Journal of Cellular Biochemistry
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In vitro and in silico analyses of <i>Vicia faba</i> L. on Peroxisome proliferator–activated receptor gamma Abstract The agonists of peroxisome proliferator–activated receptor gamma (PPARγ) from natural victual products were used as antidiabetic agents. Faba bean (Vicia faba L.) is a consequential legume that was known to possess potential antidiabetic activity, whose mechanism of action was unknown. The current study was focused to ascertain gene expression of the nuclear receptor PPARγ by Faba bean pod extract in rat cell lines (RINm5F).The real‐time polymerase chain reaction analysis demonstrated that Faba bean pod extract in concentrations of 160 µg/mL have shown 4.97‐fold stimulation compared with control. The cells treated with 320 µg/mL has shown 5.89‐fold upregulation, respectively. Furthermore, in silico docking analysis was carried out against PPARγ, using the bioactive compounds identified from Faba bean pod extracts, which were known reported compounds from the literature. The results suggest that gene expression of PPARγ was inhibited by the constituents in Faba bean. In silico analysis prognosticates, butein has a high binding energy (−8.6 kcal/mol) with an atomic contact energy of −214.10, followed by Apigenin and Quercetin against PPARγ. Similarly, the percentage of interaction was high for butein, followed by Apigenin and Quercetin than other compounds comparatively. Hence, the results conclude inhibition of PPARγ by the bioactive compounds from Faba bean, which may provide insights into developing future therapeutic molecules for diabetes mellitus.
Journal of Cellular Biochemistry - Tập 119 Số 9 - Trang 7729-7737 - 2018
Silibinin protects human endothelial cells from high glucose‐induced injury by enhancing autophagic response Abstract Silibin, a flavonoid from the seeds of Silybum marianum (L.) Gaertn. (Asteraceae) has been reported to produce curative properties in diabetes. Autophagy is generated by a vast array of insults for removal of damaged proteins and organelles from the cell. Inadequate autophagy promotes endothelial cells dysfunction and delays in diabetic ulcers recovery. We hypothesized that silibinin could protect endothelial cells against high glucose‐induced damage by engaging autophagic responses. HUVECs viability was evaluated by MTT assay. The Griess method and TBARS assay were used to monitor changes in the levels of nitric oxide and malondialdehyde, respectively. ROS generation was recorded in DCFDA‐stained cells analyzed by flow cytometry. To investigate the role of silibinin on migration, we used scratch test. The level of autophagy proteins LC3, Becline‐1, and P62 were measured by Western blotting. Our data showed that silibinin had potential to increase cell survival after exposure to high glucose condition. Total levels of oxidative stress markers were profoundly reduced and the activity of GSH was increased by silibinin. High glucose suppressed HUVECs migration to the scratched area. However, a significant increase in cell migration was observed after exposure to silibinin. Autophagy was blocked at the late stage by high glucose concentration and silibinin initiated an autophagic response by reducing P62 and enhancing Beclin‐1 and LC3‐II‐LC3‐I ratio. These effects were blocked by autophagy inhibitor of 3‐Methyladenine. These observations suggest that silibinin could protect HUVECs from high glucose induced‐damage possibly by activation of autophagy pathway.
Journal of Cellular Biochemistry - Tập 119 Số 10 - Trang 8084-8094 - 2018
Growth factor transgenes interactively regulate articular chondrocytes Abstract Adult articular chondrocytes lack an effective repair response to correct damage from injury or osteoarthritis. Polypeptide growth factors that stimulate articular chondrocyte proliferation and cartilage matrix synthesis may augment this response. Gene transfer is a promising approach to delivering such factors. Multiple growth factor genes regulate these cell functions, but multiple growth factor gene transfer remains unexplored. We tested the hypothesis that multiple growth factor gene transfer selectively modulates articular chondrocyte proliferation and matrix synthesis. We tested the hypothesis by delivering combinations of the transgenes encoding insulin‐like growth factor I (IGF‐I), fibroblast growth factor‐2 (FGF‐2), transforming growth factor beta1 (TGF‐β1), bone morphogenetic protein‐2 (BMP‐2), and bone morphogenetic protien‐7 (BMP‐7) to articular chondrocytes and measured changes in the production of DNA, glycosaminoglycan, and collagen. The transgenes differentially regulated all these chondrocyte activities. In concert, the transgenes interacted to generate widely divergent responses from the cells. These interactions ranged from inhibitory to synergistic. The transgene pair encoding IGF‐I and FGF‐2 maximized cell proliferation. The three‐transgene group encoding IGF‐I, BMP‐2, and BMP‐7 maximized matrix production and also optimized the balance between cell proliferation and matrix production. These data demonstrate an approach to articular chondrocyte regulation that may be tailored to stimulate specific cell functions, and suggest that certain growth factor gene combinations have potential value for cell‐based articular cartilage repair. J. Cell. Biochem. 114: 908–919, 2013. © 2012 Wiley Periodicals, Inc.
Journal of Cellular Biochemistry - Tập 114 Số 4 - Trang 908-919 - 2013
Cell‐penetrable nanobodies (transbodies) that inhibit the tyrosine kinase activity of EGFR leading to the impediment of human lung adenocarcinoma cell motility and survival Abstract Most patients suffering from non–small cell lung cancer (NSCLC) have epidermal growth factor receptor (EGFR) overexpression. Currently, EGFR tyrosine kinase inhibitors (TKIs) that act as the ATP‐analogs and monoclonal antibodies (MAbs) to EGFR‐ectodomain that block intracellular signaling are used for the treatment of advanced NSCLC. Unfortunately, adverse effects due to the TKI off‐target and drug resistance occur in a significant number of the treated patients while some NSCLC genotypes do not respond to the therapeutic MAbs. Thus, a more effective remedy for the treatment of EGFR‐overexpressed cancers is deemed necessary. In this study, VH/VH H displayed‐phage clones that are bound to recombinant EGFR‐TK were fished‐out from a humanized‐camel VH/VH H phage display library. VH/VH H of three phage‐infected Escherichia coli clones (VH18, VH H35, and VH36) were linked molecularly to nonaarginine (R9) for making them cell penetrable. R9‐VH18, R9‐VH H35, and R9‐VH36 were cytotoxic to human adenocarcinomic alveolar basal epithelial cells (A549) at the fifty percent inhibitory concentration (IC50 ) 0.181 ± 0.132, 0.00961 ± 0.00516, and 0.00996 ± 0.00752 μM, respectively, which were approximately 1000‐fold more effective than small molecular TKIs. R9‐VH18 and R9‐VH36 also delayed cancer cell migration in a scratch‐wound assay. Computerized homology modeling and intermolecular docking revealed that VH18 and VH H35 used CDR3 to interact with EGFR‐TK residues close to the catalytic site, which might sterically hinder the ATP‐binding of the TK; VH36 used CDR2 to bind at the asymmetric dimerization surface, which might disrupt EGFR dimerization leading to inhibition of intracellular signaling. The humanized‐cell penetrable nanobodies have a high potential for developing further towards a clinical application.
Journal of Cellular Biochemistry - Tập 120 Số 10 - Trang 18077-18087 - 2019
Endoplasmic reticulum stress induces the phosphorylation of small heat shock protein, Hsp27 Abstract There are several reports describing participation of small heat shock proteins (sHsps) in cellular protein quality control. In this study, we estimated the endoplasmic reticulum (ER) stress‐induced response of Hsp27 and αB‐crystallin in mammalian cells. Treatment targeting the ER with tunicamycin or thapsigargin induced the phosphorylation of Hsp27 but not of αB‐crystallin in U373 MG cells, increase being observed after 2–10 h and decline at 24 h. Similar phosphorylation of Hsp27 by ER stress was also observed with U251 MG and HeLa but not in COS cells and could be blocked using SB203580, an inhibitor of p38 MAP kinase. Other protein kinase inhibitors, like Gö6983, PD98059, and SP600125, inhibitors of protein kinase C (PKC), p44/42 MAP kinase, and JNK, respectively, were without major influence. Prolonged treatment with tunicamycin but not thapsigargin for 48 h caused the second induction of the phosphorylation of Hsp27 in U251 MG cells. Under these conditions, the intense perinuclear staining of Hsp27, with some features of aggresomes, was observed in 10%–20% of the cells. © 2005 Wiley‐Liss, Inc.
Journal of Cellular Biochemistry - Tập 95 Số 5 - Trang 932-941 - 2005
Akt signaling regulates actin organization via modulation of MMP‐2 activity during chondrogenesis of chick wing limb bud mesenchymal cells Abstract Endochondral ossification is initiated by the differentiation of mesenchymal precursor cells to chondrocytes. This process is characterized by a strong interdependence of cell shape and cytoskeletal organization accompanying the onset of chondrogenic gene expression, but the molecular mechanisms mediating these interactions are not known. In this study, we hypothesized that the activation of matrix metalloproteinase (MMP)‐2 would be involved in the reorganization of the actin cytoskeleton and that this would require an Akt‐dependent signaling pathway in chick wing bud mesenchymal cells. The pharmacological inhibition of Akt signaling resulted in decreased glycosaminoglycan synthesis and reduced the level of active MMP‐2, leading to suppressed cortical actin organization which is characteristic of differentiated chondrocytes. In addition, the exposure of cells to bafilomycin A1 reversed these chondro‐inhibitory effects induced by inhibition of Akt signaling. In conclusion, our data indicate that Akt signaling is involved in the activation of MMP‐2 and that this Akt‐induced activation of MMP‐2 is responsible for reorganization of the actin cytoskeleton into a cortical pattern with parallel rounding of chondrogenic competent cells. J. Cell. Biochem. 102: 252–261, 2007. © 2007 Wiley‐Liss, Inc.
Journal of Cellular Biochemistry - Tập 102 Số 1 - Trang 252-261 - 2007
Biology and pathology of Rho GTPase, PI‐3 kinase‐Akt, and MAP kinase signaling pathways in chondrocytes Abstract Chondrocytes provide the framework for the developing skeleton and regulate long‐bone growth through the activity of the growth plate. Chondrocytes in the articular cartilage, found at the ends of bones in diarthroidial joints, are responsible for maintenance of the tissue through synthesis and degradation of the extracellular matrix. The processes of growth, differentiation, cell death and matrix remodeling are regulated by a network of cell signaling pathways in response to a variety of extracellular stimuli. These stimuli consist of soluble ligands, including growth factors and cytokines, extracellular matrix proteins, and mechanical factors that act in concert to regulate chondrocyte function through a variety of canonical and non‐canonical signaling pathways. Key chondrocyte signaling pathways include, but are not limited to, the p38, JNK and ERK MAP kinases, the PI‐3 kinase‐Akt pathway, the Jak‐STAT pathway, Rho GTPases and Wnt‐β‐catenin and Smad pathways. Modulation of the activity of any of these pathways has been associated with various pathological states in cartilage. This review focuses on the Rho GTPases, the PI‐3 kinase‐Akt pathway, and some selected aspects of MAP kinase signaling. Most studies to date have examined these pathways in isolation but it is becoming clear that there is significant cross‐talk among the pathways and that the overall effects on chondrocyte function depend on the balance in activity of multiple signaling proteins. J. Cell. Biochem. 110: 573–580, 2010. © 2010 Wiley‐Liss, Inc.
Journal of Cellular Biochemistry - Tập 110 Số 3 - Trang 573-580 - 2010
The diagnostic accuracy of procalcitonin and C‐reactive protein for sepsis: A systematic review and meta‐analysis Abstract Background The objective of this study was to systematically evaluate the clinical value of procalcitonin and C‐reactive protein in the diagnosis of adult patients with sepsis. Method PubMed, Cochrane, Embase, Wanfang, China National Knowledge Infrastructure, and VIP database were searched by the index words to identify the qualified prospective studies, and relevant literature sources were also searched. The most recent research was done in the April 2017. The only languages included were English or Chinese. In the experiment group, patients were diagnosed with sepsis, severe sepsis, or septic shock; in the control group, the patients were of noninfectious origin or a systemic inflammatory response syndrome. The diagnostic accuracy was analyzed by heterogeneity, diagnostic odds ratio (DOR), sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and the summary receiver‐operating characteristic curve. Results At least nine studies were involved in the meta‐analysis with 495 patients in the sepsis group and 873 patients in the nonsepsis group. In terms of the diagnostic accuracy of C‐reactive protein (CRP) for sepsis, the overall area under the summary receiver operator characteristic (SROC) curve was 0.73 (95% confidence interval [CI], 0.69‐0.77), with a sensitivity and specificity of 0.80 (95% CI, 0.63‐0.90) and 0.61 (95% CI, 0.50‐0.72) respectively, and the DOR was 6.89 (95% CI, 3.86‐12.31). In terms of the diagnostic accuracy of procalcitonin (PCT) for sepsis, the overall area under the SROC curve was 0.85 (95% CI, 0.82‐0.88), with a sensitivity and specificity of 0.80 (95% CI, 0.69‐0.87) and 0.77 (95% CI, 0.60‐0.88) respectively, and the DOR was 12.50 (95% CI, 3.65‐42.80). Conclusion In this meta‐analysis, our results together indicate a moderate degree of value of PCT and CRP for the diagnosis of sepsis in adult patients. The diagnosis accuracy and specificity of PCT are higher than those of CRP.
Journal of Cellular Biochemistry - Tập 120 Số 4 - Trang 5852-5859 - 2019
Photodynamic treatment with anionic nanoclays containing curcumin on human triple‐negative breast cancer cells: Cellular and biochemical studies Abstract Photodynamic treatment is a minimally invasive and clinically approved procedure for eliminating selected malignant cells with activation of a photosensitizer agent at a specific light. Little is known, however, about the phototoxic properties of curcumin, as a natural phenolic compound, against different types of cancers. It is generally accepted that cellular damage occurs during photo treatment. There is a limitation in using of curcumin as a drug due to its low solubility, but nanoparticles such as anionic nanoclays or layered double hydroxide (LDH) could overcome it. The aim of this study was to investigate cellular responses to curcumin‐LDH nanoparticles after photodynamic treatment of MDA‐MB‐231 human breast cancer cells. For this purpose, the MDA‐MB‐231 human breast cancer cell line treated with curcumin‐LDH nanoparticle and then irradiated (photodynamic treatment). After irradiation, lactate dehydrogenase assay, clonogenic cell survival, cell death mechanisms such as autophagy and apoptosis were determined. Cell cycle distribution after photodynamic therapy (PDT) and also intracellular reactive oxygen species (ROS) generation were measured. The result showed that curcumin‐LDH–PDT has a cytotoxic and antiprolifrative effect on MDA‐MB‐231 human breast cancer cells. Curcumin‐LDH–PDT induced autophagy, apoptosis, and G0/G1 cell cycle arrest in human breast cancer cell line. Intracellular ROS increased in MDA‐MB‐231 cancer cell line after treatment with curcumin‐LDH along with irradiation. The results suggest that curcumin‐LDH nanoparticle could be considered as a novel approach in the photodynamic treatment of breast cancer.
Journal of Cellular Biochemistry - Tập 120 Số 4 - Trang 4998-5009 - 2019
Mesenchymal stem cells as trophic mediators Abstract Adult marrow‐derived Mesenchymal Stem Cells (MSCs) are capable of dividing and their progeny are further capable of differentiating into one of several mesenchymal phenotypes such as osteoblasts, chondrocytes, myocytes, marrow stromal cells, tendon‐ligament fibroblasts, and adipocytes. In addition, these MSCs secrete a variety of cytokines and growth factors that have both paracrine and autocrine activities. These secreted bioactive factors suppress the local immune system, inhibit fibrosis (scar formation) and apoptosis, enhance angiogenesis, and stimulate mitosis and differentiation of tissue‐intrinsic reparative or stem cells. These effects, which are referred to as trophic effects, are distinct from the direct differentiation of MSCs into repair tissue. Several studies which tested the use of MSCs in models of infarct (injured heart), stroke (brain), or meniscus regeneration models are reviewed within the context of MSC‐mediated trophic effects in tissue repair. J. Cell. Biochem. 98: 1076–1084, 2006. © 2006 Wiley‐Liss, Inc.
Journal of Cellular Biochemistry - Tập 98 Số 5 - Trang 1076-1084 - 2006
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