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The transcription factor nuclear factor of kappa-light-chain-enhancer of activated B cells (NF- κ B) is expressed in brown adipocytes, but its role remains largely unknown in the cells. This issue was addressed in current study by examining NF- κ B in brown adipocytes in vitro and in vivo. NF- κ B activity was increased by differentiation of brown adipocytes through elevation of p65 (RelA) expression. The transcriptional activity of NF- κ B was induced by the cold stimulation with an elevation in S276 phosphorylation of p65 protein. Inactivation of NF- κ B in brown adipocytes made the knockout mice [uncoupling protein 1 (Ucp1)–CreER–p65f/f, U-p65-KO] intolerant to the cold environment. The brown adipocytes exhibited an increase in apoptosis, a decrease in cristae density and uncoupling activity in the interscapular brown adipose tissue (iBAT) of p65-KO mice. The alterations became severer after cold exposure of the KO mice. The brown adipocytes of mice with NF- κ B activation (p65 overexpression, p65-OE) exhibited a set of opposite alterations with a reduction in apoptosis, an increase in cristae density and uncoupling activity. In mechanism, NF- κ B inhibited expression of the adenine nucleotide translocase 2 (ANT2) in the control of apoptosis. Data suggest that NF- κ B activity is increased in brown adipocytes by differentiation and cold stimulation to protect the cells from apoptosis through down-regulation of ANT2 expression. Nuclear factor of kappa-light-chain-enhancer of activated B cells (NF- κ B) activity is increased in brown adipocytes by differentiation and cold stimulation to down-regulate adenine nucleotide translocase 2 (ANT2) expression in preservation of cells from apoptosis. Absence of the activity leads to ANT2-mediated apoptosis to impair the thermogenic function of brown fat in uncoupling protein 1 (Ucp1)–p65-KO mice. [Display omitted] [ABSTRACT FROM AUTHOR]

The transcription factor nuclear factor of kappa-light-chain-enhancer of activated B cells (NF- κ B) is expressed in brown adipocytes, but its role remains largely unknown in the cells. This issue was addressed in current study by examining NF- κ B in brown adipocytes in vitro and in vivo . NF- κ B activity was increased by differentiation of brown adipocytes through elevation of p65 (RelA) expression. The transcriptional activity of NF- κ B was induced by the cold stimulation with an elevation in S276 phosphorylation of p65 protein. Inactivation of NF- κ B in brown adipocytes made the knockout mice [uncoupling protein 1 ( Ucp1 )-CreER-p65 f/f , U-p65-KO] intolerant to the cold environment. The brown adipocytes exhibited an increase in apoptosis, a decrease in cristae density and uncoupling activity in the interscapular brown adipose tissue (iBAT) of p65-KO mice. The alterations became severer after cold exposure of the KO mice. The brown adipocytes of mice with NF- κ B activation (p65 overexpression, p65-OE) exhibited a set of opposite alterations with a reduction in apoptosis, an increase in cristae density and uncoupling activity. In mechanism, NF- κ B inhibited expression of the adenine nucleotide translocase 2 (ANT2) in the control of apoptosis. Data suggest that NF- κ B activity is increased in brown adipocytes by differentiation and cold stimulation to protect the cells from apoptosis through down-regulation of ANT2 expression., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.)