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postgraduate thesis: The pathological role of A-FABP in the development of liver fibrosis

TitleThe pathological role of A-FABP in the development of liver fibrosis
Authors
Issue Date2015
PublisherThe University of Hong Kong (Pokfulam, Hong Kong)
Citation
Xu, X. [徐小惠]. (2015). The pathological role of A-FABP in the development of liver fibrosis. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659870
AbstractBackground and objectives: Circulating levels of adipocyte fatty acid binding protein (A-FABP) are closely associated with liver fibrosis and inflammation in patients with nonalcoholic fatty liver disease (NAFLD). However, there are no in vivo studies to explore the role of A-FABP in liver fibrosis. In the present study, A-FABP knockout (KO) mice were generated for the loss of function study and three liver fibrosis mouse models: carbon tetrachloride (CCl4) injection, bile duct ligation (BDL) and high fat high cholesterol (HFHC) diet induced mouse models were employed to investigate the pathological role of A-FABP in liver fibrosis. Key findings: 1. Morphological analysis of liver and quantitative PCR of the hepatic expression of fibrotic markers showed that liver fibrosis was successfully established on wild-type (WT) mice treated with CCl4 injection or BDL, and wild type and A-FABP knockout (KO) mice fed on HFHC diet. 2. HFHC diet induced liver fibrosis was alleviated in A-FABP KO mice when compared to WT control. 3. Circulating A-FABP was significantly increased in both CCl4 injection and BDL induced mouse models. 4. The mRNA expression of A-FABP was elevated in the liver tissue of BDL-, CCl4- and WT-HFHC diet induced mouse models. Conclusions: Circulating and hepatic A-FABP increased in CCL4- and BDL-induced liver fibrosis mouse models. A-FABP deficiency protects against HFHC-induced liver fibrosis in mice. These results indicate that A-FABP is associated with the development of liver fibrosis and may be a potential fibrotic biomarker and therapeutic target for anti-fibrotic drug development.
DegreeMaster of Medical Sciences
SubjectFatty acid-binding proteins
Liver - Fibrosis
Dept/ProgramMedicine
Persistent Identifierhttp://hdl.handle.net/10722/221503

 

DC FieldValueLanguage
dc.contributor.authorXu, Xiaohui-
dc.contributor.author徐小惠-
dc.date.accessioned2015-11-26T23:38:08Z-
dc.date.available2015-11-26T23:38:08Z-
dc.date.issued2015-
dc.identifier.citationXu, X. [徐小惠]. (2015). The pathological role of A-FABP in the development of liver fibrosis. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659870-
dc.identifier.urihttp://hdl.handle.net/10722/221503-
dc.description.abstractBackground and objectives: Circulating levels of adipocyte fatty acid binding protein (A-FABP) are closely associated with liver fibrosis and inflammation in patients with nonalcoholic fatty liver disease (NAFLD). However, there are no in vivo studies to explore the role of A-FABP in liver fibrosis. In the present study, A-FABP knockout (KO) mice were generated for the loss of function study and three liver fibrosis mouse models: carbon tetrachloride (CCl4) injection, bile duct ligation (BDL) and high fat high cholesterol (HFHC) diet induced mouse models were employed to investigate the pathological role of A-FABP in liver fibrosis. Key findings: 1. Morphological analysis of liver and quantitative PCR of the hepatic expression of fibrotic markers showed that liver fibrosis was successfully established on wild-type (WT) mice treated with CCl4 injection or BDL, and wild type and A-FABP knockout (KO) mice fed on HFHC diet. 2. HFHC diet induced liver fibrosis was alleviated in A-FABP KO mice when compared to WT control. 3. Circulating A-FABP was significantly increased in both CCl4 injection and BDL induced mouse models. 4. The mRNA expression of A-FABP was elevated in the liver tissue of BDL-, CCl4- and WT-HFHC diet induced mouse models. Conclusions: Circulating and hepatic A-FABP increased in CCL4- and BDL-induced liver fibrosis mouse models. A-FABP deficiency protects against HFHC-induced liver fibrosis in mice. These results indicate that A-FABP is associated with the development of liver fibrosis and may be a potential fibrotic biomarker and therapeutic target for anti-fibrotic drug development.-
dc.languageeng-
dc.publisherThe University of Hong Kong (Pokfulam, Hong Kong)-
dc.relation.ispartofHKU Theses Online (HKUTO)-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThe author retains all proprietary rights, (such as patent rights) and the right to use in future works.-
dc.subject.lcshFatty acid-binding proteins-
dc.subject.lcshLiver - Fibrosis-
dc.titleThe pathological role of A-FABP in the development of liver fibrosis-
dc.typePG_Thesis-
dc.identifier.hkulb5659870-
dc.description.thesisnameMaster of Medical Sciences-
dc.description.thesislevelMaster-
dc.description.thesisdisciplineMedicine-
dc.description.naturepublished_or_final_version-

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