Regulation of hepatocyte growth factor expression by NF-κB and PPARγ in adipose tissue.
Yin J., Lee JH., Zhang J., Gao Z., Polotsky VY., Ye J.
Animal Study, published in Am J Physiol Endocrinol Metab (2014) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Am J Physiol Endocrinol Metab (2014)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 24569592
- PMCID
- PMC3989740
- DOI
- 10.1152/ajpendo.00687.2013
- Citations
- 18
Abstract (original English)
Hepatocyte growth factor (HGF) is expressed as an angiogenic factor in adipose tissue. However, the molecular mechanism of Hgf expression remains largely unknown in the tissue. We addressed the issue by studying Hgf expression in adipocytes and macrophages. Hgf was expressed more in the stromal-vascular fraction than the adipocyte fraction. The expression was fivefold more in macrophages than the stromal-vascular faction and was reduced by 50% after macrophage deletion in adipose tissue. The expression was reduced by differentiation in adipocytes and by tumor necrosis factor-α or lipopolysaccharide treatment in macrophages. The expression was suppressed by nuclear factor (NF)-κB in C57BL/6 mice with NF-κB p65 overexpression under the aP2 gene promoter (aP2-p65 mice) but enhanced by inactivation of NF-κB p65 in mouse embryonic fibroblasts. The Hgf gene promoter was suppressed by p65 overexpression, which blocked peroxisome proliferator-activated receptor-γ (PPARγ) interaction with RNA polymerase II. The p65 activity was abolished by knockdown of histone deacetylase 3. Hgf expression was upregulated by hypoxia in vitro and in vivo. Compared with vascular endothelial growth factor (Vegf), which was predominately expressed in mature adipocytes, Hgf was mainly expressed in nonadipocytes, suggesting that Hgf and Vegf may have different cell sources in adipose tissue. In mechanism, Hg
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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