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Hill AA, Anderson-Baucum EK, Kennedy AJ, et al. Activation of NF-κB drives the enhanced survival of adipose tissue macrophages in an obesogenic environment. Mol Metab. 2015;4(10):665-77doi: 10.1016/j.molmet.2015.07.005.
Hill, A. A., Anderson-Baucum, E. K., Kennedy, A. J., Webb, C. D., Yull, F. E., & Hasty, A. H. (2015). Activation of NF-κB drives the enhanced survival of adipose tissue macrophages in an obesogenic environment. Molecular metabolism, 4(10), 665-77. https://doi.org/10.1016/j.molmet.2015.07.005
Hill, Andrea A, et al. "Activation of NF-κB drives the enhanced survival of adipose tissue macrophages in an obesogenic environment." Molecular metabolism vol. 4,10 (2015): 665-77. doi: https://doi.org/10.1016/j.molmet.2015.07.005
Hill AA, Anderson-Baucum EK, Kennedy AJ, Webb CD, Yull FE, Hasty AH. Activation of NF-κB drives the enhanced survival of adipose tissue macrophages in an obesogenic environment. Mol Metab. 2015 Jul 28;4(10):665-77. doi: 10.1016/j.molmet.2015.07.005. eCollection 2015 Oct. PMID: 26779432; PMCID: PMC4588436.
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Mol Metab. 2015 Jul 28;4(10):665-77. doi: 10.1016/j.molmet.2015.07.005. eCollection 2015 Oct.

Activation of NF-κB drives the enhanced survival of adipose tissue macrophages in an obesogenic environment.

Molecular metabolism

Andrea A Hill, Emily K Anderson-Baucum, Arion J Kennedy, Corey D Webb, Fiona E Yull, Alyssa H Hasty

Affiliations

  1. Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, United States.
  2. Department of Cancer Biology, Vanderbilt University School of Medicine, United States.
  3. Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, United States; Department of Veterans Affairs, Tennessee Valley Healthcare System, United States.

PMID: 26779432 PMCID: PMC4588436 DOI: 10.1016/j.molmet.2015.07.005

Abstract

OBJECTIVE: Macrophage accumulation in adipose tissue (AT) during obesity contributes to inflammation and insulin resistance. Recruitment of monocytes to obese AT has been the most studied mechanism explaining this accumulation. However, recent evidence suggests that recruitment-independent mechanisms may also regulate pro-inflammatory AT macrophage (ATM) numbers. The role of increased ATM survival during obesity has yet to be explored.

RESULTS: We demonstrate that activation of apoptotic pathways is significantly reduced in ATMs from diet-induced and genetically obese mice. Concurrently, pro-survival Bcl-2 family member protein levels and localization to the mitochondria is elevated in ATMs from obese mice. This increased pro-survival signaling was associated with elevated activation of the transcription factor, NF-κB, and increased expression of its pro-survival target genes. Finally, an obesogenic milieu increased ATM viability only when NF-κB signaling pathways were functional.

CONCLUSIONS: Our data demonstrate that obesity promotes survival of inflammatory ATMs, possibly through an NF-κB-regulated mechanism.

Keywords: Adipose tissue; Apoptosis; Cleaved caspase-3; Macrophage; NF-κB; Survival

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