FABP4

Official Full Name

fatty acid binding protein 4

Organism

Homo sapiens

GeneID

2167

Background

FABP4 encodes the fatty acid binding protein found in adipocytes. Fatty acid binding proteins are a family of small, highly conserved, cytoplasmic proteins that bind long-chain fatty acids and other hydrophobic ligands. It is thought that FABPs roles include fatty acid uptake, transport, and metabolism. [provided by RefSeq, Jul 2008]

Synonyms

aP2; ALBP; AFABP; A-FABP; HEL-S-104;

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Detailed Information

Fatty acid-binding proteins (FABPs) are a group of homologous low molecular weight intracellular lipid-binding proteins. Its molecular weight is 14-15 kD and contains 125-134 amino acids. It can be used as a fat molecular chaperone to participate in the transport of fatty acids in cells and other signal transduction pathways. FABP4 is one of the most characteristic intracellular lipid transporters in the FABPs family, and plays a central regulatory role in energy metabolism and inflammation.

Function of FABP4

FABP4 is mainly expressed in adipocytes, macrophages, dendritic cells and microvascular endothelial cells. The functions of FABP4 are as follows.

Regulating lipid metabolism: FABP4 participates in the uptake, transport and release of fatty acids. When non-esterified fatty acids enter adipocytes or macrophages through free diffusion or passively, FABP4 is transported to various parts and participates in metabolism, or enters mitochondrial esterification, or enters the endoplasmic reticulum to participate in triacylglycerol synthesis.
Participating in inflammatory response: Studies have found that selective blocking of FABP4 expression in fat cells of nude mice can reduce the release of inflammatory factors in macrophages. By inducing the expression of FABP4 in macrophages, it can promote the development of atherosclerosis.
Participating in the formation of vascular endothelium: Studies have found that vascular endothelial factors can promote the production of endothelial cells FABP4, and down-regulation of FABP4 can inhibit the proliferation, migration and sprouting of vascular endothelial cells. This leads to a significant reduction in lipid transfer between fat cells and cancer cells, reduces tumor hemoperfusion, and inhibits its growth and new blood vessel formation.

Figure 1. Schematic view recapitulating the involvement of endothelial FABP4 in liver carcinogenesis related to metabolic syndrome. (Laouirem, S., et al. 2019)

FABP4 and Asthma

Studies have confirmed that IL-4 mediated STAT6 signal transduction in airway epithelial cells leads to downstream FABP4 gene expression; Th2 cytokines IL-4 and IL-13 up-regulate FABP4 expression; Th1 cytokine IFN-γ down-regulates FABP4 expression. The results of this study indicate that FABP4 expression in airway epithelial cells depends on STAT6 signal transduction, and FABP4 participates in Th2 cell response. STAT6 is a transcription factor that plays a major regulatory role in allergic inflammation. It transduces the cytokines IL-4 and IL-13 through the JAK/STAT signaling pathway to mediate airway inflammation and airway hyperresponsiveness in asthma. Therefore, FABP4 may be closely related to the occurrence and development of asthma.

Another study found that the staining intensity of FABP4 in airway epithelial cells in a mouse model of allergic airway inflammation was more significant than that in wild-type mice. In mouse asthma models induced by ovalbumin sensitization and airborne allergens, FABP4 knockout mice had significantly fewer inflammatory cells in bronchoalveolar lavage fluid than wild-type mice. In addition, the levels of cytokines IL-5 and IL-13 are significantly reduced, and inflammation around the bronchus and blood vessels is also significantly reduced.

FABP4 and EMT Related Signaling Pathways

EMT refers to the biological process of epithelial cells transforming into cells with mesenchymal phenotype under specific physiological or pathological conditions. FABP4 overexpression is associated with hyperlipidemia. Studies have confirmed that hyperlipidemia is very likely to cause hypoxia, and hypoxia-inducible factor-α in the hypoxic microenvironment in tumors exerts its activity. It up-regulates Snail by regulating the transcription of downstream target genes such as zinc finger transcription factor Snail, vimentin, epithelial cadherin, and nuclear factor κB, thereby reducing the level of epithelial cadherin and promoting tumor invasion and metastasis, such as liver cancer, pancreatic cancer, etc.

References:

Laouirem, S., Sannier, A., Norkowski, E., Cauchy, F., Doblas, S., Rautou, P., & Paradis, V. (2019). Endothelial fatty liver binding protein 4: a new targetable mediator in hepatocellular carcinoma related to metabolic syndrome. Oncogene, 38(16), 3033-3046.
Bervejillo, M. L., Bonanata, J., Franchini, G. R., Richeri, A., Marques, J. M., Freeman, B. A.,& Ferreira, A. M..(2020). A FABP4-PPARγ signaling axis regulates human monocyte responses to electrophilic fatty acid nitroalkenes. Redox biology.
Gharpure, K. M., Pradeep, S., Sans, M., Rupaimoole, R., Ivan, C., Wu, S. Y.,& Sood, A. K. (2018). FABP4 as a key determinant of metastatic potential of ovarian cancer. Nature Communications, 9(1).

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