scholarly journals Recovery of Vocal Fold Epithelium after Acute Phonotrauma

2017 ◽  
Vol 204 (2) ◽  
pp. 93-104 ◽  
Author(s):  
Bernard Rousseau ◽  
Tsuyoshi Kojima ◽  
Carolyn K. Novaleski ◽  
Emily E. Kimball ◽  
Carla V. Valenzuela ◽  
...  
Keyword(s):  
Tissue Repair ◽  
Vocal Fold ◽  
Structural Changes ◽  
Transforming Growth Factor ◽  
Rabbit Model ◽  
Transforming Growth Factor Β1 ◽  
Epithelial Cell Surface ◽  
Polymerase Chain ◽  
Junction Proteins

We investigated the timeline of tissue repair of vocal fold epithelium after acute vibration exposure using an in vivo rabbit model. Sixty-five New Zealand white breeder rabbits were randomized to 120 min of modal- or raised-intensity phonation. After the larynges were harvested at 0, 4, 8, and 24 h, and at 3 and 7 days, the vocal fold tissue was evaluated using electron microscopy and quantitative real-time polymerase chain reaction. There was an immediate decrease in the microprojection depth and height following raised-intensity phonation, paired with upregulation of cyclooxygenase-2. This initial 24-h period was also characterized by the significant downregulation of junction proteins. Interleukin 1β and transforming growth factor β1 were upregulated for 3 and 7 days, respectively, followed by an increase in epithelial cell surface depth at 3 and 7 days. These data appear to demonstrate a shift from inflammatory response to the initiation of a restorative process in the vocal fold epithelium between 24 h and 3 days. Despite the initial damage from raised-intensity phonation, the vocal fold epithelium demonstrates a remarkable capacity for the expeditious recovery of structural changes from transient episodes of acute phonotrauma. While structurally intact, the return of functional barrier integrity may be delayed by repeated episodes of phonotrauma and may also play an important role in the pathophysiology of vocal fold lesions.

scholarly journals In Vivo Engineering of the Vocal Fold ECM With Injectable HA Hydrogels—Late Effects on Tissue Repair and Biomechanics in a Rabbit Model

2011 ◽  
Vol 25 (2) ◽  
pp. 249-253 ◽  
Author(s):  
Susan L. Thibeault ◽  
Sarah A. Klemuk ◽  
Xia Chen ◽  
Beatriz H. Quinchia Johnson
Keyword(s):  
Late Effects ◽  
Tissue Repair ◽  
Vocal Fold ◽  
Rabbit Model

scholarly journals In Vivo Investigation of the Ameliorating Effect of Tempol against MIA-Induced Knee Osteoarthritis in Rats: Involvement of TGF-β1/SMAD3/NOX4 Cue

Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 6993
Author(s):  
Hagar B. Abo-zalam ◽  
Rehab F. Abdel-Rahman ◽  
Mohamed F. Abd-Ellah ◽  
Rania M. Abdelsalam ◽  
Mahmoud M. Khattab
Keyword(s):  
Structural Changes ◽  
Complex Disease ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Bone Alkaline Phosphatase ◽  
Mitogen Activated Protein Kinase ◽  
Knee Oa ◽  
Nadph Oxidase 4 ◽  
Tgf Β1

Osteoarthritis (OA) is a complex disease characterized by structural, functional, and metabolic deteriorations of the whole joint and periarticular tissues. In the current study, we aimed to investigate the possible effects of tempol on knee OA induced by the chemical chondrotoxic monosodium iodoacetate (MIA) which closely mimics both the pain and structural changes associated with human OA. Rats were administrated oral tempol (100 mg/kg) one week post-MIA injection (3 mg/50 μL saline) at the right knee joints for 21 consecutive days. Tempol improved motor performance and debilitated the MIA-related radiological and histological alterations. Moreover, it subsided the knee joint swelling. Tempol decreased the cartilage degradation-related biomarkers as matrix metalloproteinase-13, bone alkaline phosphatase (bone ALP), and fibulin-3. The superoxide dismutase mimetic effect of tempol was accompanied by decreased NADPH oxidase 4 (NOX4), inflammatory mediators, nuclear factor-kappa B (NF-κB), over-released transforming growth factor-β1 (TGF-β1). Tempol decreased the expression of chemokine (C-C motif) ligand 2 (CCL2). On the molecular level, tempol reduced the phosphorylated protein levels of p38 mitogen-activated protein kinase (MAPK), and small mother against decapentaplegic 3 homologs (SMAD3). These findings suggest the promising role of tempol in ameliorating MIA-induced knee OA in rats via collateral suppression of the catabolic signaling cascades including TGF-β1/SMAD3/NOX4, and NOX4/p38MAPK/NF-κB and therefore modulation of oxidative stress, catabolic inflammatory cascades, chondrocyte metabolic homeostasis.

Effect of Growth Factors on Hyaluronan Production by Canine Vocal Fold Fibroblasts

2003 ◽  
Vol 112 (7) ◽  
pp. 617-624 ◽  
Author(s):  
Shigeru Hirano ◽  
Dennis Heisey ◽  
Diane M. Bless ◽  
Charles N. Ford
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Lamina Propria ◽  
Vocal Fold ◽  
Transforming Growth Factor ◽  
Vocal Folds ◽  
Transforming Growth Factor Β1 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Positive Effects

Hyaluronan (HYA) is considered to be a crucial factor in scarless wound healing and in maintaining tissue viscosity of the vocal fold lamina propria. In this study focusing on the effects of growth factors, we examined how HYA is produced and controlled in canine cultured vocal fold fibroblasts. Fibroblasts were taken from the lamina propria of the vocal folds of 8 dogs and cultured with and without growth factors. The production of HYA in the supernatant culture was quantitatively examined by enzyme-linked immunosorbent assay. Hepatocyte growth factor, epidermal growth factor, basic fibroblast growth factor, and transforming growth factor β1 all stimulated HYA synthesis from vocal fold fibroblasts. These effects differed with the concentration of growth factors and the incubation period. We also examined how frequently the growth factors had to be administered in order to maintain appropriate levels of HYA. A single administration was sufficient to maintain appropriate HYA levels for at least 7 days. The present studies have demonstrated positive effects of growth factors in stimulating HYA production. Further in vivo study is needed to clarify the usefulness of these growth factors in the management of vocal fold scarring.

scholarly journals Unraveling the molecular pathobiology of vocal fold systemic dehydration using an in vivo rabbit model

PLoS ONE ◽  
2020 ◽  
Vol 15 (7) ◽  
pp. e0236348
Author(s):  
Naila Cannes do Nascimento ◽  
Andrea P. dos Santos ◽  
M. Preeti Sivasankar ◽  
Abigail Cox
Keyword(s):  
Vocal Fold ◽  
Rabbit Model

scholarly journals Effect of valproic acid on functional bleb morphology in a rabbit model of minimally invasive surgery

2021 ◽  
pp. bjophthalmol-2020-318691
Author(s):  
Zhu Li Yap ◽  
Li-Fong Seet ◽  
Stephanie WL Chu ◽  
Li Zhen Toh ◽  
Farah Ilyana Ibrahim ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Cell Growth ◽  
Minimally Invasive ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Rabbit Model ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Label Free ◽  
Collagen Fibres

AbstractPurposeTo determine the effect of valproic acid (VPA) on bleb morphology and scar characteristics in a rabbit model of minimally invasive glaucoma surgery (MIGS).MethodsNine New Zealand white rabbits were subjected to MIGS with intraoperative implantation of the PreserFlo MicroShunt. Rabbits were then administered with subconjunctival injections of phosphate buffered saline (PBS) (n=4) or with VPA (n=5). Bleb morphology was examined by slit-lamp biomicroscopy and in vivo confocal microscopy. Postoperative day 28 tissues were examined by immunohistochemical evaluation and label-free multiphoton microscopy to visualise the collagen matrix, by terminal deoxynucleotidyl transferase dUTP nick-end labelling assay and immunofluorescent labelling for Ki67 expression to detect apoptosis and cell growth, and by real-time quantitative PCR to measure Col1a1, Fn, and Smad6 transcript expression.ResultsVPA-treated blebs were detectable on day 28, while the PBS-treated blebs were not detectable by day 14. VPA-treated blebs were diffuse, extended posteriorly with near normal conjunctival vascularity and featured a combination of reticular/blurred stromal pattern with evidence of relatively large stromal cysts. Instead of the deposition of thick, disorganised collagen fibres characteristic of the PBS bleb, the VPA bleb contained conspicuously thinner collagen fibres which were associated with similarly thinner fibronectin fibres. In corroboration, Col1a1 and Fn mRNA expression was reduced in the VPA blebs, while increased Smad6 expression implicated the disruption of the transforming growth factor beta pathway. Apoptosis and cell growth profiles appeared similar with both treatments.ConclusionsThe results support the application of VPA to enhance bleb morphology associated with good bleb function in MIGS with no apparent cytotoxicity.

scholarly journals Intravenous Injection of Clinical Grade Human MSCs after Experimental Stroke: Functional Benefit and Microvascular Effect

2016 ◽  
Vol 25 (12) ◽  
pp. 2157-2171 ◽  
Author(s):  
Anaïck Moisan ◽  
Isabelle Favre ◽  
Claire Rome ◽  
Florence De Fraipont ◽  
Emmanuelle Grillon ◽  
...  
Keyword(s):  
Transforming Growth Factor ◽  
Ex Vivo ◽  
Quantitative Polymerase Chain Reaction ◽  
Transforming Growth Factor Β1 ◽  
Angiogenic Factors ◽  
Experimental Stroke ◽  
Vascular Density ◽  
Human Mscs ◽  
Functional Benefit

Stroke is the leading cause of disability in adults. Many current clinical trials use intravenous (IV) administration of human bone marrow-derived mesenchymal stem cells (BM-MSCs). This autologous graft requires a delay for ex vivo expansion of cells. We followed microvascular effects and mechanisms of action involved after an IV injection of human BM-MSCs (hBM-MSCs) at a subacute phase of stroke. Rats underwent a transient middle cerebral artery occlusion (MCAo) or a surgery without occlusion (sham) at day 0 (D0). At D8, rats received an IV injection of 3 million hBM-MSCs or PBS-glutamine. In a longitudinal behavioral follow-up, we showed delayed somatosensory and cognitive benefits 4 to 7 weeks after hBM-MSC injection. In a separate longitudinal in vivo magnetic resonance imaging (MRI) study, we observed an enhanced vascular density in the ischemic area 2 and 3 weeks after hBM-MSC injection. Histology and quantitative polymerase chain reaction (qPCR) revealed an overexpression of angiogenic factors such as Ang1 and transforming growth factor-β1 (TGF-β1) at D16 in hBM-MSC-treated MCAo rats compared to PBS-treated MCAo rats. Altogether, delayed IV injection of hBM-MSCs provides functional benefits and increases cerebral angiogenesis in the stroke lesion via a release of endogenous angiogenic factors enhancing the stabilization of newborn vessels. Enhanced angiogenesis could therefore be a means of improving functional recovery after stroke.

In vivo induction of bone by recombinant human transforming growth factor β1

2009 ◽  
Vol 6 (9) ◽  
pp. 961-968 ◽  
Author(s):  
L. Steven Beck ◽  
Arthur J. Ammann ◽  
Thomas B. Aufdemorte ◽  
Leo Deguzman ◽  
Yvette Xu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
In Vivo Induction

scholarly journals Hyperstimulation of CaSR in human MSCs by biomimetic apatite inhibits endochondral ossification via temporal down-regulation of PTH1R

2018 ◽  
Vol 115 (27) ◽  
pp. E6135-E6144 ◽  
Author(s):  
Melika Sarem ◽  
Miriam Heizmann ◽  
Andrea Barbero ◽  
Ivan Martin ◽  
V. Prasad Shastri
Keyword(s):  
Endochondral Ossification ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
In Vivo Studies ◽  
Human Mscs ◽  
Down Regulation ◽  
Calcium Sensing ◽  
Biomimetic Apatite ◽  
The Impact

In adult bone injuries, periosteum-derived mesenchymal stem/stromal cells (MSCs) form bone via endochondral ossification (EO), whereas those from bone marrow (BM)/endosteum form bone primarily through intramembranous ossification (IMO). We hypothesized that this phenomenon is influenced by the proximity of MSCs residing in the BM to the trabecular bone microenvironment. Herein, we investigated the impact of the bone mineral phase on human BM-derived MSCs’ choice of ossification pathway, using a biomimetic bone-like hydroxyapatite (BBHAp) interface. BBHAp induced hyperstimulation of extracellular calcium-sensing receptor (CaSR) and temporal down-regulation of parathyroid hormone 1 receptor (PTH1R), leading to inhibition of chondrogenic differentiation of MSCs even in the presence of chondroinductive factors, such as transforming growth factor-β1 (TGF-β1). Interestingly rescuing PTH1R expression using human PTH fragment (1–34) partially restored chondrogenesis in the BBHAp environment. In vivo studies in an ectopic site revealed that the BBHAp interface inhibits EO and strictly promotes IMO. Furthermore, CaSR knockdown (CaSR KD) disrupted the bone-forming potential of MSCs irrespective of the absence or presence of the BBHAp interface. Our findings confirm the expression of CaSR in human BM-derived MSCs and unravel a prominent role for the interplay between CaSR and PTH1R in regulating MSC fate and the choice of pathway for bone formation.

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