A synthetic peptide from transforming growth factor β type III receptor inhibits liver fibrogenesis in rats with carbon tetrachloride liver injury

Ezquerro, Ignacio-José; Lasarte, Juan José; Dotor, Javier; Castilla‐Cortázar, Inma; Bustos, Matilde; Peñuelas, Iván; Blanco, Gemma; Rodrı́guez, Carlos; Lechuga, Marı́a del Carmen G.; Greenwel, Patricia; Rojkind, Marcos; Prieto, Jesús; Borrás‐Cuesta, Francisco

doi:10.1016/s1043-4666(03)00101-7

Cited by 115 publications

(109 citation statements)

References 30 publications

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“…[42][43][44][45] We show that intraperitoneal administration of these blocking peptides to mice exposed to PD fluid preserved the peritoneal morphology and function and decreased the accumulation of different subpopulations of "fibroblast-specific protein-1" (FSP-1) fibroblasts, especially of those co-expressing the mesothelial marker cytokeratin. These cells with intermediate phenotype (Cyto ϩ /FSP-1 ϩ ) displayed myofibroblastlike characteristics including fibrogenic capacity.…”

mentioning

confidence: 89%

“…42 P144 is a synthetic 14-mer peptide designed from the TGF-␤1 type III receptor (TSLDASIIWAMMQN) that has been shown to bind TGF-␤1 and to inhibit its activity in vitro and in vivo. 43,44 As a control, Figure 7. TGF-␤1-blocking peptides reduce the number of fibroblasts derived from bone-marrow-recruited cells.…”

Section: Peptides and Adenoviral Vectorsmentioning

confidence: 99%

“…This dose of P17 was similar to that used in previous studies. [42][43][44][45] For quantitative RT-PCR analysis, mesothelial cells were lysed in TRI reagent (Ambion, Inc., Austin, TX), and RNA was extracted as per fabricant instructions. Complementary DNA was synthesized from 2 g of total RNA by reverse transcription (RNA PCR Core Kit, Applied Biosystems, Inc.).…”

Section: Culture Of Mesothelial Cells and Treatmentsmentioning

confidence: 99%

“…The doses of P17 and P144 used in this study were similar to those used previously. [42][43][44]51 Two animals of the PDF group and one in each of the others groups were not used in the final analysis, with the main causes of dropouts being catheter port infection or traumatic catheter removal (control group, n ϭ 7; PDF group, n ϭ 10; PDFϩP17 group, n ϭ 11; PDFϩP144 group, n ϭ 11). A peritoneal equilibrium test was performed during the last day of treatments.…”

Section: Pd Fluid Exposure Model In Micementioning

confidence: 99%

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Blocking TGF-β1 Protects the Peritoneal Membrane from Dialysate-Induced Damage

Loureiro

Aguilera

Selgas

et al. 2011

Journal of the American Society of Nephrology

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159

211

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During peritoneal dialysis (PD), mesothelial cells undergo mesothelial-to-mesenchymal transition (MMT), a process associated with peritoneal-membrane dysfunction. Because TGF-␤1 can induce MMT, we evaluated the efficacy of TGF-␤1-blocking peptides in modulating MMT and ameliorating peritoneal damage in a mouse model of PD. Exposure of the peritoneum to PD fluid induced fibrosis, angiogenesis, functional impairment, and the accumulation of fibroblasts. In addition to expressing fibroblast-specific protein-1 (FSP-1), some fibroblasts co-expressed cytokeratin, indicating their mesothelial origin.

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mentioning

confidence: 89%

Section: Peptides and Adenoviral Vectorsmentioning

confidence: 99%

Section: Culture Of Mesothelial Cells and Treatmentsmentioning

confidence: 99%

Section: Pd Fluid Exposure Model In Micementioning

confidence: 99%

See 2 more Smart Citations

Blocking TGF-β1 Protects the Peritoneal Membrane from Dialysate-Induced Damage

Loureiro

Aguilera

Selgas

et al. 2011

Journal of the American Society of Nephrology

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159

211

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“…To inhibit the activity of TGF-b and COX-2, these mice were treated for 15 days with TGF-b inhibitory peptide P144 [49], a control peptide, or indomethacin during the course of blood-stage infection. We found that both TGF-b and COX-2 activities appear to mediate the inhibition of CD8 + T cell responses in vivo, as inhibiting either of these activities restored the CD8 + T cell response (Fig.…”

Section: Pge 2 and Tgf-b Inhibit Cd8 + T Cell Responses Against The Lmentioning

confidence: 99%

Role of TGF‐β and PGE₂in T cell responses during Plasmodium yoelii infection

et al. 2007

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During an acute blood-stage malaria infection, T cell responses to malaria and other bystander antigens are inhibited. Plasmodium infection induces strong cytokine responses that facilitate parasite clearance but may interfere with T cell functions, as some of the soluble immune mediators induced are also general inhibitors of T cell responses. Using a malaria mouse model, we have analyzed the cytokines produced by dendritic cells in response to P. yoelii infection that have potential T cell inhibitory activity. We found that during acute infection DC migrate to the spleen and secrete TGF-b, prostaglandin E 2 (PGE 2 ) and IL-10. We have analyzed the role of these general T cell inhibitors in a particular T cell response of evident importance in malaria infections: the CD8 + T cells generated against the liver-stage of the disease. During blood-stage infection, inhibition of the activity of TGF-b and PGE 2 restores the CD8 + T cell responses generated by sporozoites, increasing protection against re-infection. Our findings suggest that the strong cytokine response induced by blood-stage P. yoelii infection affects host T cell responses, inhibiting protective CD8 + T cells against the liver-stage of the disease.

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