Comparative effects of TGF-β1 and TGF-β2 on extracellular matrix production, proliferation, migration, and collagen contraction of human Tenon's capsule fibroblasts in pseudoexfoliation and primary open-angle glaucoma

Kottler, Ulrike B.; Jünemann, Anselm; Aigner, Thomas; Zenkel, Matthias; Rummelt, C.; Schlötzer‐Schrehardt, Ursula

doi:10.1016/j.exer.2004.08.018

Cited by 82 publications

(60 citation statements)

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“…Results in this study indicated that emodin suppressed inflammation caused by CCl4, which might lead to the protection of the liver from injury. It is now widely accepted that the pro-inflammatory cytokine TGF-β1 is a major cytokine in the regulation of the production, degradation, and accumulation of ECM [38] , and it has been suggested that overexpression of TGF-β1 for a prolonged period of time after tissue damage may induce a fibroproliferative response and deposition of ECM, resulting in fibrosis in vital organs [39] . Many studies have detected the presence of TGF-β1, in the form of either protein or message, in the fibrotic tissues of animal models or human samples [40] .…”

Section: Discussionmentioning

confidence: 99%

Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation

Dong¹,

Yan²,

Zhang³

et al. 2009

WJG

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AIM: To investigate the role of emodin in protecting the liver against fibrogenesis caused by carbon tetrachloride (CCl4) in rats and to further explore the underlying mechanisms. METHODS:Rat models of experimental hepatic fibrosis were established by injection with CCl4; the treated rats received emodin via oral administration at a dosage of 20 mg/kg twice a week at the same time. Rats injected with olive oil served as a normal group. Histopathological changes were observed by hematoxylin and eosin staining. The activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum and hepatic hydroxyproline content were assayed by biochemical analyses. The mRNA and protein relevant to hepatic stellate cell (HSC) activation in the liver were assessed using real-time reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry, western blotting and enzymelinked immunosorbent assay. RESULTS:The degree of hepatic fibrosis increased markedly in the CCl4 group compared to the normal group (P < 0.01), and decreased markedly in the emodin group compared to the CCl4 group according to METAVIR scale (P < 0.01) compared with those in the normal control group (51.02 ± 10.64 IU/L and 132.28 ± 18.14 IU/L). The activities of serum ALT and AST were significantly higher in rats injected with CCl4 (289.25 ± 68.84 IU/L and 423.89 ± 35.67 IU/L, both P < 0.05).The activities of serum ALT and AST were significantly reduced by administration of emodin (176.34 ± 4 7. 2 9 I U / L a n d 2 2 6 . 1 ± 4 4. 5 2 I U / L , b o t h P < 0.05). Compared with the normal controls (54.53 ± 13.46 mg/g), hepatic hydroxyproline content was significantly higher in rats injected with CCl4 (120.27 ± 28.47 mg/g, P < 0.05). Hepatic hydroxyproline content was significantly reduced in the rats treated with emodin at 20 mg/kg (71.25 ± 17.02 mg/g, P < 0.05).Emodin significantly protected the liver from injury by reducing serum AST and ALT activities and reducing hepatic hydroxyproline content. The mRNA levels of transforming growth factor-β1 (TGF-β1), Smad4 and α-SMA in liver tissues were significantly down-regulated in SD rats that received emodin treatment. Furthermore, significant down-regulation of serum TGF-β1 protein levels and protein expression of Smad4 and α-SMA in liver tissues was also observed in the rats. Emodin inhibited HSC activation by reducing the abundance of TGF-β1 and Smad4. CONCLUSION:Emodin protects the rat liver from CCl4-induced fibrogenesis by inhibiting HSC activation. Emodin might be a therapeutic antifibrotic agent for the treatment of hepatic fibrosis.

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Section: Discussionmentioning

confidence: 99%

Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation

Dong¹,

Yan²,

Zhang³

et al. 2009

WJG

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“…Hcy can induce deposition of extracellular matrix components, fibrosis [11] , oxidative stress, and production of those subtypes of matrix metalloproteinases [8] , transforming growth factors, collagens [12] , and proinflammatory factors [13] , which were found to be increased in dry eye syndrome [7] and insufficient filtering blebs [4,5] . Therefore, further studies are warranted to investigate whether increased Hcy levels in tear fluid might be implicated in dry eye syndrome or failure of filtering blebs in POAG eyes.…”

Section: Discussionmentioning

confidence: 99%

“…There is accumulating evidence that vascular [1] , extracellular matrix [2] , and neurotoxic [3] changes contribute to the development of POAG besides increased intraocular pressure (IOP). Extracellular matrix and proinflammatory changes are also involved in ocular surface disorders seen in POAG including fibrosis of the filtering bleb after trabeculectomy [4,5] and dry eye syndrome [6,7] .…”

Section: Introductionmentioning

confidence: 99%

Increased Homocysteine Levels in Tear Fluid of Patients with Primary Open-Angle Glaucoma

et al. 2008

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Aims: We assessed homocysteine (Hcy) levels in tear fluid and plasma of patients with primary open-angle glaucoma (POAG). We determined the association between Hcy levels, dry eye syndrome and B vitamin status. Methods: This prospective case-control study included 36 patients with POAG and 36 controls. Hcy concentrations were measured by high-performance liquid chromatography. Results: Patients with POAG had significantly higher mean Hcy levels both in tear fluid (205 ± 84 nmol/l; p < 0.001, t test) and in plasma (13.43 ± 3.53 µmol/l; p = 0.001, t test) than control subjects (130 ± 53 nmol/l and 10.50 ± 3.33 µmol/l, respectively). Hcy in tear fluid was significantly correlated with plasma Hcy in POAG patients (r = 0.459; p = 0.005, Pearson’s correlation), but not in controls (r = 0.068; p = 0.695). POAG patients with dry eye disease had significantly higher Hcy levels both in tear fluid and plasma than POAG patients without dry eye disease. There was no association between Hcy levels and B vitamin status in subjects with POAG. Conclusions: The study suggests increased Hcy levels in tear fluid and plasma of patients with POAG. Elevated Hcy levels might be a risk factor for POAG and dry eye syndrome in subjects with glaucoma.

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“…27,28 TGFb alters ECM production and turnover in both the LC and TM and has been shown in numerous studies to play a role in ocular wound healing, 29,30 while its role in the pathogenesis of glaucoma is also well documented. [31][32][33] Several studies have reported elevated AqH levels of TGFb2 in POAG 34,35 and TGFb1 in PXFG patients. 23 Our studies have shown that TGFb1 has an effect on global gene expression profiles, especially profibrotic ECM genes in nerve head LC cells.…”

mentioning

confidence: 99%

Anti-Connective Tissue Growth Factor Antibody Treatment Reduces Extracellular Matrix Production in Trabecular Meshwork and Lamina Cribrosa Cells

Wallace

Clark

Lipson

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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Comparative effects of TGF-β1 and TGF-β2 on extracellular matrix production, proliferation, migration, and collagen contraction of human Tenon's capsule fibroblasts in pseudoexfoliation and primary open-angle glaucoma

Cited by 82 publications

References 45 publications

Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation

Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation

Increased Homocysteine Levels in Tear Fluid of Patients with Primary Open-Angle Glaucoma

Anti-Connective Tissue Growth Factor Antibody Treatment Reduces Extracellular Matrix Production in Trabecular Meshwork and Lamina Cribrosa Cells

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Comparative effects of TGF-β1 and TGF-β2 on extracellular matrix production, proliferation, migration, and collagen contraction of human Tenon's capsule fibroblasts in pseudoexfoliation and primary open-angle glaucoma

Cited by 82 publications

References 45 publications

Emodin protects rat liver from CCl4-induced fibrogenesis via inhibition of hepatic stellate cells activation

Emodin protects rat liver from CCl4-induced fibrogenesis via inhibition of hepatic stellate cells activation

Increased Homocysteine Levels in Tear Fluid of Patients with Primary Open-Angle Glaucoma

Anti-Connective Tissue Growth Factor Antibody Treatment Reduces Extracellular Matrix Production in Trabecular Meshwork and Lamina Cribrosa Cells

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Product

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Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation

Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation