1, 25(OH)2D3-induced interaction of vitamin D receptor with p50 subunit of NF-κB suppresses the interaction between KLF5 and p50, contributing to inhibition of LPS-induced macrophage proliferation

Biochemical and Biophysical Research Communications

Volumn 482, Issue 2, 2017, Pages 366-374

  Ma, Dong ^a,b   Zhang, Ruo nan ^a   Wen, Ya ^a   Yin, Wei na ^c   Bai, Disi ^b   Zheng, Guo ying ^b   Li, Jin shui ^a   Zheng, Bin ^a   Wen, Jin kun ^a  

^a HEBEI MEDICAL UNIVERSITY   (China)

^b NORTH CHINA UNIVERSITY OF SCIENCE AND TECHNOLOGY   (China)

^c Handan City First Hospital   (China)

Author keywords

1,25(OH)2D3; KLF5; Macrophage; NF B; Proliferation; Vitamin D receptor

Indexed keywords

CALCITRIOL; CYCLIN B1; CYCLIN DEPENDENT KINASE 1; CYCLIN DEPENDENT KINASE 2; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; KRUPPEL LIKE FACTOR 5; LIPOPOLYSACCHARIDE; VITAMIN D RECEPTOR; CALCITRIOL RECEPTOR; DIHYDROXY-VITAMIN D3; KLF5 PROTEIN, MOUSE; KRUPPEL LIKE FACTOR; PROTEIN BINDING; PROTEIN SUBUNIT; VITAMIN D;

ANIMAL CELL; ANTIINFLAMMATORY ACTIVITY; ANTIPROLIFERATIVE ACTIVITY; ARTICLE; ASSOCIATION; BINDING COMPETITION; CELL PROLIFERATION; CONTROLLED STUDY; GENE EXPRESSION; MACROPHAGE; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN FUNCTION; PROTEIN PROTEIN INTERACTION; RECEPTOR UPREGULATION; ANALOGS AND DERIVATIVES; ANIMAL; BINDING SITE; DOSE RESPONSE; DRUG EFFECTS; MACROPHAGE ACTIVATION; METABOLISM; PHYSIOLOGY; PROTEIN SUBUNIT; RAW 264.7 CELL LINE;

ANIMALS; BINDING SITES; CELL PROLIFERATION; DOSE-RESPONSE RELATIONSHIP, DRUG; KRUPPEL-LIKE TRANSCRIPTION FACTORS; LIPOPOLYSACCHARIDES; MACROPHAGE ACTIVATION; MICE; NF-KAPPA B; PROTEIN BINDING; PROTEIN SUBUNITS; RAW 264.7 CELLS; RECEPTORS, CALCITRIOL; VITAMIN D;

EID: 85006634996     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2016.11.069     Document Type: Article

References (27)

1. [1] Medzhitov, R., Horng, T., Transcriptional control of the inflammatory response. Nat. Rev. Immunol. 9 (2009), 692–703.
2. [2] Liao, X., Sharma, N., Kapadia, F., Zhou, G., Lu, Y., Hong, H., Paruchuri, K., Mahabeleshwar, G.H., Dalmas, E., Venteclef, N., Flask, C.A., Kim, J., Doreian, B.W., Lu, K.Q., Kaestner, K.H., Hamik, A., Clément, K., Jain, M.K., Krüppel-like factor 4 regulates macrophage polarization. J. Clin. Investig. 121 (2011), 2736–2749.
3. [3] Smale, S.T., Natoli, G., Transcriptional control of inflammatory responses. Cold Spring Harb. Perspect. Biol., 6, 2014, a016261.
4. [4] McConnell, B.B., Ghaleb, A.M., Nandan, M.O., Yang, V.W., The diverse functions of Krüppel-like factors 4 and 5 in epithelial biology and pathobiology. Bioessays 29 (2007), 549–557.
5. [5] Ma, X., Becker Buscaglia, L.E., Barker, J.R., Li, Y., MicroRNAs in NF-kappaB signaling. J. Mol. Cell Biol. 3 (2011), 159–166.
6. [6] Fujiu, K., Manabe, I., Nagai, R., Renal collecting duct epithelial cells regulate inflammation in tubulointerstitial damage in mice. J. Clin. Investig. 121 (2011), 3425–3441.
7. [7] Xu, Z., Yoshida, T., Wu, L., Maiti, D., Cebotaru, L., Duh, E.J., Transcription factor MEF2C suppresses endothelial cell inflammation via regulation of NF-κB and KLF2. J. Cell Physiol. 230 (2015), 1310–1320.
8. [8] Bobryshev, Y.V., Vitamin D3 suppresses immune reactions in atherosclerosis, affecting regulatory T cells and dendritic cell function. Arterioscler. Thromb. Vasc. Biol. 30 (2010), 2317–2319.
9. [9] Oh, J., Riek, A.E., Darwech, I., Funai, K., Shao, J., Chin, K., Sierra, O.L., Carmeliet, G., Ostlund, R.E. Jr., Bernal-Mizrachi, C., Deletion of macrophage Vitamin D receptor promotes insulin resistance and monocyte cholesterol transport to accelerate atherosclerosis in mice. Cell Rep. 10 (2015), 1872–1886.
10. [10] Krishnan, A.V., Feldman, D., Mechanisms of the anti-cancer and anti-inflammatory actions of vitamin D. Annu. Rev. Pharmacol. Toxicol. 51 (2011), 311–336.
11. [11] Sun, J., Kong, J., Duan, Y., Szeto, F.L., Liao, A., Madara, J.L., Li, Y.C., Increased NF-kappaB activity in fibroblasts lacking the vitamin D receptor. Am. J. Physiol. Endocrinol. Metab. 291 (2006), E315–E322.
12. [12] Shi, J.H., Zheng, B., Chen, S., Ma, G.Y., Wen, J.K., Retinoic acid receptor α mediates all-trans-retinoic acid-induced Klf4 gene expression by regulatingKlf4 promoter activity in vascular smooth muscle cells. J. Biol. Chem. 287 (2012), 10799–10811.
13. [13] Satoh, T., Saika, T., Ebara, S., Kusaka, N., Timme, T.L., Yang, G., Wang, J., Mouraviev, V., Cao, G., Fattah el, M.A., Thompson, T.C., Macrophages transduced with an adenoviral vector expressing interleukin 12 suppress tumor growth and metastasis in a preclinical metastatic prostate cancer model. Cancer Res. 63 (2003), 7853–7860.
14. [14] Straszewski-Chavez, S.L., Visintin, I.P., Karassina, N., Los, G., Liston, P., Halaban, R., Fadiel, A., Mor, G., XAF1 mediates tumor necrosis factor-alpha-induced apoptosis and X-linked inhibitor of apoptosis cleavage by acting through the mitochondrial pathway. J. Biol. Chem. 282 (2007), 13059–13072.
15. [15] Looi, C.Y., Arya, A., Cheah, F.K., Muharram, B., Leong, K.H., Mohamad, K., Wong, W.F., Rai, N., Mustafa, M.R., Induction of apoptosis in human breast cancer cells via caspase pathway by vernodalin isolated from Centratherum anthelminticum (L.) seeds. PLoS One, 8, 2013, e56643.
16. [16] Zhang, X.H., Zheng, B., Yang, Z., He, M., Yue, L.Y., Zhang, R.N., Zhang, M., Zhang, W., Zhang, X., Wen, J.K., TMEM16A and myocardin form a positive feedback loop that is disrupted by KLF5 during Ang II-induced vascular remodeling. Hypertension 66 (2015), 412–421.
17. [17] Zhang, X.H., Zheng, B., Gu, C., Fu, J.R., Wen, J.K., TGF-β1 downregulates AT1 receptor expression via PKC-δ-mediated Sp1 dissociation from KLF4 and Smad-mediated PPAR-γ association with KLF4. Arterioscler. Thromb. Vasc. Biol. 32 (2012), 1015–1023.
18. [18] Sølvsten, H., Svendsen, M.L., Fogh, K., Kragballe, K., Upregulation of vitamin D receptor levels by 1,25(OH)2 vitamin D3 in cultured human keratinocytes. Arch. Dermatol. Res. 289 (1997), 367–372.
19. [19] Aizawa, K., Suzuki, T., Kada, N., Ishihara, A., Kawai-Kowase, K., Matsumura, T., Sasaki, K., Munemasa, Y., Manabe, I., Kurabayashi, M., Collins, T., Nagai, R., Regulation of platelet-derived growth factor-A chain by Krüppel-like factor 5: new pathway of cooperative activation with nuclear factor-kappaB. J. Biol. Chem. 279 (2004), 70–76.
20. [20] Jiao, H.W., Jia, X.X., Zhao, T.J., Rong, H., Zhang, J.N., Cheng, Y., Zhu, H.P., Xu, K.L., Guo, S.Y., Shi, Q.Y., Zhang, H., Wang, F.Y., Chen, C.F., Du, L., Up-regulation of TDAG51 is a dependent factor of LPS-induced RAW264.7 macrophages proliferation and cell cycle progression. Immunopharmacol. Immunotoxicol. 38 (2016), 124–130.
21. [21] Kim, K.Y., Kang, H., Sakuranetin inhibits inflammatory enzyme, cytokine, and costimulatory molecule expression in macrophages through modulation of JNK, p38, and STAT1. Evid. Based Complement. Altern. Med., 2016, 9824203.
22. [22] Li, X., Li, X., Zheng, Z., Liu, Y., Ma, X., Unfractionated heparin suppresses lipopolysaccharide-induced monocyte chemoattractant protein-1 expression in human microvascular endothelial cells by blocking Krüppel-like factor 5 and nuclear factor-κB pathway. Immunobiology 219 (2014), 778–785.
23. [23] Nandan, M.O., Chanchevalap, S., Dalton, W.B., Yang, V.W., Krüppel-like factor 5 promotes mitosis by activating the cyclin B1/Cdc2 complex during oncogenic Ras-mediated transformation. FEBS Lett. 579 (2005), 4757–4762.
24. [24] Fujiu, K., Manabe, I., Ishihara, A., Oishi, Y., Iwata, H., Nishimura, G., Shindo, T., Maemura, K., Kagechika, H., Shudo, K., Nagai, R., Synthetic retinoid Am80 suppresses smooth muscle phenotypic modulation and in-stent neointima formation by inhibiting KLF5. Circ. Res. 97 (2005), 1132–1141.
25. [25] Matsumura, T., Suzuki, T., Aizawa, K., Munemasa, Y., Muto, S., Horikoshi, M., Nagai, R., The deacetylase HDAC1 negatively regulates the cardiovascular transcription factor Krüppel-like factor 5 through direct interaction. J. Biol. Chem. 280 (2005), 12123–12129.
26. [26] Zhang, X.H., Zheng, B., Han, M., Miao, S.B., Wen, J.K., Synthetic retinoid Am80 inhibits interaction of KLF5 with RAR alpha through inducing KLF5 dephosphorylation mediated by the PI3K/Akt signaling in vascular smooth muscle cells. FEBS Lett. 583 (2009), 1231–1236.
27. [27] Guo, P., Dong, X.Y., Zhao, K.W., Sun, X., Li, Q., Dong, J.T., Estrogen-induced interaction between KLF5 and estrogen receptor (ER) suppresses the function of ER in ER-positive breast cancer cells. Int. J. Cancer 126 (2010), 81–89.