|
|
Cite this paper: |
|
|
YANG Yue, XING Rong'e, LIU Song, QIN Yukun, LI Kecheng, YU Huahua, LI Pengcheng. PI3K/Akt pathway is involved in the activation of RAW 264.7 cells induced by hydroxypropyltrimethyl ammonium chloride chitosan[J]. Journal of Oceanology and Limnology, 2020, 38(3): 834-840 |
|
|
|
|
|
|
|
PI3K/Akt pathway is involved in the activation of RAW 264.7 cells induced by hydroxypropyltrimethyl ammonium chloride chitosan |
|
YANG Yue1,2,3, XING Rong'e1,2, LIU Song1,2, QIN Yukun1,2, LI Kecheng1,2, YU Huahua1,2, LI Pengcheng1,2 |
|
1 Key Laboratory of Experimental Marine Biology, Center for Ocean Mega-Science, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China; 2 Laboratory for Marine Drugs and Bioproducts of Qingdao National Laboratory for Marine Science and Technology, Qingdao 266237, China; 3 University of Chinese Academy of Sciences, Beijing 100049, China |
|
Abstract: |
We previously demonstrated that 2-hydroxypropyltrimethyl ammonium chloride chitosan (HACC) promoted the production of nitric oxide (NO) and proinflammatory cytokines by activating the mitogen-activated protein kinases (MAPK) and Janus kinase (JAK)/STAT pathways in RAW 264.7 cells, indicating good immunomodulatory activity of HACC. In this study, to further investigate the immunomodulatory mechanisms of HACC, we determined the roles of phosphatidylinositol 3-kinase (PI3K)/Akt, activating protein (AP-1) and nuclear factor kappa B (NF-κB) in HACC-induced activation of RAW 264.7 cells by the western blotting. The results suggest that HACC promoted the phosphorylation of p85 and Akt. Furthermore, c-Jun and p65 were also increased after the treatment of RAW 264.7 cells with HACC, indicating the translocation of NF-κB and AP-1 from cytoplasm to nucleus. In addition, as scanning electron microscopy (SEM) analysis shows, the cell morphology changed after HACC treatment. These findings indicate that HACC activated MAPK, JAK/STAT, and PI3K/Akt signaling pathways dependent on AP-1 and NF-κB activation in RAW 264.7 cells, ultimately leading to the increase of NO and cytokines. |
|
Key words:
hydroxypropyltrimethyl ammonium chloride chitosan|RAW 264.7 cells|PI3K/Akt pathway|nuclear factor-κB|activating protein 1
|
|
Received: 2019-01-19 Revised: 2019-06-28 |
|
|
|
|
References:
Cantley L C. 2002. The phosphoinositide 3-kinase pathway.Science, 296(5573):1 655-1 657. Chae H S, Kang O H, Lee Y S, Choi J G, Oh Y C, Jang H J, Kim M S, Kim J H, Jeong S I, Kwon D Y. 2009. Inhibition of LPS-induced iNOS, COX-2 and inflammatory mediator expression by paeonol through the MAPKs inactivation in RAW 264.7 cells. Am. J. Chinese Med., 37(1):181-194. Cheever M L, Sato T K, de Beer T, Kutateladze T G, Emr S D, Overduin M. 2001. Phox domain interaction with PtdIns(3)P targets the Vam7 t-SNARE to vacuole membranes. Nature Cell Biology, 3(7):613-618. Chen J J, Huang W C, Chen C C. 2005. Transcriptional regulation of cyclooxygenase-2 in response to proteasome inhibitors involves reactive oxygen species-mediated signaling pathway and recruitment of CCAAT/enhancerbinding protein δ and CREB-binding protein. Mol. Biol.Cell, 16(12):5 579-5 591. Fang R H, Zhang L F. 2016. Nanoparticle-based modulation of the immune system. Annu. Rev. Chem. Biomol. Eng., 7(1):305-326. Gugasyan R, Grumont R, Grossmann M, Nakamura Y, Pohl T, Nesic D, Gerondakis S. 2000. Rel/NF-κB transcription factors:key mediators of B-cell activation. Immunol.Rev., 176(1):134-140. Guha M, Mackman N. 2001. LPS induction of gene expression in human monocytes. Cellular Signalling, 13(2):85-94. Gukovsky I, Gukovskaya A S, Blinman T A, Zaninovic V, Pandol S J. 1998. Early NF-κB activation is associated with hormone-induced pancreatitis. Am. J. Physiol., 275(6):G1 402-G1 414. Hartley J W, Evans L H, Green K Y, Naghashfar Z, Macias A R, Zerfas P M, Ward J M. 2008. Expression of infectious murine leukemia viruses by RAW264.7 cells, a potential complication for studies with a widely used mouse macrophage cell line. Retrovirology, 5:1. Hattori Y, Hattori S, Kasai K. 2003. Lipopolysaccharide activates Akt in vascular smooth muscle cells resulting in induction of inducible nitric oxide synthase through nuclear factor-kappa B activation. European Journal of Pharmacology, 481(2-3):153-158. Johnson G L, Lapadat R. 2002. Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases. Science, 298(5600):1 911-1 912. Kao S J, Lei H C, Kuo C T, Chang M S, Chen B C, Chang Y C, Chiu W T, Lin C H. 2005. Lipoteichoic acid induces nuclear factor-kappaB activation and nitric oxide synthase expression via phosphatidylinositol 3-kinase, Akt, and p38 MAPK in RAW 264.7 macrophages. Immunology, 115(3):366-374. Karin M, Liu Z G, Zandi E. 1997. AP-1 function and regulation.Curr. Opin. Cell Biol., 9(2):240-246. Katso R, Okkenhaug K, Ahmadi K, White S, Timms J, Waterfield M D. 2001. Cellular function of phosphoinositide 3-kinases:implications for development, immunity, homeostasis, and cancer. Annual Review of Cell and Developmental Biology, 17(1):615-675. Koyasu S. 2003. The role of PI3K in immune cells. Nat.Immunol., 4(4):313-319. Kurita K. 2006. Chitin and chitosan:functional biopolymers from marine crustaceans. Mar. Biotechno., 8(3):203-226. Lee C G, Da Silva C A, Lee J Y, Hartl D, Elias J A. 2008.Chitin regulation of immune responses:an old molecule with new roles. Curr. Opin. Immunol., 20(6):684-689. Li K K, Shen S S, Deng X Y, Shiu H T, Siu W S, Leung P C, Ko C H, Cheng B H. 2018. Dihydrofisetin exerts its antiinflammatory effects associated with suppressing ERK/p38 MAPK and Heme Oxygenase-1 activation in lipopolysaccharide-stimulated RAW 264.7 macrophages and carrageenan-induced mice paw edema. International Immunopharmacology, 54:366-374. Li L, Wang L Y, Wu Z Q, Yao L J, Wu Y H, Huang L, Liu K, Zhou X, Gou D M. 2014. Anthocyanin-rich fractions from red raspberries attenuate inflammation in both RAW264.7 macrophages and a mouse model of colitis. Sci. Rep., 4:6 234. Li Y, Qin Y K, Liu S, Li P C, Xing R E. 2016. Preparation, characterization, and antifungal activity of hymexazollinked chitosan derivatives. Chinese Journal of Oceanology and Limnology, 35(5):1 079-1 085. Liang N, Sang Y X, Liu W H, Yu W L, Wang X H. 2018. AntiInflammatory effects of gingerol on lipopolysaccharidestimulated RAW 264.7 cells by inhibiting NF-κB signaling pathway. Inflammation, 41(3):835-845. Liaqat F, Eltem R. 2018. Chitooligosaccharides and their biological activities:a comprehensive review. Carbohydr.Polym., 184:243-259. Ma P, Liu H T, Wei P, Xu Q S, Bai X F, Du Y G, Yu C. 2011.Chitosan oligosaccharides inhibit LPS-induced overexpression of IL-6 and TNF-α in RAW264.7 macrophage cells through blockade of mitogen-activated protein kinase (MAPK) and PI3K/Akt signaling pathways.Carbohydr. Polym., 84(4):1 391-1 398. Musti A M, Treier M, Bohmann D. 1997. Reduced ubiquitindependent degradation of c-Jun after phosphorylation by MAP Kinases. Science, 275(5298):400-402. Nishimura K, Nishimura S, Nishi N, Saiki I, Tokura S, Azuma I. 1984. Immunological activity of chitin and its derivatives. Vaccine, 2(1):93-99. Nyati K K, Masuda K, Zaman M M U, Dubey P K, Millrine D, Chalise J P, Higa M, Li S L, Standley D M, Saito K, Hanieh H, Kishimoto T. 2017. TLR4-induced NF-κB and MAPK signaling regulate the IL-6 mRNA stabilizing protein Arid5a. Nucleic Acids Res., 45(5):2 687-2 703. Pillai C K S, Paul W, Sharma C P. 2009. Chitin and chitosan polymers:chemistry, solubility and fiber formation.Progress in Polymer Science, 34(7):641-678. Poltorak A, He X L, Smirnova I, Liu M Y, van Huffel C, Du X, Birdwell D, Alejos E, Silva M, Galanos C, Freudenberg M, Ricciardi-Castagnoli P, Layton B, Beutler B. 1998. Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice:mutations in Tlr4 gene. Science, 282(5396):2 085-2 088. Raschke W C, Baird S, Ralph P, Nakoinz I. 1978. Functional macrophage cell lines transformed by abelson leukemia virus. Cell, 15(1):261-267. Schindler C, Levy D E, Decker T. 2007. JAK-STAT signaling:from interferons to cytokines. J. Biol. Chem., 282(28):20 059-20 063. Shen T, Yang W S, Yi Y S, Sung G H, Rhee M H, Poo H, Kim M Y, Kim K W, Kim J H, Cho J Y. 2013. AP-1/IRF-3 targeted anti-Inflammatory activity of andrographolide isolated from Andrographis paniculata. Evid. Based Complement Alternat. Med., 2013(4):210 736. Sun H X, Zhang J, Chen F Y, Chen X F, Zhou Z H, Wang H. 2015. Activation of RAW264.7 macrophages by the polysaccharide from the roots of Actinidia eriantha and its molecular mechanisms. Carbohydr. Polym., 121:388-402. Tang B, Li X, Ren Y, Wang J, Xu D, Hang Y, Zhou T, Li F, Wang L. 2017. MicroRNA-29a regulates lipopolysaccharide (LPS)-induced inflammatory responses in murine macrophages through the Akt1/NFkappaB pathway. Exp. Cell Res., 360(2):74-80. Wen Q, Mei L Y, Ye S, Liu X, Xu Q, Miao J F, Du S H, Chen D F, Li C, Li H. 2018. Chrysophanol demonstrates antiinflammatory properties in LPS-primed RAW 264.7 macrophages through activating PPAR-γ. International Immunopharmacology, 56:90-97. Wymann M P, Pirola L. 1998. Structure and function of phosphoinositide 3-kinases. BBA-Mol. Cell. Biol. Lipids, 1436(1-2):127-150. Yang Y, Xing R E, Liu S, Qin Y K, Li K C, Yu H H, Li P C. 2019. Hydroxypropyltrimethyl ammonium chloride chitosan activates RAW 264.7 macrophages through the MAPK and JAK-STAT signaling pathways. Carbohydr.Polym., 205:401-409. Youn G S, Lee K W, Choi S Y, Park J. 2016. Overexpression of HDAC6 induces pro-inflammatory responses by regulating ROS-MAPK-NF-κB/AP-1 signaling pathways in macrophages. Free Radical Biology and Medicine, 97:14-23. Yu Y, Shen M Y, Wang Z J, Wang Y X, Xie M Y, Xie J H. 2017.Sulfated polysaccharide from Cyclocarya paliurus enhances the immunomodulatory activity of macrophages.Carbohydr. Polym., 174:669-676. Zhang Q, Wang L R, Chen B H, Zhuo Q, Bao C Y, Lin L. 2017.Propofol inhibits NF-κB activation to ameliorate airway inflammation in ovalbumin (OVA)-induced allergic asthma mice. International Immunopharmacology, 51:158-164. Zhang Y, Igwe O J. 2018. Exogenous oxidants activate nuclear factor kappa B through Toll-like receptor 4 stimulation to maintain inflammatory phenotype in macrophage.Biochem. Pharmacol., 147:104-118.
|
|
|