Effect of prolotherapy on cellular proliferation and collagen deposition in MC3T3-E1 and patellar tendon fibroblast populations

2011 ◽  
Vol 158 (3) ◽  
pp. 132-139 ◽  
Author(s):  
Joseph W. Freeman ◽  
Yvonne M. Empson ◽  
Emmanuel C. Ekwueme ◽  
Danielle M. Paynter ◽  
P. Gunnar Brolinson
Keyword(s):  
Patellar Tendon ◽  
Cellular Proliferation ◽  
Collagen Deposition ◽  
Tendon Fibroblast

Relation of Internal Elastic Lamellar Layer Disruption to Neointimal Cellular Proliferation and Type III Collagen Deposition in Human Peripheral Artery Restenosis

2016 ◽  
Vol 117 (7) ◽  
pp. 1173-1179 ◽  
Author(s):  
Prakash Krishnan ◽  
K-Raman Purushothaman ◽  
Meerarani Purushothaman ◽  
Usman Baber ◽  
Arthur Tarricone ◽  
...  
Keyword(s):  
Cellular Proliferation ◽  
Type Iii Collagen ◽  
Collagen Deposition ◽  
Peripheral Artery ◽  
Type Iii ◽  
Lamellar Layer

scholarly journals The effect of 5α-oleandrin on keloid fibroblast activities

2019 ◽  
Vol 13 (S11) ◽  
Author(s):  
Ishandono Dachlan ◽  
Yohanes Widodo Wirohadidjojo ◽  
Mae Sri Hartati Wahyuningsih ◽  
Teguh Aryandono ◽  
Hardyanto Soebono ◽  
...  
Keyword(s):  
Mitomycin C ◽  
Cellular Proliferation ◽  
Treated Group ◽  
Negative Control ◽  
Proliferation Index ◽  
Collagen Deposition ◽  
Keloid Fibroblast ◽  
And Migration ◽  
Migration Capacity ◽  
Better Than

Abstract Background Keloids develop due to hyperactivity of keloid fibroblast (KF) in proliferation, migration, and collagen deposition along with low rates of collagen degradation. These are a result of the Wnt/β catenin signaling pathways under stimulation of TGF-β. 5α-oleandrin can suppress Wnt-targeted genes of osteosarcoma cells. We aimed to evaluate the anti-fibrotic effects of 5α-oleandrin on KF activities. Methods We collected the core of keloid materials from six patients who underwent keloid debulking surgery. Passage 4 of KF cells were then treated with mitomycin-C, 5α-oleandrin, and dilution medium as the negative control. To determine the effective dose of 5α-oleandrin, we diluted 5α-oleandrin into various concentrations. The incubation periods were 24 h, 48 h, and 72 h. The anti-proliferation and anti-fibrotic properties were measured using standard assay. Results Both the mitomycin-C and 5α-oleandrin treated groups indicated decrease in proliferation index (86.16 ± 4.20% and 73.76 ± 4.94%, respectively), collagen deposition index (90.26 ± 1.72% and 71.35 ± 4.26%, respectively), and migration capacity (33.51 ± 1.50% and 28.57 ± 1.58%, respectively). These were significant changes (p ≤ 0.05) compared to the non-treated group. Antifibrotic activities of 5α-oleandrin in cellular proliferation and collagen deposition were better than mitomycin-C. Conclusions The 5α-oleandrin has good antifibrotic effect in keloid fibroblast activities.

scholarly journals The Addition of Hyaluronic Acid into Platelet-Rich Fibrin Lysate in Restoration of Senescent Human Dermal Fibroblasts Activities

2018 ◽  
Vol 5 (2) ◽  
pp. 85-92
Author(s):  
Rika Azyenela ◽  
Indah Julianto ◽  
Yohanes Widodo Wirohadidjojo
Keyword(s):  
Hyaluronic Acid ◽  
Cellular Proliferation ◽  
Clinical Signs ◽  
Dermal Fibroblasts ◽  
Proliferation Index ◽  
Serum Starvation ◽  
Human Dermal Fibroblasts ◽  
Collagen Deposition ◽  
Platelet Rich Fibrin ◽  
Tgf Β1

Senescent human dermal fibroblasts had reduced capacity in proliferation and collagen synthesis. It is due to unresponsiveness against transforming growth factor-β1 (TGF-β1) stimulation. Either platelet-rich fibrin (PRF)-lysate or hyaluronic acid (HA) can restore TGF-β1 signaling pathway. To determine whether HA addition to PRF lysate has a better activity than PRF-lysate alone in restoring senescent human dermal fibroblasts (HDFs) activities. HDF isolated from six different human skins was divided into normal HDFs and senescent HDFs which are induced by serum starvation. The senescent groups were then given 50% PRF-lysate and various levels of HA. Amelioration of TGF-β1 signaling was measured by cellular proliferation index and collagen deposition.  Addition of HA into PRF-lysate resulted in a significant increase in proliferation index and collagen deposition index than PRF-lysate alone. The best level of HA for this mixture ranged from 20.83 mM to 41.67 mM. HA in PRF lysate is an excellent candidate material for treating clinical signs related to senescent human dermal fibroblasts.   Ethical permission: This experiment had gain approval from the local ethical committee, Ref: KE/FK/471/EC/2016 dated 17-05-2016.

scholarly journals Neurotrophin 3 upregulates proliferation and collagen production in human aortic valve interstitial cells: a potential role in aortic valve sclerosis

2017 ◽  
Vol 312 (6) ◽  
pp. C697-C706 ◽  
Author(s):  
Qingzhou Yao ◽  
Rui Song ◽  
Lihua Ao ◽  
Joseph C. Cleveland ◽  
David A. Fullerton ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Cyclin D1 ◽  
Cellular Proliferation ◽  
D1 Protein ◽  
Collagen Deposition ◽  
Aortic Valves ◽  
Aortic Valve Sclerosis ◽  
Collagen Production ◽  
Neurotrophin 3 ◽  
Human Aortic Valve

Calcific aortic valve disease (CAVD) is a leading cardiovascular disorder in the elderly. Diseased aortic valves are characterized by sclerosis (fibrosis) and nodular calcification. Sclerosis, an early pathological change, is caused by aortic valve interstitial cell (AVIC) proliferation and overproduction of extracellular matrix (ECM) proteins. However, the mechanism of aortic valve sclerosis remains unclear. Recently, we observed that diseased human aortic valves overexpress growth factor neurotrophin 3 (NT3). In the present study, we tested the hypothesis that NT3 is a profibrogenic factor to human AVICs. AVICs isolated from normal human aortic valves were cultured in M199 growth medium and treated with recombinant human NT3 (0.10 µg/ml). An exposure to NT3 induced AVIC proliferation, upregulated the production of collagen and matrix metalloproteinase (MMP), and augmented collagen deposition. These changes were abolished by inhibition of the Trk receptors. NT3 induced Akt phosphorylation and increased cyclin D1 protein levels in a Trk receptor-dependent fashion. Inhibition of Akt abrogated the effect of NT3 on cyclin D1 production. Furthermore, inhibition of either Akt or cyclin D1 suppressed NT3-induced cellular proliferation and MMP-9 and collagen production, as well as collagen deposition. Thus, NT3 upregulates cellular proliferation, ECM protein production, and collagen deposition in human AVICs. It exerts these effects through the Trk-Akt-cyclin D1 cascade. NT3 is a profibrogenic mediator in human aortic valve, and overproduction of NT3 by aortic valve tissue may contribute to the mechanism of valvular sclerosis.

scholarly journals Regenerative Effects of Wharton’s Jelly Stem Cells-Conditioned Medium in UVA-Irradiated Human Dermal Fibroblasts

2018 ◽  
Vol 5 (1) ◽  
pp. 45-50
Author(s):  
Yohanes Widodo Wirohadidjojo ◽  
Arief Budiyanto ◽  
Hardyanto Soebono
Keyword(s):  
Stem Cells ◽  
Conditioned Medium ◽  
Cellular Proliferation ◽  
Positive Control ◽  
Dermal Fibroblasts ◽  
Wharton’S Jelly ◽  
Cellular Migration ◽  
Human Dermal Fibroblasts ◽  
Collagen Deposition ◽  
Wharton's Jelly

Background: Ultraviolet A radiation (UVA) can photo-age skin by suppressing the proliferation, migration, and collagen deposition of human dermal fibroblasts (HDFs). This process occurs because UVA light can inhibit the gene expression of the TGF-β receptor in HDFs. Moreover, Wharton’s Jelly Stem Cells-Conditioned Medium (WJSC-CM) is hypothesized to release microvesicles that contain short m-RNA with regenerative properties. Objectives: This study aimed to determine the regenerative properties of WJSC-CM on UVA-Irradiated Human Dermal Fibroblasts (UVA-HDFs) Methods: Passaged fourth of  HDFs obtained from the foreskin of six (11- to 13-year-old) boys were repeatedly irradiated with a total of 10 J/cm2 UVA and treated with various concentrations of WJSC-CM. We used non-irradiated HDFs as positive control. After that, the consumption of TGF-β, cellular proliferation, cellular migration, and collagen deposition of each group were measured and compared. Results: Compared to the non-irradiated groups, the proliferation rates, migration rates, and collagen deposition of UVA-HDFs significantly decreased (p<0.05). WJSC-CM can improve the consumption of TGF-β, proliferation, and cellular migration of UVA-HDFs. However, WJSC-CM failed to improve the collagen deposition of UVA-HDFs (p>0.05). Conclusions: WJSC-CM has regenerative properties and is a candidate material for the treatment of prematurely ageing skin induced by UVA-irradiation.   Ethical permission: This experiment was permitted by the local ethical permission committee Ref:KE/FK/382/EC with permission letter dated 17-04-2013.

scholarly journals Cardiac Morphology and Collagen Deposition in A Glucose-6-Phosphatase Catalytic Subunit 3 (G6PC3) Knockout Mouse model

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Austin Lubkemann ◽  
Heidi Carpenter ◽  
Richard O’Brien ◽  
Scott Baldwin ◽  
Rolanda Lister
Keyword(s):  
Knockout Mice ◽  
Cellular Proliferation ◽  
Cardiac Tissue ◽  
Heart Defects ◽  
Left Ventricular ◽  
Severe Neutropenia ◽  
Collagen Deposition ◽  
Ki 67 ◽  
Hematopoietic Stem ◽  
Knock Out

Background: Glucose-6-phosphatase-- β (3), one of multiple isoforms of glucose-6-phosphatase, catalyzes the final step in gluconeogenesis. It is known that mutated G6P3 is associated with severe neutropenia in addition to congenital heart defects, but little is known about the histological changes in cardiac tissue as a result of mutated or deleted G6PC34. Objectives: We sought to further characterize the histological alterations caused by deleted G6PC3 and determine the role of collagen deposition, myocyte proliferation and apoptosis in these changes. Methods: Cardiac tissue from G6PC3 knockout mice and WT mice were harvested, imbedded and stained for markers of collagen (Trichrome), proliferation (KI-67), apoptosis (caspase 3) and hematopoietic stem cells (CD34). Slides were digitally uploaded, and Leica stain quantification was calculated. Results: We demonstrated that in G6PC3 knock out adult mice have significant differences in heart morphology including decreased left ventricular collagen, decreased cellular proliferation and increased apoptosis histologically. Conclusions: As compared to wild type, the hearts of G6PC3 knockout mice demonstrated significantly decreased collagen globally, a crucial component for adequate strength and contractility of myocardial tissue. More investigation should be done to further explore the functional effects of such alterations via echocardiograms.

Correlation Between Cellular Functions and Morphological Changes of Human Trophoblast in Vitro

1975 ◽  
Vol 33 ◽  
pp. 600-601
Author(s):  
John C. Garancis ◽  
Robert O. Hussa ◽  
Michael T. Story ◽  
Donald Yorde ◽  
Roland A. Pattillo
Keyword(s):  
Electron Microscopy ◽  
Cellular Proliferation ◽  
Morphological Changes ◽  
Culture Fluid ◽  
Cellular Functions ◽  
Human Trophoblast ◽  
Transmission Electron ◽  
Marked Activity ◽  
Malignant Trophoblast

Human malignant trophoblast cells in continuous culture were incubated for 3 days in medium containing 1 mM N6-O2'-dibutyryl cyclic adenosine 3':5'-monophosphate (dibutyryl cyclic AMP) and 1 mM theophylline. The culture fluid was replenished daily. Stimulated cultures secreted many times more chorionic gonadotropin and estrogens than did control cultures in the absence of increased cellular proliferation. Scanning electron microscopy revealed remarkable surface changes of stimulated cells. Control cells (not stimulated) were smooth or provided with varying numbers of microvilli (Fig. 1). The latter, usually, were short and thin. The surface features of stimulated cells were considerably different. There was marked increase of microvilli which appeared elongated and thick. Many cells were covered with confluent polypoid projections (Fig. 2). Transmission electron microscopy demonstrated marked activity of cytoplasmic organelles. Mitochondria were increased in number and size; some giant forms with numerous cristae were observed.

Vascular adaptations to hypoxia: molecular and cellular mechanisms regulating vascular tone

2007 ◽  
Vol 43 ◽  
pp. 105-120 ◽  
Author(s):  
Michael L. Paffett ◽  
Benjimen R. Walker
Keyword(s):  
Vascular Tone ◽  
Cellular Proliferation ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Hypoxia Inducible Factor ◽  
Systemic Circulation ◽  
Cellular Mechanisms ◽  
Hypoxia Inducible Factor 1 ◽  
Pulmonary Vasoconstriction ◽  
Adaptive Mechanisms ◽  
Adaptive Processes

Several molecular and cellular adaptive mechanisms to hypoxia exist within the vasculature. Many of these processes involve oxygen sensing which is transduced into mediators of vasoconstriction in the pulmonary circulation and vasodilation in the systemic circulation. A variety of oxygen-responsive pathways, such as HIF (hypoxia-inducible factor)-1 and HOs (haem oxygenases), contribute to the overall adaptive process during hypoxia and are currently an area of intense research. Generation of ROS (reactive oxygen species) may also differentially regulate vascular tone in these circulations. Potential candidates underlying the divergent responses between the systemic and pulmonary circulations may include Nox (NADPH oxidase)-derived ROS and mitochondrial-derived ROS. In addition to alterations in ROS production governing vascular tone in the hypoxic setting, other vascular adaptations are likely to be involved. HPV (hypoxic pulmonary vasoconstriction) and CH (chronic hypoxia)-induced alterations in cellular proliferation, ionic conductances and changes in the contractile apparatus sensitivity to calcium, all occur as adaptive processes within the vasculature.

Gut-enriched kruppel-like factor (GKLF) inhibits cellular proliferation by blocking the G1/S boundary of the cell cycle

2001 ◽  
Vol 120 (5) ◽  
pp. A103-A103
Author(s):  
X CHEN ◽  
D JOHNS ◽  
D GEIMAN ◽  
E MARBAN ◽  
V YANG
Keyword(s):  
Cell Cycle ◽  
Cellular Proliferation
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