TOBACCO SMOKE EXPOSURE COMBINED WITH GENETICALLY ENGINEERED MICE COPD DRUGS APPLICATION PROGRESS OF TARGET AND MECHANISM RESEARCH
Volume 1, Issue 2, Pp 20-24, 2023
DOI:10.61784/wjbs231240
Author(s)
S. Lungwitz
Affiliation(s)
Department of Pharmaceutical Technology, University of Regensburg, Regensburg, Germany.
Corresponding Author
S. Lungwitz
ABSTRACT
Chronic obstructive pulmonary disease (chronic obstructive pulmonary disease) pulmonary disease, chronic obstructive, COPD) is a common respiratory disease that seriously threatens human life and health. COPD The formation and development of the disease are determined by the internal genes and external environment. the combined effect of environmental factors. Tobacco smoke exposure combined with genetically engineered mice mimics the effects of specific genes under disease-causing conditions COPD biological effects. Check this article Research literature in recent years summarizes the application of the above methods in drug targets, inflammation and immunity. Applications of mechanism studies and their findings outline the research process of this approach. Should Written by COPD Provide reference for pathogenesis and drug research.
KEYWORDS
Chronic obstructive pulmonary disease; Tobacco smoke; Genetically engineered mice; Purpose Genes; Pathology; Drug development
CITE THIS PAPER
S. Lungwitz. Tobacco smoke exposure combined with genetically engineered mice copd drugs application progress of target and mechanism research. World Journal of Biomedical Sciences. 2023, 1(2): 20-24. DOI:10.61784/wjbs231240.
REFERENCES
[1] Liu Di, Zhang Hongchun. Research progress on genetically engineered animal models of chronic obstructive pulmonary disease Exhibition. Chinese Journal of Bioengineering, 2020, 40(4): 59-6 8.
[1] Liu D, Zhang H C. Advances in genetically engineered animal models of chronic obstructive pulmonary disease. Chin Biotechnol, 2020, 40(4): 59-68.
[2] Brooks S A, Blackshear P J. Tristetraprolin (TTP): interactions with mRNA and proteins, and current thoughts on mechanisms of action. Biochim Biophys Acta, 2013, 1829(6-7): 666-79.
[3] Clark A R, Dean J L. The control of inflammation via the phospho- rylation and dephosphorylation of tristetraprolin: a tale of two phosphatases. Biochem Soc Trans, 2016, 44(5): 1321-37.
[4] Chrestensen C A, Schroeder M J, Shabanowitz J, et al. MAPKAP kinase 2 phosphorylates tristetraprolin on in vivo sites including Ser178, a site required for 14-3-3binding. J Biol Chem, 2004, 279(11): 10176-84.
[5] Nair P M, Starkey M R, Haw T J, et al. Enhancing tristetraprolin activity reduces the severity of cigarette smoke-induced experimental chronic obstructive pulmonary disease. Clin Transl Immunology, 2019, 8(10): e01084.
[6] Ross E A, Smallie T, Ding Q, et al. Dominant suppression of in- flammation via targeted mutation of the mRNA destabilizing protein Tristetraprolin. J Immunol, 2015, 195(1): 265-76.
[7] Chen M, Wang T, Shen Y, et al. Knockout of RAGE ameliorates mainstream cigarette smoke-induced airway inflammation in mice. Int Immunopharmacol, 2017, 50: 230-5.
[8] Sanders K A, Delker D A, Huecksteadt T, et al. RAGE is a criti- cal mediator of pulmonary oxidative stress, alveolar macrophage ac- tivation and emphysema in response to cigarette smoke. Sci Rep, 2019, 9(1): 231.
[9] Ben-Porath I, Weinberg R A. The signals and pathways activating cellular senescence. Int J Biochem Cell Biol, 2005, 37 (5 ): 961-76.
[10] Hashimoto M, Asai A, Kawagishi H, et al. Elimination of p19ARF - expressing cells enhances pulmonary function in mice. JCI In- sight, 2016, 1(12): e87732.
[11] Mikawa R, Suzuki Y, Baskoro H, et al. Elimination of p19ARF -ex- pressing cells protects against pulmonary emphysema in mice. Aging Cell, 2018, 17(5): e12827.
[12] Mikawa R, Sato T,Suzuki Y,et to lp19 ARF exacerbates cigarette smoke-induced pulmonary dysfunction, J Biomolecules,2020,1 (3): 462.
[13] Saini Y, Dang H, Livraghi-Butrico A, et al. Gene expression in whole lung and pulmonary macrophages reflects the dynamic pathol- ogy associated with airway surface dehydration. BMC Genom- ics, 2014, 15(1): 726.
[14] Engle M L, Monk J N, Jania C M, et al. Dynamic changes in lung responses after single and repeated exposures to cigarette smoke in mice. PLoS One, 2019, 14(2): e0212866.
[15] Maeno T, Houghton A M, Quintero P A, et al. CD8 + T cells are required for inflammation and destruction in cigarette smoke-in-duced emphysema in mice. J Immunol, 2007, 178(12): 8090 - 6.
[16] Motz G T, Eppert B L, Wesselkamper S C, et al. Chronic cigarette smoke exposure generates pathogenic T cells capable of driving- COPD-like disease in Rag2/mice. Am J Respir Crit Care Med, 2010, 181(11): 1223-33.
[17] Donovan C, Starkey M R, Kim R Y, et al. Roles for T/B lympho- cytes and ILC2s in experimental chronic obstructive pulmonary dis- ease. J Leukoc Biol, 2019, 105(1): 143-50.
[18] Monticelli L A, Buck M D, Flamar A L, et al. Arginase 1 is an innate lymphoid-cell-intrinsic metabolic checkpoint controlling type 2 inflammation. Nat Immunol, 2016, 17(6): 656-65.
[19] Silver J S, Kearley J, Copenhaver A M, et al. Inflammatory triggers associated with exacerbations of COPD orchestrate plasticity of group 2 innate lymphoid cells in the lungs. Nat Immunol, 2016, 17(6): 626-35.
[20] Silverman E K. Genetics of COPD. Annu Rev Physiol, 2020, 82: 413-31.
[21] Busch R, Hobbs B D, Zhou J, et al. Genetic association and risk scores in a chronic obstructive pulmonary disease meta-analysis of 16, 707 subjects. Am J Respir Cell Mol Biol, 2017, 57(1): 35 - 46.
[22] D ’Souza B, Meloty-Kapella L, Weinmaster G. Canonical and non- canonical Notch ligands. Curr Top Dev Biol, 2010, 92: 73 - 129.
[23] Ballester-López C, Conlon T M, Ertüz Z, et al. The Notch ligand DNER regulates macrophage IFNγ release in chronic obstructive pulmonary disease. EBiomedicine, 2019, 43: 562-75.
[24] Singh D, Agusti A, Anzueto A, et al. Global strategy for the diag- nosis, management, and prevention of chronic obstructive lung dis- ease: the GOLD science committee report 2019. Eur Respir J, 2019, 53(5): 1900164.