scholarly journals Geniposide Ameliorated Dexamethasone-Induced Cholesterol Accumulation in Osteoblasts by Mediating the GLP-1R/ABCA1 Axis

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3424
Author(s):  
Yizhou Zheng ◽  
Yaosheng Xiao ◽  
Di Zhang ◽  
Shanshan Zhang ◽  
Jing Ouyang ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Micro Ct ◽  
Micro Structure ◽  
Cholesterol Accumulation ◽  
Bone Trabecula ◽  
Clinical Complications ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Intracellular Cholesterol ◽  
Ct Data

Background: Overexposure to glucocorticoid (GC) produces various clinical complications, including osteoporosis (OP), dyslipidemia, and hypercholesterolemia. Geniposide (GEN) is a natural iridoid compound isolated from Eucommia ulmoides. Our previous study found that GEN could alleviate dexamethasone (DEX)-induced differentiation inhibition of MC3T3-E1 cells. However, whether GEN protected against Dex-induced cholesterol accumulation in osteoblasts was still unclear. Methods: DEX was used to induce rat OP. Micro-CT data was obtained. The ALP activity and mineralization were determined by the staining assays, and the total intracellular cholesterol was determined by the ELISA kits. The protein expression was detected by western blot. Results: GEN ameliorated Dex-induced micro-structure damages and cell differentiation inhibition in the bone trabecula in rats. In MC3T3-E1 cells, Dex enhanced the total intracellular cholesterol, which reduced the activity of cell proliferation and differentiation. Effectively, GEN decreased DEX-induced cholesterol accumulation, enhanced cell differentiation, and upregulated the expression of the GLP-1R/ABCA1 axis. In addition, inhibition of ABAC1 expression reversed the actions of GEN. Treatment with Exendin9-39, a GLP-1R inhibitor, could abrogate the protective activity of GEN. Conclusions: GEN ameliorated Dex-induced accumulation of cholesterol and inhibition of cell differentiation by mediating the GLP-1R/ABCA1 axis in MC3T3-E1 cells.

Microenvironment of Apatite-Fiber Scaffold Affects Cell Proliferation and Resulting Cell Differentiation

2007 ◽  
Vol 361-363 ◽  
pp. 1075-1078
Author(s):  
Michiyo Honda ◽  
Shigeki Izumi ◽  
Nobuyuki Kanzawa ◽  
Takahide Tsuchiya ◽  
Mamoru Aizawa
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Cell Differentiation ◽  
Bone Marrow Cells ◽  
Three Dimensional ◽  
Bone Marrow Stem Cells ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation

Appropriate culture conditions cause bone marrow stem cells to differentiate into multilineage cells such as adipocytes, chondrocytes, and osteoblasts. One key factor that regulates intercellular signaling and cell differentiation is the extracellular matrix microenvironment. The composition of the extracellular matrix influences cellular functions. In the present study, we investigated the effects of a microenvironment comprising a three-dimensional apatite-fiber scaffold (AFS) that has two kinds of pores (micro- and macro pores) on proliferation and subsequent differentiation of bone marrow stem cells. Morphologic observation revealed that osteoblastic cells in the AFS were distributed primarily in the same location on the fibrous scaffold and formed bridges within micro- and macro pores. We used molecular approaches to evaluate cell proliferation and differentiation in detail. Reverse transcription-polymerase chain reaction (RT-PCR) analysis showed that culturing bone marrow cells on AFS increases expression of osteocalcin (OC) mRNA compared with culture in a dish. Furthermore, cells cultured in AFS expressed type X collagen (Col X), which is a marker of hypertrophic cartilage. These data suggest that the three-dimensional microenvironment of AFS facilitates cell proliferation and differentiation, and promotes endochondral ossification of bone marrow cells.

Depletion in nuclear spermine during human spermatogenesis, a natural process of cell differentiation

1992 ◽  
Vol 263 (2) ◽  
pp. C343-C347 ◽  
Author(s):  
V. Quemener ◽  
Y. Blanchard ◽  
D. Lescoat ◽  
R. Havouis ◽  
J. P. Moulinoux
Keyword(s):  
Cell Proliferation ◽  
Cell Differentiation ◽  
Mammalian Cells ◽  
Gradient Centrifugation ◽  
Cell Nuclei ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Human Spermatogenesis

Polyamines (PA), polycations present in all mammalian cells, are essential for cell proliferation and differentiation. In vitro, PA are known to bind to DNA with a high affinity. In vivo, the intimate association of endogenous PA with highly condensed chromatin has been reported. During spermatogenesis, when processes of cell proliferation and differentiation take place, the potential role of polyamines has not been studied in depth. We report here the PA levels measured in human spermatogenic cell nuclei at different stages of differentiation. Cell populations (spermatocytes and round, elongating, or elongated spermatids) were obtained after submitting human testes to a trypsin-deoxyribonuclease digestion, then to a centrifugal elutriation and Percoll gradient centrifugation. A significant and progressive nuclear spermine level decrease was observed from primary spermatocytes to elongated spermatids. This release of spermine from nuclei was concomitant with three major events in mammalian spermiogenesis: the reduction of DNA transcription activity, the replacement of histone proteins by protamines, and the compaction of chromatin. This is the first report arguing a release of nuclear spermine during an in vivo physiological cell differentiation process.

The Effect of LRAP on Enamel Organ Epithelial Cell Differentiation

2007 ◽  
Vol 86 (11) ◽  
pp. 1095-1099 ◽  
Author(s):  
T.Q. Le ◽  
Y. Zhang ◽  
W. Li ◽  
P.K. DenBesten
Keyword(s):  
Cell Proliferation ◽  
Cell Differentiation ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Enamel Organ ◽  
E Coli ◽  
Cell Proliferation And Differentiation ◽  
Human Enamel ◽  
Proliferation And Differentiation ◽  
Alternatively Spliced

Leucine-rich amelogenin peptide (LRAP) is an alternatively spliced amelogenin found in the developing enamel organ. LRAP functions to regulate the development of mesenchymal-derived cells; however, its effect on cells of the enamel organ remains unclear. The hypothesis tested in this study is that LRAP also regulates human enamel organ epithelial cells. Recombinant human LRAP (rH58) was synthesized in E. coli, purified, and exogenously added to cultures of human primary enamel epithelial cells, which were analyzed for changes in cell proliferation and differentiation. rH58 had no effect on cell proliferation, but altered enamel epithelial cell morphology, resulting in larger, more rounded cells. Immunofluorescence showed that rH58 treatment increased amelogenin synthesis, but down-regulated Notch1 expression in enamel epithelial cells. LAMP-1, a membrane receptor for LRAP in mesenchymal cells, was identified and was up-regulated in the presence of rH58. These results suggest that rH58 promotes differentiation of human enamel organ epithelial cells.

scholarly journals Regulation of Redox Homeostasis by Nonthermal Biocompatible Plasma Discharge in Stem Cell Differentiation

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Ying Li ◽  
Eun Ha Choi ◽  
Ihn Han
Keyword(s):  
Tissue Engineering ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Cell Differentiation ◽  
Redox Homeostasis ◽  
Stem Cell Differentiation ◽  
Redox Biology ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation

Recently, a growing body of evidence has shown the role of reactive species as secondary messengers in cell proliferation and differentiation, as opposed to the harmful metabolism byproducts that they were previously solely recognized as. Thus, the balance of intracellular reduction-oxidation (redox) homeostasis plays a vital role in the regulation of stem cell self-renewal and differentiation. Nonthermal biocompatible plasma (NBP) has emerged as a novel tool in biomedical applications. Recently, NBP has also emerged as a powerful tool in the tissue engineering field for the surface modification of biomaterial and the promotion of stem cell differentiation by the regulation of intracellular redox biology. NBP can generate various kinds of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which may play the role of the second passenger in the cell signaling network and active antioxidant system in cells. Herein, we review the current knowledge on mechanisms by which NBP regulates cell proliferation and differentiation through redox modification. Considering the importance of redox homeostasis in the regulation of stem cell differentiation, understanding the underlying molecular mechanisms involved will provide important new insights into NBP-induced stem cell differentiation for tissue engineering.

scholarly journals mTOR modulates CD8+ T cell differentiation in mice with invasive pulmonary aspergillosis

2018 ◽  
Vol 13 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Hao Wang ◽  
Yu Xiao ◽  
Longxiang Su ◽  
Na Cui ◽  
Dawei Liu
Keyword(s):  
Cell Proliferation ◽  
Cell Differentiation ◽  
T Cell ◽  
Invasive Pulmonary Aspergillosis ◽  
Mtor Pathway ◽  
Effector Memory ◽  
Pulmonary Aspergillosis ◽  
Tem Cell ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation

AbstractCD8+ T cells are a vital component of the adaptive immune system and important for eliminating intracellular pathogens. Notably, mTOR activity is associated with CD8+ T effector memory (Tem) cell differentiation in fungal infections. This study investigates the molecular mechanisms of CD8+ Tem cell proliferation and differentiation mediated by the mTOR pathway in immunosuppressed mice with invasive pulmonary aspergillosis (IPA). We first established the immunosuppressed IPA mouse model, then mice were subjected to rapamycin treatment daily or interleukin (IL)-12 treatment every other day. Lung tissues and blood samples were obtained seven days later. Aspergillus fumigatus was cultured from the lung tissue of mice inoculated with A. fumigatus spores. After IL-12 treatment, the expression of mTOR and its downstream signaling molecule S6 kinase, number of CD8+ Tem cells and interferon-γ expression were significantly increased, while they were significantly decreased after treatment with rapamycin. Additionally, IL-12 treatment induced T-bet but inhibited Eomesodermin expression, while the opposite was seen when the mTOR pathway was blocked by rapamycin. In conclusion, we found that the mTOR pathway induced CD8+ T cell proliferation and differentiation by regulating T-bet and Eomesodermin expression, which significantly influenced immune regulation during IPA and enhanced the immune response against fungal infection.

Impaired B-cell development at the pre-BII-cell stage in galectin-1–deficient mice due to inefficient pre-BII/stromal cell interactions

Blood ◽  
2009 ◽  
Vol 113 (23) ◽  
pp. 5878-5886 ◽  
Author(s):  
Marion Espeli ◽  
Stéphane J. C. Mancini ◽  
Caroline Breton ◽  
Françoise Poirier ◽  
Claudine Schiff
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Cell Differentiation ◽  
B Cell ◽  
Stromal Cell ◽  
Cell Phenotype ◽  
Cell Proliferation And Differentiation ◽  
Hydroxyurea Treatment ◽  
Proliferation And Differentiation ◽  
Deficient Mice

Abstract Activation of the pre-B-cell receptor (pre-BCR) in the bone marrow depends on both tonic and ligand-induced signaling and leads to pre-BII-cell proliferation and differentiation. Using normal mouse bone marrow pre-BII cells, we demonstrate that the ligand-induced pre-BCR activation depends on pre-BCR/galectin-1/integrin interactions leading to pre-BCR clustering at the pre-BII/stromal cell synapse. In contrast, heparan sulfates, shown to be pre-BCR ligands in mice, are not implicated in pre-BCR relocalization. Inhibition of pre-BCR/galectin-1/integrin interactions has functional consequences, since pre-BII-cell proliferation and differentiation are impaired in an in vitro B-cell differentiation assay, without affecting cellular apoptosis. Most strikingly, although galectin-1–deficient mice do not show an apparent B-cell phenotype, the kinetics of de novo B-cell reconstitution after hydroxyurea treatment indicates a specific delay in pre-BII-cell recovery due to a decrease in pre-BII-cell differentiation and proliferation. Thus, although it remains possible that the pre-BCR interacts with other ligands, these results highlight the role played by the stromal cell–derived galectin-1 for the efficient development of normal pre-BII cells and suggest the existence of pre-BII–specific stromal cell niches in normal bone marrow.

scholarly journals Akt-Fas to Quell Aberrant T Cell Differentiation and Apoptosis in Covid-19

2020 ◽  
Vol 11 ◽  
Author(s):  
Anthony J. Leonardi ◽  
Rui B. Proenca
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Cell Function ◽  
T Cell Differentiation ◽  
Serine Threonine Kinase ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
T Cell Lymphopenia ◽  
Infected Cells

Aberrant T cell differentiation and lymphopenia are hallmarks of severe COVID-19 disease. Since T cells must race to cull infected cells, they are quick to differentiate and achieve cytotoxic function. With this responsiveness, comes hastened apoptosis, due to a coupled mechanism of death and differentiation in both CD4+ and CD8+ lymphocytes via CD95 (Fas) and serine-threonine kinase (Akt). T cell lymphopenia in severe cases may represent cell death or peripheral migration. These facets depict SARS-Cov-2 as a lympho-manipulative pathogen; it distorts T cell function, numbers, and death, and creates a dysfunctional immune response. Whether preservation of T cells, prevention of their aberrant differentiation, and expansion of their population may alter disease course is unknown. Its investigation requires experimental interrogation of the linked differentiation and death pathway by agents known to uncouple T cell proliferation and differentiation in both CD4+ and CD8+ T cells.

scholarly journals Akt Fas to Quell Aberrant T Cell Differentiation and Death in Covid-19

2020 ◽  
Author(s):  
Anthony Joseph Leonardi
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Cell Function ◽  
T Cell Differentiation ◽  
Serine Threonine Kinase ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Hastened Death ◽  
Infected Cells

Aberrant T cell differentiation and lymphopenia are hallmarks of severe COVID-19 disease. Since T cells must race to cull infected cells, they are quick to differentiate and achieve cytotoxic function. With this responsiveness, unfortunately, comes hastened death, due to a coupled mechanism of death and differentiation in both CD4+ and CD8+ lymphocytes via CD95 (Fas) and serine-threonine kinase (Akt). T cell lymphopenia in severe cases may represent cell death or peripheral migration. These facets depict SARS-Cov-2 as a lympho-manipulative pathogen; it distorts T cell function, numbers, and death, and creates a dysfunctional immune response. Whether preservation of T cells, prevention of their differentiation, and expansion of their population may alter disease course is unknown. Its investigation requires experimental interrogation of the linked differentiation and death pathway by agents known to uncouple T cell proliferation and differentiation in both CD4+ and CD8+ T cells.

Role of melatonin in regulating neurogenesis: Implications for the neurodegenerative pathology and analogous therapeutics for Alzheimer’s disease

2020 ◽  
Vol 3 (2) ◽  
pp. 216-242 ◽  
Author(s):  
Mayuri Shukla ◽  
Areechun Sotthibundhu ◽  
Piyarat Govitrapong
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Adult Neurogenesis ◽  
Adult Brain ◽  
Therapeutic Approaches ◽  
Therapeutic Implications ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Progenitor Cell Proliferation

The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.   

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