.

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24

Liu, Lei, Lan Zhang, Xiaobo Mao, Lin Niu, Yanlian Yang, and Chen Wang. "Chaperon-Mediated Single Molecular Approach Toward Modulating Aβ Peptide Aggregation." Nano Letters 9, no. 12 (December 9, 2009): 4066–72. http://dx.doi.org/10.1021/nl902256b.

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25

Wang, Zi-Yuan, Ze-Fan Yao, Yang Lu, Li Ding, Zi-Di Yu, Hao-Yang You, Xin-Yi Wang, et al. "Precise tracking and modulating aggregation structures of conjugated copolymers in solutions." Polymer Chemistry 11, no. 22 (2020): 3716–22. http://dx.doi.org/10.1039/d0py00456a.

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Different backbone shape of BDOPV-based polymers generates distinct aggregation structures in dilute solutions, which could be retained into the solid-state microstructures, further exhibiting different electron mobility and doping efficiency.

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26

Yu, Rui, Fanglei Zuo, Huiqin Ma, and Shangwu Chen. "Exopolysaccharide-Producing Bifidobacterium adolescentis Strains with Similar Adhesion Property Induce Differential Regulation of Inflammatory Immune Response in Treg/Th17 Axis of DSS-Colitis Mice." Nutrients 11, no. 4 (April 4, 2019): 782. http://dx.doi.org/10.3390/nu11040782.

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Intestinal bifidobacteria benefit human health by promoting and modulating the gut flora, and boosting therapeutic efficiency for chronic metabolic diseases and cancer. Recently, Bifidobacterium adolescentis strains with high adhesion to intestinal epithelial cells were associated with induction of T-helper 17 (Th17) cells in humans and rodents. Here, two B. adolescentis strains with similar adhesive ability but different aggregation properties were investigated for specific immunoregulatory effects, including the underlying cellular pathway, on macrophage and T-regulatory (Treg)/Th17 axis activation in vitro and in the colon of dextran sodium sulfate (DSS)-colitis mice in vivo. In-vitro, the auto-aggregative B. adolescentis strain IF1-11 induced significantly higher IL-6 and lower IL-10 secretion from immune cells, and it induced abundant Th17 cells. The non-aggregating strain IF1-03 induced significantly higher IL-10, less IL-6 and a high proportion of Treg/Th17 cells compared to total T cells. In vivo, orally administered IF1-03 protected DSS-colitis mice via activation of dendritic cells or macrophages and skewing of Treg/Th17 cells, consistent with Treg cell induction in vitro. IF1-03 exopolysaccharides showed a functional recognition pattern similar to IF1-03 for IL-10 cytokine secretion and Treg cell-differentiation induction, both dependent on the toll-like receptor 2–ERK/p38 MAPK-signaling cascade for macrophage activation. We suggest that B. adolescentis exopolysaccharide-associated enterocyte adhesion/aggregation phenotypes determine strain-specific adaptive immune responses in the gut via the macrophage-regulated Treg/Th17 axis.

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27

Liu, Changliang, Huan Huang, Lilusi Ma, Xiaocui Fang, Chen Wang, and Yanlian Yang. "Modulation of β-amyloid aggregation by graphene quantum dots." Royal Society Open Science 6, no. 6 (June 2019): 190271. http://dx.doi.org/10.1098/rsos.190271.

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Misfolding and abnormal aggregation of β-amyloid peptide is associated with the onset and progress of Alzheimer's disease (AD). Therefore, modulating β-amyloid aggregation is critical for the treatment of AD. Herein, we studied the regulatory effects and mechanism of graphene quantum dots (GQDs) on 1–42 β-amyloid (Aβ 1–42 ) aggregation. GQDs displayed significant regulatory effects on the aggregation of Aβ 1–42 peptide as detected by thioflavin T (ThT) assay. Then, the changes of confirmations and structures induced by GQDs on the Aβ 1–42 aggregation were monitored by circular dichroism (CD), dynamic light scattering (DLS) and transmission electron microscope (TEM). The in vitro cytotoxicity experiments further demonstrated the feasibility of GQDs on the regulation of Aβ 1–42 aggregation. Meanwhile, the structural changes of a Aβ 1–42 /GQDs mixture in different pH revealed that electrostatic interaction was the major driving force in the co-assembly process of Aβ 1–42 and GQDs. The proposed mechanism of the regulatory effects of GQDs on the Aβ 1–42 aggregation was also deduced reasonably. This work not only demonstrated the potential feasibility of GQDs as therapeutic drug for AD but also clarified the regulatory mechanism of GQDs on the Aβ 1–42 aggregation.

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28

Benichou Haziot, Carla, and Kulbir Singh Birak. "Therapeutic Potential of Microbiota Modulation in Alzheimer’s Disease: A Review of Preclinical Studies." Journal of Alzheimer's Disease Reports 7, no. 1 (May 12, 2023): 415–31. http://dx.doi.org/10.3233/adr-220097.

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Alzheimer’s disease (AD) is the most common neurodegenerative disease, yet it currently lacks effective treatment due to its complex etiology. The pathological changes in AD have been linked to the neurotoxic immune responses following aggregation of Aβ and phosphorylated tau. The gut microbiota (GM) is increasingly studied for modulating neuroinflammation in neurodegenerative diseases and in vivo studies emerge for AD. This critical review selected 7 empirical preclinical studies from 2019 onwards assessing therapy approaches targeting GM modulating microglia neuroinflammation in AD mouse models. Results from probiotics, fecal microbiota transplantation, and drugs were compared and contrasted, including for cognition, neuroinflammation, and toxic aggregation of proteins. Studies consistently reported significant amelioration or prevention of cognitive deficits, decrease in microglial activation, and lower levels of pro-inflammatory cytokines, compared to AD mouse models. However, there were differences across papers for the brain regions affected, and changes in astrocytes were inconsistent. Aβ plaques deposition significantly decreased in all papers, apart from Byur dMar Nyer lNga Ril Bu (BdNlRB) treatment. Tau phosphorylation significantly declined in 5 studies. Effects in microbial diversity following treatment varied across studies. Findings are encouraging regarding the efficacy of study but information on the effect size is limited. Potentially, GM reverses GM derived abnormalities, decreasing neuroinflammation, which reduces AD toxic aggregations of proteins in the brain, resulting in cognitive improvements. Results support the hypothesis of AD being a multifactorial disease and the potential synergies through multi-target approaches. The use of AD mice models limits conclusions around effectiveness, as human translation is challenging.

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Pandey, Gaurav, Prem Prakash Das, and Vibin Ramakrishnan. "Directive Effect of Chain Length in Modulating Peptide Nano-assemblies." Protein & Peptide Letters 27, no. 9 (October 15, 2020): 923–29. http://dx.doi.org/10.2174/0929866527666200224114627.

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Background: RADA-4 (Ac-RADARADARADARADA-NH2) is the most extensively studied and marketed self-assembling peptide, forming hydrogel, used to create defined threedimensional microenvironments for cell culture applications. Objectives: In this work, we use various biophysical techniques to investigate the length dependency of RADA aggregation and assembly. Methods: We synthesized a series of RADA-N peptides, N ranging from 1 to 4, resulting in four peptides having 4, 8, 12, and 16 amino acids in their sequence. Through a combination of various biophysical methods including thioflavin T fluorescence assay, static right angle light scattering assay, Dynamic Light Scattering (DLS), electron microscopy, CD, and IR spectroscopy, we have examined the role of chain-length on the self-assembly of RADA peptide. Results: Our observations show that the aggregation of ionic, charge-complementary RADA motifcontaining peptides is length-dependent, with N less than 3 are not forming spontaneous selfassemblies. Conclusion: The six biophysical experiments discussed in this paper validate the significance of chain-length on the epitaxial growth of RADA peptide self-assembly.

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Xu, Na, James Gulick, Hanna Osinska, Yang Yu, Patrick M. McLendon, Kritton Shay-Winkler, Jeffrey Robbins, and Katherine E. Yutzey. "Ube2v1 Positively Regulates Protein Aggregation by Modulating Ubiquitin Proteasome System Performance Partially Through K63 Ubiquitination." Circulation Research 126, no. 7 (March 27, 2020): 907–22. http://dx.doi.org/10.1161/circresaha.119.316444.

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Rationale: Compromised protein quality control can result in proteotoxic intracellular protein aggregates in the heart, leading to cardiac disease and heart failure. Defining the participants and understanding the underlying mechanisms of cardiac protein aggregation is critical for seeking therapeutic targets. We identified Ube2v1 (ubiquitin-conjugating enzyme E2 variant 1) in a genome-wide screen designed to identify novel effectors of the aggregation process. However, its role in the cardiomyocyte is undefined. Objective: To assess whether Ube2v1 regulates the protein aggregation caused by cardiomyocyte expression of a mutant αB crystallin (CryAB R120G ) and identify how Ube2v1 exerts its effect. Methods and Results: Neonatal rat ventricular cardiomyocytes were infected with adenoviruses expressing either wild-type CryAB (CryAB WT ) or CryAB R120G . Subsequently, loss- and gain-of-function experiments were performed. Ube2v1 knockdown decreased aggregate accumulation caused by CryAB R120G expression. Overexpressing Ube2v1 promoted aggregate formation in CryAB WT and CryAB R120G -expressing neonatal rat ventricular cardiomyocytes. Ubiquitin proteasome system performance was analyzed using a ubiquitin proteasome system reporter protein. Ube2v1 knockdown improved ubiquitin proteasome system performance and promoted the degradation of insoluble ubiquitinated proteins in CryAB R120G cardiomyocytes but did not alter autophagic flux. Lys (K) 63-linked ubiquitination modulated by Ube2v1 expression enhanced protein aggregation and contributed to Ube2v1’s function in regulating protein aggregate formation. Knocking out Ube2v1 exclusively in cardiomyocytes by using AAV9 (adeno-associated virus 9) to deliver multiplexed single guide RNAs against Ube2v1 in cardiac-specific Cas9 mice alleviated CryAB R120G -induced protein aggregation, improved cardiac function, and prolonged lifespan in vivo. Conclusions: Ube2v1 plays an important role in protein aggregate formation, partially by enhancing K63 ubiquitination during a proteotoxic stimulus. Inhibition of Ube2v1 decreases CryAB R120G -induced aggregate formation through enhanced ubiquitin proteasome system performance rather than autophagy and may provide a novel therapeutic target to treat cardiac proteinopathies.

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31

Alexandre, Gladys. "Chemotaxis Control of Transient Cell Aggregation." Journal of Bacteriology 197, no. 20 (July 27, 2015): 3230–37. http://dx.doi.org/10.1128/jb.00121-15.

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Chemotaxis affords motile cells the ability to rapidly respond to environmental challenges by navigating cells to niches favoring growth. Such a property results from the activities of dedicated signal transduction systems on the motility apparatus, such as flagella, type IV pili, and gliding machineries. Once cells have reached a niche with favorable conditions, they often stop moving and aggregate into complex communities termed biofilms. An intermediate and reversible stage that precedes commitment to permanent adhesion often includes transient cell-cell contacts between motile cells. Chemotaxis signaling has been implicated in modulating the transient aggregation of motile cells. Evidence further indicates that chemotaxis-dependent transient cell aggregation events are behavioral responses to changes in metabolic cues that temporarily prohibit permanent attachment by maintaining motility and chemotaxis. This minireview discusses a few examples illustrating the role of chemotaxis signaling in the initiation of cell-cell contacts in bacteria moving via flagella, pili, or gliding.

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32

Hanke, Marcel, Alejandro Gonzalez Orive, Guido Grundmeier, and Adrian Keller. "Effect of DNA Origami Nanostructures on hIAPP Aggregation." Nanomaterials 10, no. 11 (November 4, 2020): 2200. http://dx.doi.org/10.3390/nano10112200.

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The aggregation of human islet amyloid polypeptide (hIAPP) plays a major role in the pathogenesis of type 2 diabetes mellitus (T2DM), and numerous strategies for controlling hIAPP aggregation have been investigated so far. In particular, several organic and inorganic nanoparticles (NPs) have shown the potential to influence the aggregation of hIAPP and other amyloidogenic proteins and peptides. In addition to conventional NPs, DNA nanostructures are receiving more and more attention from the biomedical field. Therefore, in this work, we investigated the effects of two different DNA origami nanostructures on hIAPP aggregation. To this end, we employed in situ turbidity measurements and ex situ atomic force microscopy (AFM). The turbidity measurements revealed a retarding effect of the DNA nanostructures on hIAPP aggregation, while the AFM results showed the co-aggregation of hIAPP with the DNA origami nanostructures into hybrid peptide–DNA aggregates. We assume that this was caused by strong electrostatic interactions between the negatively charged DNA origami nanostructures and the positively charged peptide. Most intriguingly, the influence of the DNA origami nanostructures on hIAPP aggregation differed from that of genomic double-stranded DNA (dsDNA) and appeared to depend on DNA origami superstructure. DNA origami nanostructures may thus represent a novel route for modulating amyloid aggregation in vivo.

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Zou, Hong Yan, Fang Fang Zhang, Qing Juan Guo, Tong Yang, and Cheng Zhi Huang. "A label-free turn ON–OFF chemiluminescence strategy for lysozyme detection by target-triggered Cu2−xSe aggregation." Analytical Methods 11, no. 34 (2019): 4376–81. http://dx.doi.org/10.1039/c9ay01288e.

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A label-free and sensitive turn on-off CL probe for Lys by modulating the biocatalytic ability of the Cu_2−xSe was developed. The good catalytic ability of Cu_2−xSe were suppressed for the aggregation when Lys was added, inducing the CL signal off.

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Chung, You Jung, Byung Il Lee, and Chan Beum Park. "Multifunctional carbon dots as a therapeutic nanoagent for modulating Cu(ii)-mediated β-amyloid aggregation." Nanoscale 11, no. 13 (2019): 6297–306. http://dx.doi.org/10.1039/c9nr00473d.

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Kong, Linglong, Lu Wang, Deye Sun, Su Meng, Dandan Xu, Zaixin He, Xiaoying Dong, Yongfeng Li, and Yongcheng Jin. "Aggregation-Morphology-Dependent Electrochemical Performance of Co3O4 Anode Materials for Lithium-Ion Batteries." Molecules 24, no. 17 (August 29, 2019): 3149. http://dx.doi.org/10.3390/molecules24173149.

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The aggregation morphology of anode materials plays a vital role in achieving high performance lithium-ion batteries. Herein, Co3O4 anode materials with different aggregation morphologies were successfully prepared by modulating the morphology of precursors with different cobalt sources by the mild coprecipitation method. The fabricated Co3O4 can be flower-like, spherical, irregular, and urchin-like. Detailed investigation on the electrochemical performance demonstrated that flower-like Co3O4 consisting of nanorods exhibited superior performance. The reversible capacity maintained 910.7 mAh·g−1 at 500 mA·g−1 and 717 mAh·g−1 at 1000 mA·g−1 after 500 cycles. The cyclic stability was greatly enhanced, with a capacity retention rate of 92.7% at 500 mA·g−1 and 78.27% at 1000 mA·g−1 after 500 cycles. Electrochemical performance in long-term storage and high temperature conditions was still excellent. The unique aggregation morphology of flower-like Co3O4 yielded a reduction of charge-transfer resistance and stabilization of electrode structure compared with other aggregation morphologies.

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Devi, Shweta, Minal Chaturvedi, Siraj Fatima, and Smriti Priya. "Environmental factors modulating protein conformations and their role in protein aggregation diseases." Toxicology 465 (January 2022): 153049. http://dx.doi.org/10.1016/j.tox.2021.153049.

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Borana, Mohanish S., Pushpa Mishra, Raghuvir R. S. Pissurlenkar, Ramakrishna V. Hosur, and Basir Ahmad. "Curcumin and kaempferol prevent lysozyme fibril formation by modulating aggregation kinetic parameters." Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1844, no. 3 (March 2014): 670–80. http://dx.doi.org/10.1016/j.bbapap.2014.01.009.

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Limbocker, Ryan, Benedetta Mannini, Sean Chia, Francesco S. Ruggeri, Michele Perni, Roberta Cascella, Catherine Xu, et al. "Modulating Amyloid-Beta Aggregation to Reduce the Toxicity of its Oligomeric Aggregates." Biophysical Journal 114, no. 3 (February 2018): 430a. http://dx.doi.org/10.1016/j.bpj.2017.11.2382.

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Jiang, Runsheng, Zheng Xue, Yongjun Li, Zhihong Qin, Yuliang Li, and Daoben Zhu. "Controllable Supramolecular Architectures for Modulating Optical Properties on the Molecular Aggregation Level." European Journal of Organic Chemistry 2014, no. 23 (July 4, 2014): 5004–9. http://dx.doi.org/10.1002/ejoc.201402460.

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Zaman, Masihuz, and Maria Andreasen. "Modulating Kinetics of the Amyloid-Like Aggregation of S. aureus Phenol-Soluble Modulins by Changes in pH." Microorganisms 9, no. 1 (January 7, 2021): 117. http://dx.doi.org/10.3390/microorganisms9010117.

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The pathogen Staphylococcus aureus is recognized as one of the most frequent causes of biofilm-associated infections. The recently identified phenol-soluble modulin (PSM) peptides act as the key molecular effectors of staphylococcal biofilm maturation and promote the formation of an aggregated fibril structure. The aim of this study was to evaluate the effect of various pH values on the formation of functional amyloids of individual PSM peptides. Here, we combined a range of biophysical, chemical kinetics and microscopic techniques to address the structure and aggregation mechanism of individual PSMs under different conditions. We established that there is a pH-induced switch in PSM aggregation kinetics. Different lag times and growth of fibrils were observed, which indicates that there was no clear correlation between the rates of fibril elongation among different PSMs. This finding confirms that pH can modulate the aggregation properties of these peptides and suggest a deeper understanding of the formation of aggregates, which represents an important basis for strategies to interfere and might help in reducing the risk of biofilm-related infections.

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Vicente-Zurdo, David, Leonardo Brunetti, Luca Piemontese, Beatriz Guedes, Sandra M. Cardoso, Daniel Chavarria, Fernanda Borges, Yolanda Madrid, Sílvia Chaves, and M. Amélia Santos. "Rivastigmine–Benzimidazole Hybrids as Promising Multitarget Metal-Modulating Compounds for Potential Treatment of Neurodegenerative Diseases." International Journal of Molecular Sciences 24, no. 9 (May 5, 2023): 8312. http://dx.doi.org/10.3390/ijms24098312.

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With the goal of combating the multi-faceted Alzheimer’s disease (AD), a series of Rivastigmine-Benzimidazole (RIV–BIM) hybrids was recently reported by us as multitarget-directed ligands, thanks to their capacity to tackle important hallmarks of AD. In particular, they exhibited antioxidant activity, acted as cholinesterase inhibitors, and inhibited amyloid-β (Aβ) aggregation. Herein, we moved forward in this project, studying their ability to chelate redox-active biometal ions, Cu(II) and Fe(III), with widely recognized roles in the generation of oxidative reactive species and in protein misfolding and aggregation in both AD and Parkinson’s disease (PD). Although Cu(II) chelation showed higher efficiency for the positional isomers of series 5 than those of series 4 of the hybrids, the Aβ-aggregation inhibition appears more dependent on their capacity for fibril intercalation than on copper chelation. Since monoamine oxidases (MAOs) are also important targets for the treatment of AD and PD, the capacity of these hybrids to inhibit MAO-A and MAO-B was evaluated, and they showed higher activity and selectivity for MAO-A. The rationalization of the experimental evaluations (metal chelation and MAO inhibition) was supported by computational molecular modeling studies. Finally, some compounds showed also neuroprotective effects in human neuroblastoma (SH-SY5Y cells) upon treatment with 1-methyl-4-phenylpyridinium (MPP+), a neurotoxic metabolite of a Parkinsonian-inducing agent.

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Morrill, André, Ólafur K. Nielsen, Karl Skírnisson, and Mark R. Forbes. "Identifying sources of variation in parasite aggregation." PeerJ 10 (August 24, 2022): e13763. http://dx.doi.org/10.7717/peerj.13763.

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Aggregation of macroparasites among hosts is a near-universal pattern, and has important consequences for the stability of host-parasite associations and the impacts of disease. Identifying which potential drivers are contributing to levels of aggregation observed in parasite-host associations is challenging, particularly for observational studies. We apply beta regressions in a Bayesian framework to determine predictors of aggregation, quantified using Poulin’s index of discrepancy (D), for 13 species of parasites infecting Icelandic Rock Ptarmigan (Lagopus muta) collected over 12 years. 1,140 ptarmigan were collected using sampling protocols maximizing consistency of sample sizes and of composition of host ages and sexes represented across years from 2006–2017. Parasite species, taxonomic group (insect, mite, coccidian, or nematode), and whether the parasite was an ecto- or endoparasite were tested as predictors of aggregation, either alone or by modulating an effect of parasite mean abundance on D. Parasite species was an important predictor of aggregation in models. Despite variation in D across samples and years, relatively consistent aggregation was demonstrated for each specific host-parasite association, but not for broader taxonomic groups, after taking sample mean abundance into account. Furthermore, sample mean abundance was consistently and inversely related to aggregation among the nine ectoparasites, however no relationship between mean abundance and aggregation was observed among the four endoparasites. We discuss sources of variation in observed aggregation, sources both statistical and biological in nature, and show that aggregation is predictable, and distinguishable, among infecting species. We propose explanations for observed patterns and call for the review and re-analysis of parasite and other symbiont distributions using beta regression to identify important drivers of aggregation—both broad and association-specific.

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McIntire, Larry, Joel Moake, Huey-Ju Kuo, Rui-Qing Qian, Robert Glanville, Elaine Schwartz, Jacob Rand, and Julia Ross. "Fibrillin Containing Elastic Microfibrils Support Platelet Adhesion under Dynamic Shear Conditions." Thrombosis and Haemostasis 79, no. 01 (1998): 155–61. http://dx.doi.org/10.1055/s-0037-1614236.

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SummaryThe vascular subendothelium contains macromolecular structures called microfibrils. Type VI collagen is one protein found in microfibrils that supports platelet adhesion and aggregation and we have previously evaluated the roles of platelet receptors and vWf involved in these processes under physiological shear conditions. Here we investigate the ability of fibrillin containing elastic microfibrils to support mural thrombus formation. Our results show that elastic microfibril surfaces support platelet adhesion under low shear conditions at a level similar to collagen VI tetramers. However, the degree of aggregation on the elastic microfibril surface is much higher. Both adhesion and aggregation were shown to be mediated by the GPIIb-IIIa platelet receptor. Elastic microfibrils do not support the formation of mural thrombi under high shear conditions. These results suggest roles for both collagen VI and fibrillin containing elastic microfibrils in modulating the platelet response to blood vessel injury.

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Thompson, Kiara, Holly Hosking, Wayne Pederick, Indu Singh, and Abishek B. Santhakumar. "The effect of anthocyanin supplementation in modulating platelet function in sedentary population: a randomised, double-blind, placebo-controlled, cross-over trial." British Journal of Nutrition 118, no. 5 (September 13, 2017): 368–74. http://dx.doi.org/10.1017/s0007114517002124.

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AbstractThe anti-thrombotic properties of anthocyanin (ACN) supplementation was evaluated in this randomised, double-blind, placebo (PBO) controlled, cross-over design, dietary intervention trial in sedentary population. In all, sixteen participants (three males and thirteen females) consumed ACN (320 mg/d) or PBO capsules for 28 d followed by a 2-week wash-out period. Biomarkers of thrombogenesis and platelet activation induced by ADP; platelet aggregation induced by ADP, collagen and arachidonic acid; biochemical, lipid, inflammatory and coagulation profile were evaluated before and after supplementation. ACN supplementation reduced monocyte-platelet aggregate formation by 39 %; inhibited platelet endothelial cell adhesion molecule-1 expression by 14 %; reduced platelet activation-dependant conformational change and degranulation by reducing procaspase activating compound-1 (PAC-1) (↓10 %) and P-selectin expression (↓14 %), respectively; and reduced ADP-induced whole blood platelet aggregation by 29 %. Arachidonic acid and collagen-induced platelet aggregation; biochemical, lipid, inflammatory and coagulation parameters did not change post-ACN supplementation. PBO treatment did not have an effect on the parameters tested. The findings suggest that dietary ACN supplementation has the potential to alleviate biomarkers of thrombogenesis, platelet hyperactivation and hyper-aggregation in sedentary population.

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Mauro, D., D. Iacono, I. Pantano, M. Raimondi, M. L. Marchesano, F. Riccio, A. Pellegrino, V. Liakouli, and F. Ciccia. "AB0470 EFFECT OF TOFACITINIB IN MODULATING PLATELET FUNCTION IN PATIENTS WITH RHEUMATOID ARTHRITIS." Annals of the Rheumatic Diseases 82, Suppl 1 (May 30, 2023): 1428.1–1428. http://dx.doi.org/10.1136/annrheumdis-2023-eular.5861.

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BackgroundRecent data suggested an association between Tofacitinib treatment and increased cardiovascular events in patients with Rheumatoid arthritis. Janus Kinase inhibitors (JAKi), specifically JAK3, have been demonstrated to be one of the regulators of platelet function. Treating platelets with thrombin induces tyrosine phosphorylation of the JAK3 target substrates STAT1 and STAT3, and JAK3 deficiency in mice reduces platelet aggregation and improves event-free survival in thromboplastin-induced thromboembolism.ObjectivesThis study aimed to study the ability of the JAK1/JAK3 inhibitor, Tofacitinib, to influence platelet activity in patients with Rheumatoid Arthritis.MethodsWe enrolled patients with a diagnosis of RA according to the ACR/EULAR 2010 ACR/EULAR criteria. Peripheral blood was obtained from RA patients at the baseline and after 1, 3 and 6 months of Tofacitinib therapy.Platelet aggregation assay was performed by optical aggregometry stimulated with the thromboxane A2receptor in RA patients and controls. The aggregation test was performed before starting the therapy with Tofacitinib and after one month, three months and six months.Results25 RA patients treated with Tofacitinib were recruited, 86% female and 14 % male, with a mean age of 56.5 years (SD 9.7 yrs.), mean disease duration of 16.3 years, mean ESR 28.2 mm, mean CRP 0.9 mg/dl, mean SDAI 18.2 and mean prednisone equivalent dose 3.75 mg/die. 78% of the patients were positive for Rheumatoid factor and 57.1% for ACPA. Looking at the classical risk factors, 35.7 had hypertension, 21.4% had hypercholesterolemia, 16.2% had diabetes, and 14.2% were smokers.; only one patient had a previous cardiovascular event.The platelet aggregation was not influenced by Tofacitinib treatment at any time points (T1, T3 and T6) at any Thromboxane dose (5uM and 20 uM), furthermore did not differ from patients and controls basally (64%, SD 15.84% vs 62%, SD 10.5%).ConclusionIn conclusion, Tofacitinib does not increase platelet aggregation in patients treated for Rheumatoid Arthritis.References[1]Lu, W.-J., Lin, K.-C., Huang, S.-Y., Thomas, P. A., Wu, Y.-H., Wu, H.-C., Lin, K.-H., & Sheu, J.-R. (2014). Role of a Janus kinase 2-dependent signaling pathway in platelet activation.Thrombosis Research,133(6), 1088–1096.[2]Parra-Izquierdo, I., Melrose, A. R., Pang, J., Lakshmanan, H. H. S., Reitsma, S. E., Vavilapalli, S. H., Larson, M. K., Shatzel, J. J., McCarty, O. J. T., & Aslan, J. E. (2022). Janus kinase inhibitors ruxolitinib and baricitinib impair glycoprotein-VI mediated platelet function.Platelets,33(3), 404–415.AcknowledgementsResearch was supported by an unrestricted grant by Pfizer.Disclosure of InterestsDaniele Mauro Grant/research support from: Research was supported by an unrestricted grant by Pfizer, Daniela Iacono Grant/research support from: Research was supported by an unrestricted grant by Pfizer, Ilenia Pantano Grant/research support from: Some research was supported by an unrestricted grant by Pfizer, Maura Raimondi Grant/research support from: Some research was supported by an unrestricted grant by Pfizer, Maria Laura Marchesano Grant/research support from: Some research was supported by an unrestricted grant by Pfizer, Flavia Riccio Grant/research support from: Some research was supported by an unrestricted grant by Pfizer, Anna Pellegrino Grant/research support from: Some research was supported by an unrestricted grant by Pfizer, Vasiliki Liakouli Grant/research support from: Some research was supported by an unrestricted grant by Pfizer, Francesco Ciccia Grant/research support from: Some research was supported by an unrestricted grant by Pfizer.

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Fan, Cheng, Xiaofang Yang, Wan Wendy Wang, Jue Wang, Wenzhu Li, Mengyuan Guo, Shiyuan Huang, Zhaohui Wang, and Kun Liu. "Role of Kv1.3 Channels in Platelet Functions and Thrombus Formation." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 10 (October 2020): 2360–75. http://dx.doi.org/10.1161/atvbaha.120.314278.

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Objective: Platelet activation by stimulatory factors leads to an increase in intracellular calcium concentration ([Ca 2+ ] i ), which is essential for almost all platelet functions. Modulation of Ca 2+ influx and [Ca 2+ ] i in platelets has been emerging as a possible strategy for preventing and treating platelet-dependent thrombosis. Voltage-gated potassium 1.3 channels (Kv1.3) are highly expressed in platelets and able to regulate agonist-evoked [Ca 2+ ] i increase. However, the role of Kv1.3 channels in regulating platelet functions and thrombosis has not yet been elucidated. In addition, it is difficult to obtain a specific blocker for this channel, since Kv1.3 shares identical drug-binding sites with other K + channels. Here, we investigate whether specific blockade of Kv1.3 channels by monoclonal antibodies affects platelet functions and thrombosis. Approach and Results: In this study, we produced the anti-Kv1.3 monoclonal antibody 6E12#15, which could specifically recognize both human and mouse Kv1.3 proteins and sufficiently block Kv1.3 channel currents. We found Kv1.3 blockade by 6E12#15 inhibited platelet aggregation, adhesion, and activation upon agonist stimulation. In vivo treatment with 6E12#15 alleviated thrombus formation in a mesenteric arteriole thrombosis mouse model and protected mice from collagen/epinephrine-induced pulmonary thromboembolism. Furthermore, we observed Kv1.3 regulated platelet functions by modulating Ca 2+ influx and [Ca 2+ ] i elevation, and that this is mediated in part by P2X 1 . Interestingly, Kv1.3 −/− mice showed impaired platelet aggregation while displayed no abnormalities in in vivo thrombus formation. This phenomenon was related to more megakaryocytes and platelets produced in Kv1.3 −/− mice compared with wild-type mice. Conclusions: We showed specific inhibition of Kv1.3 by the novel monoclonal antibody 6E12#15 suppressed platelet functions and platelet-dependent thrombosis through modulating platelet [Ca 2+ ] i elevation. These results indicate that Kv1.3 could act as a promising therapeutic target for antiplatelet therapies.

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Ren, Zhenkui, Mei Yang, Zhizhong Guan, and Wenfeng Yu. "Astrocytic α7 Nicotinic Receptor Activation Inhibits Amyloid-β Aggregation by Upregulating Endogenous αB-crystallin through the PI3K/Akt Signaling Pathway." Current Alzheimer Research 16, no. 1 (December 31, 2018): 39–48. http://dx.doi.org/10.2174/1567205015666181022093359.

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Background: β-amyloid (Aβ) aggregation plays an important role in the pathogenesis of Alzheimer’s disease (AD), and astrocytes can significantly inhibit Aβ aggregation. Astrocytic α7 Neuronal Nicotinic Acetylcholine Receptor (nAChR) upregulation detected in the AD brains is closely associated with Aβ deposits. However, the relationships between the astrocytic α7 nAChRs and Aβ aggregation remain unclear. Methods: The Aβ oligomers levels in astrocytic cell lysates and culture medium were measured after treatment with nicotine or co-treatment with a Phosphatidylinositol 3-Kinase (PI3K)-protein kinase B (Akt) inhibitor. The level of αB-Crystallin (Cryab) in astrocytes treated with nicotine for different times or co-treated with α7 nAChR antagonists as well as co-incubated with a PI3K or mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor was determined by western blotting. Results: In this study, nicotine pre-treatment in primary astrocytes markedly inhibited Aβ aggregation and upregulated endogenous astrocytic Cryab, while the nicotine-mediated neuroprotective effect was reversed by pre-treatment with a selective α7 nAChR antagonist. Furthermore, this neuroprotection against Aβ aggregation was suppressed by LY294002, a PI3K inhibitor. Pre-treatment with nicotine significantly increased the levels of phosphorylated Akt, an effector of PI3K in astrocytes. Conclusion: α7 nAChR activation and PI3K/Akt signaling transduction contributed to nicotinemediated neuroprotection against Aβ aggregation by modulating endogenous astrocytic Cryab.

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Alemanno, Laura, Isabella Massimi, Vanessa Klaus, Maria Guarino, Teresa Maltese, Luigi Frati, Dominick Angiolillo, and Fabio Pulcinelli. "Impact of Multidrug Resistance Protein-4 Inhibitors on Modulating Platelet Function and High on-Aspirin Treatment Platelet Reactivity." Thrombosis and Haemostasis 118, no. 03 (February 15, 2018): 490–501. http://dx.doi.org/10.1055/s-0038-1629920.

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AbstractPlatelet multidrug resistance protein 4 (MRP4) plays a modulating role on platelet activation. Platelet function and thrombus formation are impaired in MRP4 knockout mice models, and, among aspirin-treated patients, high on-aspirin residual platelet reactivity (HARPR) positively correlates with MRP4 levels. To better understand the effects of MRP4 on platelet function, the aim of this investigation was to assess the impact of cilostazol-induced inhibition of MRP4-mediated transport and assess aspirin-induced antiplatelet effects and rates of HARPR in human subjects.Cilostazol-dependent inhibition of MRP4-mediated transport was assessed with the release of the fluorescent adduct bimane-glutathione and aspirin entrapment. Effect of Cilostazol on cAMP inhibition was evaluated by vasodilator-stimulated phosphoprotein (VASP). Platelet function was studied by collagen and TRAP-6-induced platelet aggregation and secretion.Cilostazol reduced the release of bimane-glutathione and enhanced aspirin entrapment demonstrating an inhibitory effect on MRP4 in platelets. VASP phosphorylation was absent until 10 seconds after addition of cilostazol, and becomes evident after 30 seconds. An inhibitory effect on platelet aggregation and secretion was found in activated platelets, with threshold concentration of agonists, 10 seconds after addition of cilostazol, supporting a role of MRP4 on platelet function that is cAMP independent. Cilostazol effects were also shown in aspirin-treated platelets. A reduction of platelet aggregation and secretion were observed in aspirin-treated patients with HARPR.This study supports the role of MRP4 on modulating platelet function which occurs through cAMP-independent mechanisms. Moreover, inhibition of MRP4 induced by cilostazol enhances aspirin-induced antiplatelet effects and reduces HARPR.

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Xu, Fang, Kun Gong, Dongzhi Liu, Lichang Wang, Wei Li, and Xueqin Zhou. "Enhancing photocurrent of dye-sensitized solar cells through solvent modulating aggregation of dyes." Solar Energy 240 (July 2022): 157–67. http://dx.doi.org/10.1016/j.solener.2022.05.032.

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Han, Xie, Bibo Zhang, Jianhua Chen, Sheng Hua Liu, Chunyan Tan, Haiyang Liu, Matthew J. Lang, Ying Tan, Xiaogang Liu, and Jun Yin. "Modulating aggregation-induced emission via a non-conjugated linkage of fluorophores to tetraphenylethenes." Journal of Materials Chemistry B 5, no. 26 (2017): 5096–100. http://dx.doi.org/10.1039/c7tb00623c.

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