scholarly journals Comparison of early changes in ocular surface markers and tear inflammatory mediators after femtosecond lenticule extraction and FS-LASIK

2021 ◽  
Vol 14 (2) ◽  
pp. 283-291
Author(s):  
Chi Zhang ◽  
◽  
Hong He ◽  
He Jin ◽  
Liang-Ping Liu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Inflammatory Mediators ◽  
Ocular Surface ◽  
Laser In Situ Keratomileusis ◽  
Fluorescein Staining ◽  
Female Patients ◽  
Tnf Α ◽  
Lenticule Extraction ◽  
Tgf Β1 ◽  
Femtosecond Lenticule Extraction

AIM: To compare the short-term impacts of femtosecond lenticule extraction (FLEx) and femtosecond laser-assisted laser in situ keratomileusis (FS-LASIK) on ocular surface measures and tear inflammatory mediators. METHODS: This prospective comparative nonrandomized clinical study comprised 75 eyes (75 patients). Totally 20 male and 15 female patients (age 21.62±3.25y) with 35 eyes underwent FLEx, and 26 male and 14 female patients (age 20.18±3.59y) with 40 eyes underwent FS-LASIK. Central corneal sensitivity, noninvasive tear breakup time, corneal fluorescein staining, Schirmer I test, tear meniscus height, and ocular surface disease index were evaluated in all patients. Tear concentrations of nerve growth factor (NGF), interleukin-1α (IL-1α), transforming growth factor-β1 (TGF-β1), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), and matrix metalloproteinase-9 (MMP-9) were assessed by multiplex antibody microarray. All measurements were performed preoperatively, and 1d, 1wk, and 1mo postoperatively. RESULTS: Patients who underwent FLEx exhibited a more moderate reduction in central corneal sensation and less corneal fluorescein staining than those in the FS-LASIK group 1wk after the procedure (P<0.01). NGF was significantly higher 1d and 1wk after surgery in the FS-LASIK group than in the FLEx group (P<0.01). By contrast, compared to those in the FLEx group, higher postoperative values and slower recovery of tear TGF-β1, IL-1α, and TNF-α concentrations were observed in the FS-LASIK group (P<0.01). Tear concentrations of NGF, TGF-β1, TNF-α, and IL-1α were correlated with ocular surface changes after FLEx or FS-LASIK surgery. CONCLUSION: There is less early ocular surface disruption and a reduced inflammatory response after FLEx than after FS-LASIK. NGF, TGF-β1, TNF-α, and IL-1α may contribute to the process of ocular surface recovery.

scholarly journals Centrifugation Conditions in the L-PRP Preparation Affect Soluble Factors Release and Mesenchymal Stem Cell Proliferation in Fibrin Nanofibers

Molecules ◽  
2019 ◽  
Vol 24 (15) ◽  
pp. 2729 ◽  
Author(s):  
Melo ◽  
Luzo ◽  
Lana ◽  
Santana
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Platelet Rich Plasma ◽  
Clinical Practices ◽  
Soluble Factors ◽  
Tnf Α ◽  
Platelet Concentration ◽  
Tgf Β1

Leukocyte and platelet-rich plasma (L-PRP) is an autologous product that when activated forms fibrin nanofibers, which are useful in regenerative medicine. As an important part of the preparation of L-PRP, the centrifugation parameters may affect the release of soluble factors that modulate the behavior of the cells in the nanofibers. In this study, we evaluated the influences of four different centrifugation conditions on the concentration of platelets and leukocytes in L-PRP and on the anabolic/catabolic balance of the nanofiber microenvironment. Human adipose-derived mesenchymal stem cells (h-AdMSCs) were seeded in the nanofibers, and their viability and growth were evaluated. L-PRPs prepared at 100× g and 100 + 400× g released higher levels of transforming growth factor (TGF)-β1 and platelet-derived growth factor (PDGF)-BB due to the increased platelet concentration, while inflammatory cytokines interleukin (IL)-8 and tumor necrosis factor (TNF)-α were more significantly released from L-PRPs prepared via two centrifugation steps (100 + 400× g and 800 + 400× g) due to the increased concentration of leukocytes. Our results showed that with the exception of nanofibers formed from L-PRP prepared at 800 + 400× g, all other microenvironments were favorable for h-AdMSC proliferation. Here, we present a reproducible protocol for the standardization of L-PRP and fibrin nanofibers useful in clinical practices with known platelet/leukocyte ratios and in vitro evaluations that may predict in vivo results.

scholarly journals Smooth-Muscle Calponin in Mesangial Cells: Regulation of Expression and a Role in Suppressing Glomerulonephritis

2002 ◽  
Vol 13 (2) ◽  
pp. 322-331 ◽  
Author(s):  
Youichi Sugenoya ◽  
Ashio Yoshimura ◽  
Hisako Yamamura ◽  
Kiyoko Inui ◽  
Hiroyuki Morita ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Actin Binding ◽  
Luciferase Reporter ◽  
Tnf Α ◽  
Mesangial Cell Proliferation ◽  
Tgf Β1

ABSTRACT. The basic or h1 calponin gene, which encodes an actin-binding protein involved in the regulation of smooth-muscle shortening velocity, is known to be a smooth-muscle differentiation-specific gene. It was found that basic calponin was expressed by cultured mesangial cells and localized along the actin filaments. Among the growth factors involved in the mesangial cell pathophysiology, including platelet-derived growth factor-BB (PDGF-BB), tumor necrosis factor–α (TNF-α), and transforming growth factor–β1 (TGF-β1), TNF-α potently downregulates basic calponin expression in both the mRNA and protein levels, whereas TGF-β1 upregulates the calponin expression. PDGF-BB also reduced its mRNA expression. The half-life of basic calponin mRNA was determined to be similar between TNF-α–treated and –untreated mesangial cells, whereas cell transfection assays that used a luciferase reporter gene construct containing the functional basic calponin promoter showed that TNF-α and PDGF-BB reduced the transcriptional activity. Because stimulation with TNF-α and PDGF-BB was associated with mesangial cell proliferation, basic calponin may play a role in the suppression of mesangial cell proliferation. Treatment with anti–glomerular basement membrane antibody in calponin knockout mice induced more severe nephritis than in wild type mice, as judged from an increase in the urinary protein excretion, glomerular cellularity, and number of proliferating cell nuclear antigen–positive cells in glomerulus. These results suggest that basic calponin expression may serve as one of the intrinsic regulators of glomerular nephritis. Elucidation of the molecular mechanisms for regulation of the basic calponin expression in mesangial cells may improve the understanding of the molecular basis and pathogenesis of the glomerular response to injury.

Cytokines modulate the sensitivity of human fibroblasts to stimulation with insulin-like growth factor-I (IGF-I) by altering endogenous IGF-binding protein production

1993 ◽  
Vol 137 (1) ◽  
pp. 151-159 ◽  
Author(s):  
M. E. Yateman ◽  
D. C. Claffey ◽  
S. C. Cwyfan Hughes ◽  
V. J. Frost ◽  
J. A. H. Wass ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Human Fibroblasts ◽  
Dermal Fibroblasts ◽  
Insulin Like Growth Factor ◽  
Tnf Α ◽  
Igf I ◽  
Dose Dependent ◽  
Tgf Β1 ◽  
Igfbp 3

ABSTRACT Human dermal fibroblasts produce a number of insulin-like growth factor-binding proteins (IGFBPs) including the main circulating form, IGFBP-3. It has been suggested that the regulation of IGFBP secretion may play a major role in modulating insulin-like growth factor (IGF) bioactivity. We have quantified the effects of two cytokines, transforming growth factor-β1 (TGF-β1) and tumour necrosis factor-α (TNF-α) which have opposing actions on fibroblast IGFBP-3 production, and examined their subsequent role in IGF-I mitogenesis. TGF-β1 caused a dose-dependent increase in IGFBP-3 in serum-free fibroblast-conditioned media. TGF-β1 (1 μg/l) resulted in immunoreactive IGFBP-3 levels reaching 286·5 ± 22·4% of control after 20 h, the increase being confirmed by Western ligand blot. TNF-α caused a dose-dependent decrease in fibroblast IGFBP-3 secretion, 1 μg TNG-α/l reducing IGFBP-3 levels to 32·1 ± 11·% of control. This effect was not due to cytotoxicity and was not cell-density-dependent. Fibroblast proliferation was examined using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric cytochemical bioassay. The addition of IGF-I resulted in dose-dependent growth stimulation after 48 h, the effective range being 20–100 μg/l. The IGF-I analogue Long-R3-IGF-I which has little affinity for the IGFBPs was approximately 20-fold more potent in this assay, and was unaffected by exogenous IGFBP-3. While the addition of 1 μg TGF-β1/l to increasing doses of IGF-I resulted in a fourfold decrease in mitogenic sensitivity to the IGF-I, no such effect was seen with Long-R3-IGF-I. Conversely, 1 μg TNF-α/l increased fibroblast IGF-I sensitivity five-fold, an effect not observed with the IGF-I analogue. Such data suggest that endogenous IGFBP-3 inhibits IGF-I bioactivity and that the regulation of IGF mitogenesis by TGF-β1 and TNF-α can occur via local IGFBP modulation. This may represent a mechanism by which complex growth signals are co-ordinated in vivo. Journal of Endocrinology (1993) 137, 151–159

scholarly journals Effect of Neutralizing Transforming Growth Factor β1 on the Immune Response against Mycobacterium tuberculosis in Guinea Pigs

2004 ◽  
Vol 72 (3) ◽  
pp. 1358-1363 ◽  
Author(s):  
Shannon Sedberry Allen ◽  
Lynne Cassone ◽  
Todd M. Lasco ◽  
David N. McMurray
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Growth Factor ◽  
Pleural Effusion ◽  
Pleural Fluid ◽  
Guinea Pigs ◽  
Transforming Growth Factor ◽  
Fluid Volume ◽  
Protein Levels ◽  
Tnf Α ◽  
Tgf Β1

ABSTRACT Transforming growth factor β (TGF-β) is a cytokine which has been shown to suppress the antimycobacterial immune responses of humans and experimental animals. In this study, the contributions of TGF-β to cytokine production in vivo were investigated by using the established guinea pig model of tuberculous pleurisy. Mycobacterium bovis BCG-vaccinated guinea pigs were injected intrapleurally with heat-killed virulent Mycobacterium tuberculosis. Eight days following induction of an antigen-specific pleural effusion, guinea pigs were injected intrapleurally with anti-TGF-β1 or isotype control antibody. The following day, pleural exudates were removed, and the fluid volume and characteristics of the infiltrating cells were determined. Pleural fluid was analyzed for total interferon (IFN) and tumor necrosis factor (TNF) protein levels by using appropriate bioassays. RNA from pleural effusion cells was examined to determine TGF-β1, TNF-α, IFN-γ, and interleukin-8 mRNA levels by using real-time PCR. Proliferative responses of pleural effusion lymphocytes were examined in response to concanavalin A and purified protein derivative (PPD) in vitro. Treatment with anti-TGF-β1 resulted in decreased pleural fluid volume and decreased cell numbers in the pleural space along with an increased percentage of lymphocytes and a decreased percentage of neutrophils. The bioactive TNF protein levels in pleural fluid were increased in guinea pigs treated with anti-TGF-β1, while the bioactive IFN protein concentrations were not altered. Expression of TGF-β1 and TNF-α mRNA was significantly increased following TGF-β1 neutralization. Finally, PPD-induced proliferative responses of pleural cells from anti-TGF-β1-treated animals were significantly enhanced. Thus, TGF-β1 may be involved in the resolution of this local, mycobacterial antigen-specific inflammatory response.

Modulation of Pro- and Antifibrinolytic Properties of Human Peritoneal Mesothelial Cells by Transforming Growth Factor β1 (TGF- β1), Tumor Necrosis Factor α (TNF-α) and Interleukin β1 (IL-1β)

1998 ◽  
Vol 79 (02) ◽  
pp. 362-370 ◽  
Author(s):  
Anne Elbrecht ◽  
Carsten Schauerte ◽  
Bernd Klosterhalfen ◽  
Baffour Amo-Takyi ◽  
Johanna Gehlen ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Plasminogen Activator ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Mesothelial Cells ◽  
Tnf Α ◽  
Tgf Β1 ◽  
Necrosis Factor ◽  
Pai 1

SummaryA decreased fibrinolytic activity of serosal surfaces appears to be a major factor in the development of peritoneal fibrous adhesions. Serosal fibrinolysis is regulated by mesothelial release of tissue type plasminogen activator (t-PA) and plasminogen activator inhibitor types 1 and 2 (PAI-1 and PAI-2). We investigated the influence of tumor necrosis factor alpha (TNF-α), transforming growth factor β (TGF- β1) and interleukin 1β (IL-1β) on pro- and antifibrinolytic properties of mesothelial cells (HOMC) using a cell/fibrin clot assay. TGF-β1, TNF-α and IL-1β induced a dose dependent 2.9, 2.3 and 1.9-fold increase of PAI-1 antigen, respectively, whereas t-PA concentrations decreased to one third of the control values. This modified PAI-1/t-PA secretion pattern leads to a significant delay of fibrinolysis. Analysis of m-RNA levels revealed increased PAI-1 m-RNA concentrations after 12 h and decreased m-RNA concentrations for t-PA after 6 h. Serosal hypofibrinolysis during peritonitis may be explained at least in part by cytokine effects which thus may favor adhesion formation.

scholarly journals Characterization and biological evaluation of a novel silver nanoparticle-loaded collagen-chitosan dressing

2020 ◽  
Vol 7 (4) ◽  
pp. 371-380 ◽  
Author(s):  
Rongfu Li ◽  
Zhaorong Xu ◽  
Qiong Jiang ◽  
Yunquan Zheng ◽  
Zhaohong Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Growth Factor ◽  
Silver Nanoparticle ◽  
Cytokine Expression ◽  
Inflammatory Factors ◽  
Mixed Solution ◽  
Degree Burn ◽  
Tnf Α ◽  
Tgf Β1

Abstract Effective coverage and protection is a priority in wound treatment. Collagen and chitosan have been widely used for wound dressings due to their excellent biological activity and biocompatibility. Silver nanoparticles (AgNPs) have a powerful antibacterial effect. In this study, a macromolecular and small-molecular collagen mixed solution, a macromolecular and small-molecular chitosan mixed solution were prepared, and a silver nanoparticle-loaded collagen-chitosan dressing (AgNP-CCD) has been proposed. First, the effects of a collagen-chitosan mixed solution on the proliferation of human umbilical vein endothelial cells and the secretion of cytokines were evaluated. Then, the characteristics and antibacterial effects of the AgNP-CCD were tested, and the effects on wound healing and the influence of wound cytokine expression were investigated via a deep second-degree burn wound model. The results showed that at the proper proportion and concentration, the collagen-chitosan mixed solution effectively promoted cell proliferation and regulated the levels of growth factors (vascular endothelial growth factor [VEGF], epidermal growth factor [EGF], platelet-derived growth factor [PDGF], transforming growth factor [TGF-β1], basic fibroblastic growth factor [bFGF]) and inflammatory factors (TNF-α, IL-1β, IL-6, IL-8). Moreover, AgNP solutions at lower concentrations exerted limited inhibitory effects on cell proliferation and had no effect on cytokine secretion. The AgNP-CCD demonstrated satisfactory morphological and physical properties as well as efficient antibacterial activities. An in vivo evaluation indicated that AgNP-CCD could accelerate the healing process of deep second-degree burn wounds and played an important role in the regulation of growth and inflammatory factors, including VEGF, EGFL-7, TGF-β1, bFGF, TNF-α and IL-1β. This AgNP-CCD exerted excellent biological effects on wound healing promotion and cytokine expression regulation.

scholarly journals Association of fibroblast growth factor 10 with the fibrotic and inflammatory pathogenesis of Graves’ orbitopathy

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0255344
Author(s):  
Sun Young Jang ◽  
Soo Hyun Choi ◽  
Don Kikkawa ◽  
Eun Jig Lee ◽  
Jin Sook Yoon
Keyword(s):  
Growth Factor ◽  
Protein Expression ◽  
Fibroblast Growth Factor ◽  
Transforming Growth Factor ◽  
Fibroblast Growth ◽  
Expression Levels ◽  
Tnf Α ◽  
Orbital Tissue ◽  
Graves Orbitopathy ◽  
Tgf Β1

Purpose The role of fibroblast growth factor (FGF) in orbital fibroblasts (OFs) is rarely known. In this study, we investigated the effect of FGF10 on fibrosis and the inflammation mechanism of Graves′ orbitopathy (GO). Methods Orbital tissue from GO (n = 15) and non-GO (n = 15) was obtained for this study. The mRNA and protein expression levels of FGF10 and FGF receptor 2b (FGFR2b) in orbital tissue were determined by real-time polymerase chain reaction, western blot analysis, and confocal microscopy. The effects of FGF10 on transforming growth factor (TGF)-β1 induced fibrotic proteins and interleukin (IL)-1β- or tumor necrosis factor (TNF)-α- induced inflammatory proteins were investigated using recombinant human (rh) FGF10 and small interfering (si) RNA transfection against FGF10. Results FGF10 and FGFR2b mRNA expression levels were significantly lower in GO orbital tissues than in non-GO orbital tissues (p = 0.009 and 0.005, respectively). Immunostaining of FGF10 in orbital adipose tissues showed differences in FGF10 expression between GO and control samples. Immunostaining of FGF10 was very weak in the orbital tissues of GO patients. TGF-β1-induced fibronectin, collagen Iα, α-smooth muscle actin protein expression in GO OFs was attenuated by rhFGF10 treatment and increased by knockdown of FGF10 via siFGF10 transfection. Similarly, IL-1β- or TNF-α-induced IL-6, IL-8, and cyclooxygenase-2 protein production in GO OFs was either blocked by rhFGF10 treatment or further upregulated by inhibition of FGF10 via siFGF10 transfection. Conclusions Our data demonstrate that FGF10 has beneficial effects on the inflammatory and fibrotic mechanisms of GO in primary cultured OFs, providing new insights into GO pathology and the discovery of FGF10 as a promising novel therapeutic application for the treatment of GO.

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