Liver Structural Injury in Leptin-Deficient (ob/ob) Mice: Lipogenesis, Fibrogenesis, Inflammation, and Apoptosis

SUMMARY: Nonalcoholic fatty liver disease (NAFLD) might progress the steatosis to nonalcoholic steatohepatitis (NASH), reaching a cirrhosis state and possibly hepatocellular carcinoma. The liver of three-month-old C57BL/6J mice (wild-type, WT group, n=10) and leptin- deficient obese mice (ob/ob grou...

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Autores principales:	Martins,Fabiane Ferreira, Souza-Mello,Vanessa, Carvalho,Jorge Jose de, del Sol,Mariano, Aguila,Marcia Barbosa, Mandarim-de-Lacerda,Carlos Alberto
Lenguaje:	English
Publicado:	Sociedad Chilena de Anatomía 2021
Materias:	Steatosis Stellate cell Fibrosis Confocal microscopy Stereology
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0717-95022021000300732
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spelling	oai:scielo:S0717-950220210003007322021-07-25Liver Structural Injury in Leptin-Deficient (ob/ob) Mice: Lipogenesis, Fibrogenesis, Inflammation, and ApoptosisMartins,Fabiane FerreiraSouza-Mello,VanessaCarvalho,Jorge Jose dedel Sol,MarianoAguila,Marcia BarbosaMandarim-de-Lacerda,Carlos Alberto Steatosis Stellate cell Fibrosis Confocal microscopy Stereology SUMMARY: Nonalcoholic fatty liver disease (NAFLD) might progress the steatosis to nonalcoholic steatohepatitis (NASH), reaching a cirrhosis state and possibly hepatocellular carcinoma. The liver of three-month-old C57BL/6J mice (wild-type, WT group, n=10) and leptin- deficient obese mice (ob/ob group, n=10) were studied, focusing on the mechanisms associated with the activation of the hepatic stellate cells (HSCs) and pro-fibrogenesis. The obese ob/ob animals' liver showed steatosis, increased lipogenesis gene expressions, inflammation, increased pro-inflammatory gene expressions, inflammatory infiltrate, and potential apoptosis linked to a high Caspase 3 expression. In ob/ob mice, liver sections were labeled in the fibrotic zones by anti-alpha-smooth muscle actin (alpha-SMA) and anti-Reelin, but not in the WT mice. Moreover, the alpha-SMA gene expression was higher in the ob/ob group's liver than the WT group. The pro-fibrogenic gene expressions were parallel to anti- alpha-SMA and anti-Reelin immunofluorescence, suggesting HSCs activation. In the ob/ob animals, there were increased gene expressions involved with lipogenesis (Peroxisome proliferator-activated receptor-gamma, Cell death-inducing DFFA-like effector-c, Sterol regulatory element-binding protein-1c, and Fatty acid synthase), pro-fibrogenesis (Transforming growth factor beta1, Smad proteins- 3, Yes-associated protein-1, Protein platelet-derived growth factor receptor beta), pro-inflammation (Tumor necrosis factor-alpha, and Interleukin-6), and apoptosis (Caspase 3). In conclusion, the results in obese ob/ob animals provide a clue to the events in humans. In a translational view, controlling these targets can help mitigate the hepatic effects of human obesity and NAFLD progression to NASH.info:eu-repo/semantics/openAccessSociedad Chilena de AnatomíaInternational Journal of Morphology v.39 n.3 20212021-06-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0717-95022021000300732en10.4067/S0717-95022021000300732
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	Steatosis Stellate cell Fibrosis Confocal microscopy Stereology
spellingShingle	Steatosis Stellate cell Fibrosis Confocal microscopy Stereology Martins,Fabiane Ferreira Souza-Mello,Vanessa Carvalho,Jorge Jose de del Sol,Mariano Aguila,Marcia Barbosa Mandarim-de-Lacerda,Carlos Alberto Liver Structural Injury in Leptin-Deficient (ob/ob) Mice: Lipogenesis, Fibrogenesis, Inflammation, and Apoptosis
description	SUMMARY: Nonalcoholic fatty liver disease (NAFLD) might progress the steatosis to nonalcoholic steatohepatitis (NASH), reaching a cirrhosis state and possibly hepatocellular carcinoma. The liver of three-month-old C57BL/6J mice (wild-type, WT group, n=10) and leptin- deficient obese mice (ob/ob group, n=10) were studied, focusing on the mechanisms associated with the activation of the hepatic stellate cells (HSCs) and pro-fibrogenesis. The obese ob/ob animals' liver showed steatosis, increased lipogenesis gene expressions, inflammation, increased pro-inflammatory gene expressions, inflammatory infiltrate, and potential apoptosis linked to a high Caspase 3 expression. In ob/ob mice, liver sections were labeled in the fibrotic zones by anti-alpha-smooth muscle actin (alpha-SMA) and anti-Reelin, but not in the WT mice. Moreover, the alpha-SMA gene expression was higher in the ob/ob group's liver than the WT group. The pro-fibrogenic gene expressions were parallel to anti- alpha-SMA and anti-Reelin immunofluorescence, suggesting HSCs activation. In the ob/ob animals, there were increased gene expressions involved with lipogenesis (Peroxisome proliferator-activated receptor-gamma, Cell death-inducing DFFA-like effector-c, Sterol regulatory element-binding protein-1c, and Fatty acid synthase), pro-fibrogenesis (Transforming growth factor beta1, Smad proteins- 3, Yes-associated protein-1, Protein platelet-derived growth factor receptor beta), pro-inflammation (Tumor necrosis factor-alpha, and Interleukin-6), and apoptosis (Caspase 3). In conclusion, the results in obese ob/ob animals provide a clue to the events in humans. In a translational view, controlling these targets can help mitigate the hepatic effects of human obesity and NAFLD progression to NASH.
author	Martins,Fabiane Ferreira Souza-Mello,Vanessa Carvalho,Jorge Jose de del Sol,Mariano Aguila,Marcia Barbosa Mandarim-de-Lacerda,Carlos Alberto
author_facet	Martins,Fabiane Ferreira Souza-Mello,Vanessa Carvalho,Jorge Jose de del Sol,Mariano Aguila,Marcia Barbosa Mandarim-de-Lacerda,Carlos Alberto
author_sort	Martins,Fabiane Ferreira
title	Liver Structural Injury in Leptin-Deficient (ob/ob) Mice: Lipogenesis, Fibrogenesis, Inflammation, and Apoptosis
title_short	Liver Structural Injury in Leptin-Deficient (ob/ob) Mice: Lipogenesis, Fibrogenesis, Inflammation, and Apoptosis
title_full	Liver Structural Injury in Leptin-Deficient (ob/ob) Mice: Lipogenesis, Fibrogenesis, Inflammation, and Apoptosis
title_fullStr	Liver Structural Injury in Leptin-Deficient (ob/ob) Mice: Lipogenesis, Fibrogenesis, Inflammation, and Apoptosis
title_full_unstemmed	Liver Structural Injury in Leptin-Deficient (ob/ob) Mice: Lipogenesis, Fibrogenesis, Inflammation, and Apoptosis
title_sort	liver structural injury in leptin-deficient (ob/ob) mice: lipogenesis, fibrogenesis, inflammation, and apoptosis
publisher	Sociedad Chilena de Anatomía
publishDate	2021
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0717-95022021000300732
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_version_	1718445198308016128

Liver Structural Injury in Leptin-Deficient (ob/ob) Mice: Lipogenesis, Fibrogenesis, Inflammation, and Apoptosis

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