ArticleWorld journal of gastroenterology2004
Blockage of transforming growth factor beta receptors prevents progression of pig serum-induced rat liver fibrosis.
Article in World journal of gastroenterology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Antioxidant and hepatoprotective effects of novel heteropolysaccharide isolated fromFood science & nutrition · 2022Article
- San-Cao Granule () Ameliorates Hepatic Fibrosis through High Mobility Group Box-1 Protein/Smad Signaling Pathway.Chinese journal of integrative medicine · 2018Article
- Small RNA- and DNA-based gene therapy for the treatment of liver cirrhosis, where we are?World journal of gastroenterology · 2014Review
- 3,3'-Diindolylmethane ameliorates experimental hepatic fibrosis via inhibiting miR-21 expression.British journal of pharmacology · 2013Article
- Effects of S-adenosylmethionine on liver methionine metabolism and steatosis with ethanol-induced liver injury in rats.Hepatology international · 2008Article
- Rosiglitazone prevents murine hepatic fibrosis induced by Schistosoma japonicum.World journal of gastroenterology · 2008Article
- Gene modulation for treating liver fibrosis.Critical reviews in therapeutic drug carrier systems · 2007Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo test the hypothesis that introduction of antisense T beta R I and T beta R II eukaryotic expressing plasmids into a rat model of immunologically induced liver fibrosis might block the action of TGF-beta (1) and halt the progression of liver fibrosis.
methodsRT-Nest-PCR and gene recombination techniques were used to construct rat antisense T beta R I and T beta R II recombinant plasmids which could be expressed in eukaryotic cells. The recombinant plasmids and empty vector (pcDNA3) were encapsulated by glycosyl-poly-L-lysine and then transducted into rats of pig serum-induced liver fibrosis model. Expression of exogenously transfected gene was assessed by Northern blot, and hepatic expressions of T beta R I and T beta R II were evaluated by RT-PCR and Western blot. We also performed ELISA for serum TGF-beta(1), hydroxyproline of hepatic tissues, immunohistochemistry for collagen types I and III, and VG staining for pathological study of the liver tissues.
resultsThe exogenous antisense T beta R I and T beta R II plasmids could be well expressed in vivo, and block mRNA and protein expression of T beta R I and T beta R II in the fibrotic liver at the level of mRNA respectively. These exogenous plasmid expressions reduced the level of TGF-beta(1) (antisense T beta R I group 23.998+/-3.045 ng/mL, antisense T beta R II group 23.156+/-3.131 ng/mL, disease control group 32.960+/-3.789 ng/mL; F=38.19, 36.73, P<0.01). Compared with disease control group, the contents of hepatic hydroxyproline (antisense T beta R I group 0.169+/-0.015 mg/g liver, antisense T beta R II group 0.167+/-0.009 mg/g liver, disease control group 0.296+/-0.026 mg/g liver; F=14.39, 15.48, P<0.01) and the deposition of collagen types I and III decreased in the two antisense treatment groups (antisense T beta R I group, collagen type I 669.90+/-50.67, collagen type III 657.29+/-49.48; antisense T beta R II group, collagen type I 650.26+/-51.51, collagen type III 661.58+/-55.28; disease control group, collagen type I 1209.44+/-116.60, collagen type III 1175.14+/-121.44; F=15.48 to 74.89, P<0.01). Their expression also improved the pathologic classification of liver fibrosis models (compared with disease control group, chi(2)=17.14, 17.24, P<0.01). No difference was found in the level of TGF-beta(1), the contents of hepatic hydroxyproline and collagen types I and III and pathologic grade between pcDNA3 control group and disease control group or between the two antisense treatment groups (F=0.11 to 1.06, chi(2)=0.13 to 0.16, P>0.05).
conclusionAntisense T beta R I and T beta R II recombinant plasmids have certain reverse effects on liver fibrosis and can be used as possible candidates for gene therapy.
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