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TG and VLDL cholesterol activate NLRP1 inflammasome by Nuclear Factor-κB in endothelial cells
IJCA-24335; No of Page 1 International Journal of Cardiology xxx (2016) xxx
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
TG and VLDL cholesterol activate NLRP1 inflammasome by Nuclear Factor-κB in endothelial cells Yanjun Pan a,1, Yan Wang b,1, Jianqiang Xu a, Jianfeng Wu a, Qingyong Chen a, Gaofeng Zeng a,⁎, Guojun Zhao c,⁎⁎ a b c
Department of Cardiovascular Medicine, The Second Affiliated Hospital of University of South China, Hengyang, Hunan, China Department of Anesthesiology, The Second Affiliated Hospital of University of South China, Hengyang, Hunan, China Department of Histology and Embryology, Guilin Medical University, Guilin, Guangxi, China
a r t i c l e
i n f o
Article history: Received 21 November 2016 Accepted 16 December 2016 Available online xxxx Keywords: TG VLDL NLRP1 NF-κB Atherosclerosis
induced the expression of NLRP1 inflammasomes through NF-κB, resulting in the release of mature IL-1β from THP-1cells [4]. Additionally, Im et al. [5] found that by binding the SREBP-1a promoter, NF-kB activated expression of the NLRP1a. These results indicate that the underlying molecular mechanism of TG and VLDL accelerates the expression of NLRP1 inflammasome may via activation of NF-κB. However, much more researches need to be done to supporting this view in the future. Conflicts of interest The authors report no relationships that could be construed as a conflict of interest.
Dear Editor, Bleda and colleagues [1] reported that increased triglycerides and VLDL-cholesterol of patients with atherosclerosis provoke activation of NLRP1 inflammasome in endothelial cells. The finding may provide a novel way for proatherogenic inflammation, but the precise mechanisms remained unknown. Some evidences revealed that lipids play a key role in regulation of inflammation. Dichtl et al. [2] found that VLDL may promote the development of atherosclerotic lesions by irritation of NF-κB in Endothelial Cells. Another study showed that VLDL exacerbated proinflammatory actions through binding the LDL-receptor related proteins (LRP) and downstream induction of p38 MAP kinase and stimulation of NF-κB [3]. These findings suggest that TG and VLDL contribute to inflammation by provoking NF-κB. Accumulating research indicated that NF-κB mediated innate immune response. The extra-neuronal nerve growth factor NGF/TrkA
Acknowledgment This work was supported by the grant from Natural Science Foundation of Hunan Province(14JJ5016), China. References [1] S. Bleda, J. de Haro, C. Varela, A. Ferruelo, F. Acin, Elevated levels of triglycerides and vldl-cholesterol provoke activation of nlrp1 inflammasome in endothelial cells, Int. J. Cardiol. 220 (2016) 52–55. [2] W. Dichtl, L. Nilsson, I. Goncalves, et al., Very low-density lipoprotein activates nuclear factor-kappaB in endothelial cells, Circ. Res. 84 (9) (1999) 1085–1094. [3] P. Libby, Fat fuels the flame: triglyceride-rich lipoproteins and arterial inflammation, Circ. Res. 100 (3) (2007) 299–301. [4] A. Datta-Mitra, S. Kundu-Raychaudhuri, A. Mitra, S.P. Raychaudhuri, Cross talk between neuroregulatory molecule and monocyte: nerve growth factor activates the inflammasome, PLoS One 10 (4) (2015), e0121626. [5] S.S. Im, L. Yousef, C. Blaschitz, et al., Linking lipid metabolism to the innate immune response in macrophages through sterol regulatory element binding protein-1a, Cell Metab. 13 (5) (2011) 540–549.
⁎ Correspondence to: G. Zeng, Department of Cardiovascular Medicine, The Second Affiliated Hospital of University of South China, No. 35 Jiefang Road, Hengyang City; Hunan Province 421001, China. ⁎⁎ Correspondence to: G. Zhao, Department of Histology and Embryology, Guilin Medical University, No. 1 Zhiyuan Road, Guilin City, Guangxi Province 541100, China. E-mail addresses: [email protected] (G. Zeng), [email protected] (G. Zhao). 1 Co-first author.
http://dx.doi.org/10.1016/j.ijcard.2016.12.156 0167-5273/© 2016 Published by Elsevier Ireland Ltd.
Please cite this article as: Y. Pan, et al., TG and VLDL cholesterol activate NLRP1 inflammasome by Nuclear Factor-κB in endothelial cells, Int J Cardiol (2016), http://dx.doi.org/10.1016/j.ijcard.2016.12.156
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
TG and VLDL cholesterol activate NLRP1 inflammasome by Nuclear Factor-κB in endothelial cells Yanjun Pan a,1, Yan Wang b,1, Jianqiang Xu a, Jianfeng Wu a, Qingyong Chen a, Gaofeng Zeng a,⁎, Guojun Zhao c,⁎⁎ a b c
Department of Cardiovascular Medicine, The Second Affiliated Hospital of University of South China, Hengyang, Hunan, China Department of Anesthesiology, The Second Affiliated Hospital of University of South China, Hengyang, Hunan, China Department of Histology and Embryology, Guilin Medical University, Guilin, Guangxi, China
a r t i c l e
i n f o
Article history: Received 21 November 2016 Accepted 16 December 2016 Available online xxxx Keywords: TG VLDL NLRP1 NF-κB Atherosclerosis
induced the expression of NLRP1 inflammasomes through NF-κB, resulting in the release of mature IL-1β from THP-1cells [4]. Additionally, Im et al. [5] found that by binding the SREBP-1a promoter, NF-kB activated expression of the NLRP1a. These results indicate that the underlying molecular mechanism of TG and VLDL accelerates the expression of NLRP1 inflammasome may via activation of NF-κB. However, much more researches need to be done to supporting this view in the future. Conflicts of interest The authors report no relationships that could be construed as a conflict of interest.
Dear Editor, Bleda and colleagues [1] reported that increased triglycerides and VLDL-cholesterol of patients with atherosclerosis provoke activation of NLRP1 inflammasome in endothelial cells. The finding may provide a novel way for proatherogenic inflammation, but the precise mechanisms remained unknown. Some evidences revealed that lipids play a key role in regulation of inflammation. Dichtl et al. [2] found that VLDL may promote the development of atherosclerotic lesions by irritation of NF-κB in Endothelial Cells. Another study showed that VLDL exacerbated proinflammatory actions through binding the LDL-receptor related proteins (LRP) and downstream induction of p38 MAP kinase and stimulation of NF-κB [3]. These findings suggest that TG and VLDL contribute to inflammation by provoking NF-κB. Accumulating research indicated that NF-κB mediated innate immune response. The extra-neuronal nerve growth factor NGF/TrkA
Acknowledgment This work was supported by the grant from Natural Science Foundation of Hunan Province(14JJ5016), China. References [1] S. Bleda, J. de Haro, C. Varela, A. Ferruelo, F. Acin, Elevated levels of triglycerides and vldl-cholesterol provoke activation of nlrp1 inflammasome in endothelial cells, Int. J. Cardiol. 220 (2016) 52–55. [2] W. Dichtl, L. Nilsson, I. Goncalves, et al., Very low-density lipoprotein activates nuclear factor-kappaB in endothelial cells, Circ. Res. 84 (9) (1999) 1085–1094. [3] P. Libby, Fat fuels the flame: triglyceride-rich lipoproteins and arterial inflammation, Circ. Res. 100 (3) (2007) 299–301. [4] A. Datta-Mitra, S. Kundu-Raychaudhuri, A. Mitra, S.P. Raychaudhuri, Cross talk between neuroregulatory molecule and monocyte: nerve growth factor activates the inflammasome, PLoS One 10 (4) (2015), e0121626. [5] S.S. Im, L. Yousef, C. Blaschitz, et al., Linking lipid metabolism to the innate immune response in macrophages through sterol regulatory element binding protein-1a, Cell Metab. 13 (5) (2011) 540–549.
⁎ Correspondence to: G. Zeng, Department of Cardiovascular Medicine, The Second Affiliated Hospital of University of South China, No. 35 Jiefang Road, Hengyang City; Hunan Province 421001, China. ⁎⁎ Correspondence to: G. Zhao, Department of Histology and Embryology, Guilin Medical University, No. 1 Zhiyuan Road, Guilin City, Guangxi Province 541100, China. E-mail addresses: [email protected] (G. Zeng), [email protected] (G. Zhao). 1 Co-first author.
http://dx.doi.org/10.1016/j.ijcard.2016.12.156 0167-5273/© 2016 Published by Elsevier Ireland Ltd.
Please cite this article as: Y. Pan, et al., TG and VLDL cholesterol activate NLRP1 inflammasome by Nuclear Factor-κB in endothelial cells, Int J Cardiol (2016), http://dx.doi.org/10.1016/j.ijcard.2016.12.156