Literature DB >> 22149185

Reduction of galectin-3 expression and liver fibrosis after cell therapy in a mouse model of cirrhosis.

Sheilla Andrade de Oliveira1, Bruno Solano de Freitas Souza, Elton Pereira Sá Barreto, Carla Martins Kaneto, Hélio Almeida Neto, Carine Machado Azevedo, Elisalva Teixeira Guimarães, Luiz Antonio Rodrigues de Freitas, Ricardo Ribeiro-Dos-Santos, Milena Botelho Pereira Soares.   

Abstract

BACKGROUND AIMS: Cirrhosis, end-stage liver disease, is caused by different mechanisms of injury, associated with persistent inflammation. Galectin-3 is an important regulator of fibrosis that links chronic inflammation to fibrogenesis. We investigated the role of bone marrow cell (BMC) transplantation in chronic inflammation and hepatic fibrosis.
METHODS: Liver cirrhosis was induced by administration of carbon tetrachloride and ethanol to wild-type C57BL/6 or bone marrow chimeric mice. Bone marrow chimeras were generated by lethal irradiation and transplantation with BMC obtained from green fluorescent protein (GFP(+) )donors. Wild-type cirrhotic mice were transplanted with BMC without irradiation. Livers from chimeras and cirrhotic transplanted mice were obtained for evaluation of inflammation, fibrosis and regulatory factors [galectin-3, matrix metallopeptidase (MMP)-9, tissue inhibitor of metalloproteinase (TIMP)-1 and transforming growth factor (TGF)-β].
RESULTS: The development of cirrhosis was associated with increased expression of galectin-3 by F4/80(+) cells and intense migration of BMC to the liver. Furthermore, when transplanted after the establishment of cirrhosis, BMC also migrated to the liver and localized within the fibrous septa. Two months after BMC therapy, cirrhotic mice had a significant reduction in liver fibrosis and expression of type I collagen. We did not find any difference in levels of TGF-β, TIMP-1 and MMP-9 between saline and BMC groups. However, the numbers of inflammatory cells, phagocytes and galectin-3(+) cells were markedly lower in the livers of cirrhotic mice treated with BMC.
CONCLUSIONS: Our results demonstrate an important role for BMC in the regulation of liver fibrosis and that transplantation of BMC can accelerate fibrosis regression through modulatory mechanisms.

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Year:  2011        PMID: 22149185     DOI: 10.3109/14653249.2011.637668

Source DB:  PubMed          Journal:  Cytotherapy        ISSN: 1465-3249            Impact factor:   5.414


  8 in total

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Journal:  Clin Res Cardiol       Date:  2013-09-01       Impact factor: 5.460

Review 2.  IL-33/ST2 Axis in Organ Fibrosis.

Authors:  Ourania S Kotsiou; Konstantinos I Gourgoulianis; Sotirios G Zarogiannis
Journal:  Front Immunol       Date:  2018-10-24       Impact factor: 7.561

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4.  Adoptive Transfer of Bone Marrow-Derived Monocytes Ameliorates Schistosoma mansoni -Induced Liver Fibrosis in Mice.

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Journal:  Sci Rep       Date:  2019-04-23       Impact factor: 4.379

5.  The Number of Liver Galectin-3 Positive Cells Is Dually Correlated with NAFLD Severity in Children.

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Authors:  Nada Pejnovic; Ilija Jeftic; Nemanja Jovicic; Nebojsa Arsenijevic; Miodrag L Lukic
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Authors:  C M Kaneto; J S Nascimento; M C R Moreira; N D Ludovico; A P Santana; R A A Silva; I Silva-Jardim; J L Santos; S M B Sousa; P S P Lima
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  8 in total

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