scholarly journals Triple Combination of siRNAs Targeting TGFβ1, TGFβR2, and CTGF Enhances Reduction of Collagen I and Smooth Muscle Actin in Corneal Fibroblasts

2013 ◽  
Vol 54 (13) ◽  
pp. 8214 ◽  
Author(s):  
Sriniwas Sriram ◽  
Paulette Robinson ◽  
Liya Pi ◽  
Alfred S. Lewin ◽  
Gregory Schultz
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Collagen I ◽  
Muscle Actin ◽  
Triple Combination ◽  
Corneal Fibroblasts ◽  
Combination Of Sirnas

scholarly journals Detection of Retinal Fibrosis in a Rabbit Model of Penetrating Eye Injury

2020 ◽  
Vol 185 (Supplement_1) ◽  
pp. 443-447
Author(s):  
Whitney Greene ◽  
Teresa Burke ◽  
Gregory Bramblett ◽  
Heuy-Ching Wang
Keyword(s):  
Smooth Muscle ◽  
Disease Progression ◽  
Smooth Muscle Actin ◽  
Rabbit Model ◽  
Collagen I ◽  
Fundus Photography ◽  
Eye Injury ◽  
Muscle Actin ◽  
Penetrating Eye Injury ◽  
Immunofluorescence Labeling

ABSTRACT Introduction To establish a rabbit model of posterior penetrating eye injury as a platform to test potential therapeutics. Materials and Methods Anesthetized rabbits received posterior penetrating eye injury in one eye, whereas contralateral eyes were maintained as uninjured controls. Rabbits were randomized into two experimental groups. Group A was euthanized on Day 14 postinjury to determine retinal fibrosis at an early phase of disease progression. Group B was euthanized on Day 28 postinjury to examine retinal fibrosis at a late phase of disease progression. We examined animals on postinjury Days 7, 14, 21, and 28 with indirect ophthalmoscope and fundus photography. After euthanasia, eyes were processed for histology and immunofluorescence labeling of fibrotic proteins α-smooth muscle actin and collagen I. Results Early fibrosis was detected by Day 14, as indicated by indirect ophthalmoscopy and fundus imaging. Fibrotic membranes were visible at sites of injury. Immunofluorescence analysis detected α-smooth muscle actin and collagen I within the fibrotic membranes. Conclusions These data show that ocular fibrosis can be detected within 14 days after initial injury, with more severe fibrosis detected at 28 days postinjury. These results will be used to determine the optimal time points for later studies designed to test treatment strategies.

Functional resolution of fibrosis in mdx mouse dystrophic heart and skeletal muscle by halofuginone

2008 ◽  
Vol 294 (4) ◽  
pp. H1550-H1561 ◽  
Author(s):  
Kyla D. Huebner ◽  
Davinder S. Jassal ◽  
Orna Halevy ◽  
Mark Pines ◽  
Judy E. Anderson
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Respiratory Function ◽  
Smooth Muscle Actin ◽  
Collagen I ◽  
Mdx Mouse ◽  
Muscle Actin ◽  
Hepatocyte Growth

The effect of halofuginone (Halo) on established fibrosis in older mdx dystrophic muscle was investigated. Mice (8 to 9 mo) treated with Halo (or saline in controls) for 5, 10, or 12 wk were assessed weekly for grip strength and voluntary running. Echocardiography was performed at 0, 5, and 10 wk. Respiratory function and exercise-induced muscle damage were tested. Heart, quadriceps, diaphragm, and tibialis anterior muscles were collected to study fibrosis, collagen I and III expression, collagen content using a novel collagenase-digestion method, and cell proliferation. Hepatocyte growth factor and α-smooth muscle actin proteins were assayed in quadriceps. Halo decreased fibrosis (diaphragm and quadriceps), collagen I and III expression, collagen protein, and smooth muscle actin content after 10 wk treatment. Muscle-cell proliferation increased at 5 wk, and hepatocyte growth factor increased by 10 wk treatment. Halo markedly improved both cardiac and respiratory function and reduced damage and improved recovery from exercise. The overall impact of established dystrophy and dysfunction in cardiac and skeletal muscles was reduced by Halo treatment. Marked improvements in vital-organ functions implicate Halo as a strong candidate drug to reduce morbidity and mortality in Duchenne muscular dystrophy.

scholarly journals Cytotoxic Influence of Khat (Catha edulis (Vahl) Forssk. ex Endl) on Oral Fibroblasts, Squamous Carcinoma Cells, and Expression of α Smooth Muscle Actin

2021 ◽  
Vol 11 (8) ◽  
pp. 3524
Author(s):  
Azeem Ul Yaqin Syed ◽  
Muhammad A. Ahmed ◽  
Eman I. AlSagob ◽  
Mansour Al-Askar ◽  
Abdulrahman M. AlMubarak ◽  
...  
Keyword(s):  
Cell Death ◽  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Control Cell ◽  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Muscle Actin ◽  
Catha Edulis ◽  
Squamous Carcinoma Cells ◽  
Dose Dependent

The aim was to determine the cytotoxicity of Khat (Catha edulis (Vahl) Forssk. ex Endl) on normal oral fibroblasts (NOFs) and SCC4 (squamous carcinoma cells) along with expression of α-smooth muscle actin (α-SMA) in fibroblasts. Khat filtrate was prepared to obtain a concentrated viscous solution. NOFs and SCC4 cells were cultured in biological cabinets and were grown in Dulbeccos’ modified Eagles medium. Frozen cells were thawed at 37 °C and cell seeding was performed. NOFs and SCC4 cells were seeded on 96 well plates and allowed to attach. The medium was removed and a fresh medium containing different concentrations of Khat was added. The group without Khat served as a negative control and 4% paraformaldehyde as the positive control. Cell viability was assessed using the MTT assay and effect of Khat on fibroblast and SCC4 phenotypes was evaluated by immunostaining. Analysis of variance was used to assess data (p < 0.05). NOF 316 showed cell death in response to 4% paraformaldehyde, 12.5, 6.25, and 3.12 mg/mL of Khat. The highest concentration of Khat (25 mg/mL) failed to cause cytotoxicity of NOF 316. NOF 319 and NOF 26 displayed cell death at all concentrations of Khat, however, cytotoxicity was not dose dependent. NOF 18 and SCC4 cells showed dose-dependent cell death. NOF 316 showed α-SMA expression after 1 mg/mL of Khat exposure. Not all fibroblasts were α-SMA-positive, suggesting specific activation of a subset of fibroblasts. Khat is cytotoxic to NOF and SCC4 cells. Furthermore, it can also cause activation and phenotypic changes in oral fibroblasts, indicating a potential role in progression of oral squamous cell carcinoma.

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