Comparison of trichostatin A and valproic acid treatment regimens in a mouse model of kidney fibrosis

Beneden, Katrien Van; Geers, Caroline; Pauwels, Marina; Mannaerts, Inge; Wissing, Karl Martin; Branden, Christiane Van Den; Grunsven, Leo A. van

doi:10.1016/j.taap.2013.05.013

Cited by 53 publications

(39 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, some investigators have shown that VPA has renoprotective properties . It has been reported that VPA prevented focal segmental glomerulosclerosis, proteinuria, and kidney fibrosis in a mice model .…”

Section: Discussionmentioning

confidence: 99%

“…Valproic acid-induced Fanconi syndrome Interestingly, some investigators have shown that VPA has renoprotective properties. [58][59][60] It has been reported that VPA prevented focal segmental glomerulosclerosis, proteinuria, and kidney fibrosis in a mice model. 58,60 VPA, as an effective inhibitor of histone deacetylase (HDAC), serves as an antiinflammatory and anti-fibrotic agent.…”

Section: Discussionmentioning

confidence: 99%

“…[58][59][60] It has been reported that VPA prevented focal segmental glomerulosclerosis, proteinuria, and kidney fibrosis in a mice model. 58,60 VPA, as an effective inhibitor of histone deacetylase (HDAC), serves as an antiinflammatory and anti-fibrotic agent. 58,60 Although a lower dose VPA acts as a renoprotective agent, 58,60 a higher dose of VPA was administered here to simulate VPA-induced renal injury in rats.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Mechanism of valproic acid‐induced Fanconi syndrome involves mitochondrial dysfunction and oxidative stress in rat kidney

et al. 2018

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Mechanism of valproic acid‐induced Fanconi syndrome involves mitochondrial dysfunction and oxidative stress in rat kidney

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Renal fibrosis is a well-known cause of kidney failure in DXR-induced nephropathy [27]. Several cellular pathways, including fibroblast activation and tubular epithelial-mesenchymal transition, have been identified as the major causes of renal fibrosis [28].…”

Section: Discussionmentioning

confidence: 99%

Dalbergioidin Ameliorates Doxorubicin-Induced Renal Fibrosis by Suppressing the TGF-βSignal Pathway

Ren

Fan

et al. 2016

Mediators of Inflammation

View full text Add to dashboard Cite

We investigated the effect of Dalbergioidin (DAL), a well-known natural product extracted from Uraria crinita, on doxorubicin- (DXR-) induced renal fibrosis in mice. The mice were pretreated for 7 days with DAL followed by a single injection of DXR (10 mg/kg) via the tail vein. Renal function was analyzed 5 weeks after DXR treatment. DXR caused nephrotoxicity. The symptoms of nephrotic syndrome were greatly improved after DAL treatment. The indices of renal fibrosis, the phosphorylation of Smad3, and the expression of alpha-smooth muscle actin (α-SMA), fibronectin, collagen III (Col III), E-cadherin, TGF-β, and Smad7 in response to DXR were all similarly modified by DAL. The present findings suggest that DAL improved the markers for kidney damage investigated in this model of DXR-induced experimental nephrotoxicity.

show abstract

“…Histone deacetylase (HDAC) inhibitors are extensively evaluated in numerous experimental models of cancer, in which inhibition of deacetylation regulates cell survival, proliferation, differentiation, and apoptosis. 19 In addition, recent literature demonstrates HDAC inhibitors as efficacious treatment options for choroidal angiogenesis 20 and retinal ischemic injury and degeneration. 21,22 Acetylation is a critical post-translational modification that directly modulates gene transcription of histone and nonhistone proteins and is associated with the proliferation and differentiation of a variety of cell types.…”

Section: Introductionmentioning

confidence: 99%

Trichostatin A Inhibits Retinal Pigmented Epithelium Activation in an In Vitro Model of Proliferative Vitreoretinopathy

Por

Greene

Burke

et al. 2016

Journal of Ocular Pharmacology and Therapeutics

View full text Add to dashboard Cite

Purpose: Proliferative vitreoretinopathy (PVR) is a blinding disorder that develops after a retinal tear or detachment. Activation of the retinal pigmented epithelium (RPE) is implicated in PVR; however, the mechanisms leading to enhanced RPE proliferation, migration, and contraction remain largely unknown. This study utilized an in vitro model of PVR to investigate the role of acetylation in RPE activation and its contribution to the progression of this disease.Methods: ARPE-19 cells, primary cultures of porcine RPE, and induced pluripotent stem cell-derived RPE (iPS-RPE) were utilized for cellular and molecular analyses. Cells treated with transforming growth factor beta 2 (TGFβ2; 10 ng/mL) alone or in the presence of the broad-spectrum histone deacetylase (HDAC) inhibitor, trichostatin A (TSA; 0.1 μM), were assessed for contraction and migration through collagen contraction and scratch assays, respectively. Western blotting and immunofluorescence analysis were performed to assess α-smooth muscle actin (α-SMA) and β-catenin expression after TGFβ2 treatment alone or in combination with TSA.Results: TGFβ2 significantly increased RPE cell contraction in collagen matrix and this effect was inhibited in the presence of TSA (0.1 μM). In agreement with these data, immunofluorescence analysis of TSA-treated iPS-RPE wounded monolayers revealed decreased α-SMA as compared with control. Scratch assays to assess wound healing revealed TSA inhibited TGFβ2-mediated iPS-RPE cell migration.Conclusions: Our findings indicate a role of acetylation in RPE activation. Specifically, the HDAC inhibitor TSA decreased RPE cell proliferation and TGFβ2-mediated cell contraction and migration. Further investigation of pharmacological compounds that modulate acetylation may hold promise as therapeutic agents for PVR.

show abstract

Comparison of trichostatin A and valproic acid treatment regimens in a mouse model of kidney fibrosis

Cited by 53 publications

References 59 publications

Mechanism of valproic acid‐induced Fanconi syndrome involves mitochondrial dysfunction and oxidative stress in rat kidney

Mechanism of valproic acid‐induced Fanconi syndrome involves mitochondrial dysfunction and oxidative stress in rat kidney

Dalbergioidin Ameliorates Doxorubicin-Induced Renal Fibrosis by Suppressing the TGF-βSignal Pathway

Trichostatin A Inhibits Retinal Pigmented Epithelium Activation in an In Vitro Model of Proliferative Vitreoretinopathy

Contact Info

Product

Resources

About