Human liver fatty acid binding protein (hFABP1) gene is regulated by liver-enriched transcription factors HNF3β and C/EBPα

Wu, Yunli; Peng, Xian-E; Wang, Dong; Chen, Wan-nan; Lin, Xu

doi:10.1016/j.biochi.2011.08.006

Cited by 24 publications

(21 citation statements)

References 39 publications

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“…ChIP assay was performed according to the published protocol (19). The following set of primers was used for PCR: Foxa2 forward primer 5Ј-GTCAGCTCTTCCTAGTTTTTACTTCTC-3Ј and Foxa2 reverse primer 5Ј-TCCTTTAAGACTTGGAGTGCTGT-3Ј.…”

Section: Isolation Of Primary Myoblasts-the Hind Limb Skeletal Musclementioning

confidence: 99%

Myostatin Induces DNA Damage in Skeletal Muscle of Streptozotocin-induced Type 1 Diabetic Mice

Sriram

Subramanian

Juvvuna

et al. 2014

Journal of Biological Chemistry

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Section: Isolation Of Primary Myoblasts-the Hind Limb Skeletal Musclementioning

confidence: 99%

Myostatin Induces DNA Damage in Skeletal Muscle of Streptozotocin-induced Type 1 Diabetic Mice

Sriram

Subramanian

Juvvuna

et al. 2014

Journal of Biological Chemistry

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“…pGL3B-255, pGL3B-255HNF3␤mut, and pGL3B-255C/EBP␣mut were constructed as previously described (21). pGL3B-255PPAR␣mut and pGL3B-255mut (which included triple binding site mutations for HNF3␤, C/EBP␣, and PPAR␣) were synthesized chemically by the Sangon Biotech (Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

“…pGL3B-255PPAR␣mut and pGL3B-255mut (which included triple binding site mutations for HNF3␤, C/EBP␣, and PPAR␣) were synthesized chemically by the Sangon Biotech (Shanghai, China). HNF3␤ and C/EBP␣ small interfering RNAs (siRNAs) were described in our earlier study (21). PPAR␣ siRNA mix and FABP1 siRNA mix were obtained from Santa Cruz Biotechnology, and a nontargeting siRNA was used as a negative control (NC).…”

Section: Methodsmentioning

confidence: 99%

“…To determine whether HBx induces FABP1 transcription, a reporter plasmid pGL3B-255 containing the human FABP1 promoter sequence from positions Ϫ255 to ϩ50, a region known to possess maximum FABP1 promoter activity (21), was cotransfected with Ad-HBx or Ad-GFP control into HepG2 cells. The luciferase assay revealed that the FABP1 promoter activity was markedly enhanced by the HBx protein (Fig.…”

Section: Hbv Infection Upregulates Fabp1 Expressionmentioning

confidence: 99%

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Hepatitis B Virus X Protein Induces Hepatic Steatosis by Enhancing the Expression of Liver Fatty Acid Binding Protein

Peng

Zhu

et al. 2016

J Virol

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Hepatitis B virus (HBV) has been implicated as a potential trigger of hepatic steatosis although molecular mechanisms involved in the pathogenesis of HBV-associated hepatic steatosis still remain elusive. Our prior work has revealed that the expression level of liver fatty acid binding protein 1 (FABP1), a key regulator of hepatic lipid metabolism, was elevated in HBV-producing hepatoma cells. In this study, the effects of HBV X protein (HBx) mediated FABP1 regulation on hepatic steatosis and the underlying mechanism were determined. mRNA and protein levels of FABP1 were measured by quantitative RT-PCR (qPCR) and Western blotting. HBx-mediated FABP1 regulation was evaluated by luciferase assay, coimmunoprecipitation, and chromatin immunoprecipitation. Hepatic lipid accumulation was measured by using Oil-Red-O staining and the triglyceride level. It was found that expression of FABP1 was increased in HBV-producing hepatoma cells, the sera of HBV-infected patients, and the sera and liver tissues of HBV-transgenic mice. IMPORTANCEAccumulating evidence from epidemiological and experimental studies has indicated that chronic HBV infection is associated with hepatic steatosis. However, the molecular mechanism underlying HBV-induced pathogenesis of hepatic steatosis still remains to be elucidated. In this study, we found that expression of liver fatty acid binding protein (FABP1) was dramatically increased in the sera of HBV-infected patients and in both sera and liver tissues of HBV-transgenic mice. Forced expression of HBx led to FABP1 upregulation, whereas knockdown of FABP1 remarkably diminished lipid accumulation in both in vitro and in vivo models. It is possible that HBx promotes hepatic lipid accumulation through upregulating FABP1 in the development of HBV-induced nonalcoholic fatty liver disease. Therefore, inhibition of FABP1 might have therapeutic value in steatosis-associated chronic HBV infection. H epatitis B virus (HBV) infection is a serious health problemworldwide, causing acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma (1). Emerging evidence from epidemiological and experimental studies suggests that chronic HBV infection, as well as HCV infection, is associated with hepatic steatosis (2, 3). The frequency of hepatic steatosis in subjects with a chronic HBV infection ranges from 27 to 51% (4). Furthermore, HBV X protein (HBx) is known to cause hepatic lipid deposition by inhibiting the secretion of apolipoprotein B (5). A previous report showed that the increased HBx expression can cause lipid accumulation in hepatocytes, likely mediated by sterol regulatory element binding protein 1 and peroxisome proliferator-activated receptor ␥ (PPAR␥) (4). The molecular mechanism by which HBV induces the pathogenesis of hepatic steatosis remains elusive. Using fluorescent two-dimensional difference gel electrophoresis and matrix-assisted laser desorption ionization-time of flight mass spectrometry analysis, we found that the protein level of liver fatty acid binding protein (L-FABP ...

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“…A previous study has indicated that alterations in FABP1 may be associated with the development of aspirin-exacerbated respiratory disease (22). The FABP1 gene is highly transcribed in liver-derived cells, and regulated predominantly by liver-enriched transcription factors HNF3β and C/EBPα (23). A role of L-FABP in the attenuation of hepatic steatosis has also been demonstrated (24).…”

Section: Discussionmentioning

confidence: 98%

Changes in FABP1 and gastrin receptor expression in the testes of rats that have undergone electrical injury

Huang

Liu

2015

Experimental and Therapeutic Medicine

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Abstract. Testicular trauma may occur due to accidental electrical injury. The aim of this study was to investigate alterations in the levels of fatty acid-binding protein 1 (FABP1) and gastrin receptor (gastrin R) in the testes following electrical injury. Sprague-Dawley rats were divided into control, fatal electrocution (220 V, 50 Hz, 60 sec) and electrical injury (220 V, 50 Hz, 60 sec) groups (n=8 per group). The animals in the fatal electrocution and electrical injury groups were deeply anesthetized with sodium pentobarbital prior to each treatment, in which the current was delivered via an anode connected to the left foreleg and a cathode to the right hindleg. The rats that survived were subsequently sacrificed by cervical dislocation. Control animals received cervical dislocation alone. Immunohistochemical analysis was performed to evaluate the protein expression of FABP1 and gastrin R in the testes. Sections were evaluated by digital image analysis. The expression levels of FABP1 and gastrin R were significantly increased following electrical injury, supported by an increase in the integrated optical density (IOD) when compared with that in the control group (P<0.05). However, no significant difference was found in FABP1 and gastrin R expression levels between the fatal electrocution and control groups. In summary, the protein expression levels of FABP1 and gastrin R were found to be significantly altered by electrical injury, suggesting that these two proteins may be important in underlying mechanisms of testicular injury during electrical injury. The findings indicate that such alterations would be reflected in abnormal testicular function.

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Human liver fatty acid binding protein (hFABP1) gene is regulated by liver-enriched transcription factors HNF3β and C/EBPα

Cited by 24 publications

References 39 publications

Myostatin Induces DNA Damage in Skeletal Muscle of Streptozotocin-induced Type 1 Diabetic Mice

Myostatin Induces DNA Damage in Skeletal Muscle of Streptozotocin-induced Type 1 Diabetic Mice

Hepatitis B Virus X Protein Induces Hepatic Steatosis by Enhancing the Expression of Liver Fatty Acid Binding Protein

Changes in FABP1 and gastrin receptor expression in the testes of rats that have undergone electrical injury

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