PL EN


Preferences help
enabled [disable] Abstract
Number of results
Journal
2015 | 64 | 1 | 11-20
Article title

Owady - alternatywne organizmy modelowe do badań chorób człowieka

Content
Title variants
Languages of publication
PL EN
Abstracts
PL
W ostatniej dekadzie nastąpił gwałtowny wzrost zainteresowania wykorzystaniem bezkręgowców, w tym owadów, jako organizmów modelowych w badaniach chorób człowieka. Opublikowano liczne prace, w których wykazano możliwość wykorzystania owadzich modeli w badaniach chorób neurodegeneracyjnych, cukrzycy, otyłości, czy chorób serca. Szybki rozwój technik biologii molekularnej, biotestów fizjologicznych i farmakologicznych, a także poznanie genomów muszki Drosophila melanogaster, chrząszcza Tribolium castaneum, jedwabnika Bombyx mori i pszczoły Apis mellifera dodatkowo stanowią silne wsparcie metodologiczne tego kierunku badań. Poznano szereg genów owadów, będących ortologami genów ludzkich, odpowiedzialnych za rozwój różnych chorób, zidentyfikowano wiele białek kodowanych przez te geny, scharakteryzowano ich fenotypy morfologiczne i fizjologiczne, a także opisano działanie u owadów niektórych leków stosowanych w chorobach neurodegeneracyjnych i kardiologicznych człowieka.
EN
Over the last decade the interest of using invertebrates, including insects, as model organisms in studies of human diseases has rapidly increased. Until now, hundreds of papers which demonstrate the possibility of using insect models in studies on human neurodegenerative diseases, diabetes, obesity or heart diseases were published. The rapid development of molecular biology techniques, physiological and pharmacological bioassays, as well as genome sequencing of fruit fly Drosophila melanogaster, red flour beetle Tribolium castaneum, silkworm Bombyx mori and honey bee Apis mellifera also provides a strong methodological support for this research approach. As a result of these studies a number of insect genes, orthologs of human genes known to be responsible for the development of various diseases, and many proteins encoded by these genes were identified. Also morphological and physiological phenotypes of different genes and the action of some drugs applied in neurodegenerative and cardiac diseases in humans have been characterized in insects.
Keywords
Journal
Year
Volume
64
Issue
1
Pages
11-20
Physical description
Dates
published
2015
Contributors
  • Zakład Fizjologii i Biologii Rozwoju Zwierząt, Instytut Biologii Eksperymentalnej, Wydział Biologii, Uniwersytet im. Adama Mickiewicza w Poznaniu, Umultowska 89, 61-614 Poznań, Polska
  • Zakład Fizjologii i Biologii Rozwoju Zwierząt, Instytut Biologii Eksperymentalnej, Wydział Biologii, Uniwersytet im. Adama Mickiewicza w Poznaniu, Umultowska 89, 61-614 Poznań, Polska
  • Zakład Fizjologii i Biologii Rozwoju Zwierząt, Instytut Biologii Eksperymentalnej, Wydział Biologii, Uniwersytet im. Adama Mickiewicza w Poznaniu, Umultowska 89, 61-614 Poznań, Polska
  • Zakład Fizjologii i Biologii Rozwoju Zwierząt, Instytut Biologii Eksperymentalnej, Wydział Biologii, Uniwersytet im. Adama Mickiewicza w Poznaniu, Umultowska 89, 61-614 Poznań, Polska
References
  • Abraham D. M., Wolf M. J., 2013. Disruption of sarcoendoplasmic reticulum calcium ATPase function in Drosophila leads to cardiac dysfunction. PLoS One 8, e77785.
  • Akasaka T., Ocorr K., 2009. Drug discovery through functional screening in the Drosophila heart. Meth. Mol. Biol. 577, 235-249.
  • Ambegaokar S. S., Roy B., Jackson G. R., 2010. Neurodegenerative models in Drosophila: polyglutamine disorders, Parkinson disease, and amyotrophic lateral sclerosis. Neurobiol. Dis. 40, 29-39.
  • Bier E., Bodmer R., 2004. Drosophila, an emerging model for cardiac disease. Gene 342, 1-11.
  • Birse R. T., Bodmer R., 2011. Lipotoxicity and cardiac dysfunction in mammals and Drosophila. Crit. Rev. Biochem. Mol. Biol. 46, 376-385.
  • Buechling T., Akasaka T., Vogler G., Ruiz-Lozano P., Ocorr K., Bodmer R., 2009. Non-autonomous modulation of heart rhythm, contractility and morphology in adult fruit flies. Dev. Biol. 328, 483-492.
  • Chen K. F., Possidente B., Lomas D. A., Crowther D. C., 2014. The central molecular clock is robust in the face of behavioural arrhythmia in a Drosophila model of Alzheimer's disease. Dis. Model. Mech. 7, 445-458.
  • Choma M. A., Suter M. J., Vakoc B. J., Bouma B. E., Tearney G. J., 2010. Heart wall velocimetry and exogenous contrast-based cardiac flow imaging in Drosophila melanogaster using Doppler optical coherence tomography. J. Biomed. Opt. 15, 056020-056026.
  • Cookson M. R., 2005. The biochemistry of Parkinson's disease. Annu. Rev. Biochem. 74, 29-52.
  • De Greeve P., De Leeuw W., van Zutphen B. F., 2004. Trends in animal use and animal alternatives. Altern. Lab. Anim. 32, 13-19.
  • Feliciano D. F., Bassani R. A., Oliveira P. X., Bassani J. W., 2011. Pacemaker activity in the insect (T. molitor) heart: role of the sarcoplasmic reticulum. Am. J. Physiol. Regul. Integr. Comp. Physiol. 301, R1838-R1845.
  • Gelsomino S., Lucà F., Nediani C., Orlandini S.Z., Bani D., Rubino A.S., Renzulli A., Lorusso R., Consolo A., Lo Cascio A., Maessen J., Gensini G. F., 2013. Early hemodynamic and biochemical changes in overloaded swine ventricle. Tex. Heart Inst. J. 40, 235-245.
  • Green E. W., Giorgini F., 2012. Choosing and using Drosophila models to characterize modifiers of Huntington's disease. Biochem. Soc. Trans. 40,739-745.
  • Greeve I., Kretzschmar D., Tschäpe J. A.,Beyn A., Brellinger C., Schweizer M., Nitsch R. M., Reifegerste R., 2004. Age-dependent neurodegeneration and Alzheimer-amyloid plaque formation in transgenic Drosophila. J. Neurosci. 24, 3899-3906.
  • Jackson G. R., Salecker I., Dong X., Yao X., Arnheim N., Faber P. W., MacDonald M. E., Zipursky S. L., 1998. Polyglutamine-expanded human huntingtin transgenes induce degeneration of Drosophila photoreceptor neurons. Neuron 21, 633-642.
  • Johnson E., Sherry T., Ringo J., Dowse H., 2002. Modulation of the cardiac pacemaker of Drosophila: cellular mechanisms. J. Comp. Physiol B. 172, 227-236.
  • Haywood A. F., Staveley B. E., 2004. Parkin counteracts symptoms in a Drosophila model of Parkinson's disease. BMC Neurosci. 5, 14.
  • Keil T. A, Steinbrecht R. A., 2010. Insects as model systems in cell biology. Meth. Cell Biol. 96, 363-394.
  • Krench M., Littleton J. T., 2013. Modeling Huntington disease in Drosophila: Insights into axonal transport defects and modifiers of toxicity. Fly (Austin) 7, 229-236.
  • Lenz S., Karsten P., Schulz J. B., Voigt A., 2013. Drosophila as a screening tool to study human neurodegenerative diseases. J. Neurochem. 127, 453-460.
  • Liu Z., Wang X., Yu Y., Li X., Wang T., Jiang H., Ren Q., Jiao Y., Sawa A., Moran T., Ross C. A., Montell C., Smith W. W., 2008. A Drosophila model for LRRK2-linked parkinsonism. Proc. Nat. Acad. Sci. USA 105, 2693-2698.
  • Ma L., Bradu A., Podoleanu A., Bloor J. W., 2010. Arrythmia caused by a Drosophila tropomyosin mutation is revealed using a novel optical coherence tomography instrument. Plos One 5, e14348.
  • Magny E. G., Pueyo J. I., Pearl F. M., Cespedes M. A., Niven J. E., Bishop S. A., Couso J. P., 2013. Conserved regulation of cardiac calcium uptake by peptides encoded in small open reading frames. Science 341, 1116-1120.
  • Marciniak P., Grodecki S., Konopińska D., Rosiński G., 2008. Structure activity relationships for the cardiotropic action of the Led-NPF-I peptide in the beetles Tenebrio molitor and Zophobas atratus. J. Pept. Sci.14, 329-334.
  • Markou T., Theophilidis G., 2000.The pacemaker activity generating the intrinsic myogenic contraction of the dorsal vessel of Tenebrio molitor (Coleoptera). J. Exp. Biol. 203, 3471-3483.
  • Matsumoto Y., Sumiya E., Sugita T., Sekimizu K., 2011. An invertebrate hyperglycemic model for the identification of anti-diabetic drugs. PLoS One 6, e18292.
  • Mery A., Taghli-Lamallem O., Clark K., Beckerle M., Wu X., Ocorr K., Bodmer R., 2008. The Drosophila muscle LIM protein, Mlp84B, is essential for cardiac function. J. Exp. Biol. 211, 15-23.
  • Mhatre S. D., Satyasi V., Killen M., Paddock B. E., Moir R. D., Saunders A. J, Marenda D. R., 2014. Synaptic abnormalities in a Drosophila model of Alzheimer's disease. Dis. Model Mech. 7, 373-385.
  • Mosqueira M., Willmann G., Ruohola-Baker H., Khurana T. S., 2010. Chronic hypoxia impairs muscle function in the Drosophila model of Duchenne's muscular dystrophy (DMD). PLoS One. 5, e13450.
  • Na J., Musselman L. P., Pendse J., Baranski T. J., Bodmer R., Ocorr K., Cagan R., 2013. A Drosophila model of high sugar diet-induced cardiomyopathy. PLoS Genet. 9, e1003175.
  • Nishimura M., Ocorr K., Bodmer R., Cartry J., 2011. Drosophila as a model to study cardiac aging. Exp. Gerontol. 46, 326-330.
  • Ocorr K., Reeves N., Wessells R., Fink M., Chen V., Akasaka T., Yasuda S., Metzger J., Giles W., Posakony J., Bodmer R., 2007. KCNQ potassium channel mutations cause cardiac arrhythmias in Drosophila that mimic the effects of aging. Proc. Natl. Acad. Sci. USA 104, 3943-3948.
  • Qian L., Bodmer R., 2012. Probing the polygenic basis of cardiomyopathies in Drosophila. J. Cell Mol. Med. 16, 972-977.
  • Perutz M. F., Johnson T., Suzuki M., Finch J. T., 1994. Glutamine repeats as polar zippers: their possible role in inherited neurodegenerative diseases. Proc. Natl. Acad. Sci. USA 91, 5355-5358.
  • Rosiński G., 1995. Metaboliczne i miotropowe neuropeptydy owadów. Wydawnictwo Naukowe UAM, Seria Zoologia 22.
  • Russell W. M. S., Burch R. L., 1959. The principles of humane experimental technique. Methuen, London.
  • Sang T. K., Jackson G. R., 2005. Drosophila models of neurodegenerative disease. NeuroRx 2, 438-446.
  • Setzu M., Biolchini M., Lilliu A., Manca M., Muroni P., Poddighe S., Bass C., Angioy A. M., Nichols R., 2012. Neuropeptide F peptides act through unique signaling pathways to affect cardiac activity. Peptides 33, 230-239.
  • Slama K., 2012. A new look at the comparative physiology of insect and human hearts. J. Insect Physiol. 58, 1072-1081.
  • Slama K., Lukaš J., 2011. Myogenic nature of insects heartbeat revealed by neuromuscular paralysis caused by the sting of a braconid wasp. J. Insect Physiol. 57, 251-259.
  • Slama K., Rosiński G., 2005. Delayed pharmacological effects of proctolin and CCAP on heartbeat in pupae of the tobacco hornworm, Manduca sexta. Physiol. Entomol. 30, 14-28.
  • Szymczak M., Marciniak P., Rosiński G., 2014. Miokardium owada - model do badań biomedycznych. Postępy biologii komórki. Post. Biol. Kom. 41, 59-78.
  • Taghli-Lamallem O., Akasaka T., Hogg G., Nudel U., Yaffe D., Chamberlain J. S., Ocorr K., Bodmer R., 2008a. Dystrophin deficiency in Drosophila reduces lifespan and causes a dilated cardiomyopathy phenotype. Aging Cell 7, 237-249.
  • Taghli-Lamallem O., Bodmer R., Chamberlain J. S., 2008b. Genetics and pathogenic mechanisms of cardiomyopathies in the Drosophila model. Drug Discov. Today 5, 125-134.
  • Terlau H., Stühmer W., 1998. Structure and function of voltage-gated ion channels. Naturwissenschaften 85, 437-444.
  • Thenganatt M. A., Jankovic J., 2014. Parkinson disease subtypes. JAMA Neurol. 71, 499-504.
  • Trinh K., Moore K., Wes P. D., Muchowski P. J., Dey J., Andrews L., Pallanck L. J., 2008. Induction of the phase II detoxification pathway suppresses neuron loss in Drosophila models of Parkinson's disease. J. Neurosci. 28, 465-472.
  • van der Plas M. C., Pilgram G. S., de Jong A. W., Bansraj M. R., Fradkin L. G., Noordermeer J. N., 2007. Drosophila Dystrophin is required for integrity of the musculature. Mech. Dev. 124, 617-630.
  • Viswanathan M. C., Kaushik G., Engler A. J., Lehman W., Cammarato A., 2013. A Drosophila melanogaster model of diastolic dysfunction and cardiomyopathy based on impaired troponin-T function. Circ. Res. 114, 6-17.
  • Wells D. J., Wells K. E., 2005. What do animal models have to tell us regarding Duchenne muscular dystrophy? Acta Myol. 24,172-180.
  • Wolf M. J., Amrein H., Izatt J. A., Choma M. A., Reedy M. C., Rockman H. A., 2006. Drosophila as a model for identification of genes causing adult human heart disease. Proc. Natl. Acad. Sci. USA 103, 1394-1399.
  • Yu L., Lee T., Lin N., Wolf M., 2010. Affecting rhomboid-3 function causes a dilated heart in adult Drosophila. Plos Genet. 6, e1000969.
  • Zhao X. L., Wang W. A., Tan J. X., Huang J. K., Zhang X., Zhang B. Z., Wang Y. H., YangCheng H. Y., Zhu H. L., Sun X. J., Huang F. D., 2010. Expression of beta amyloid induced age-dependent presynaptic and axonal changes in Drosophila. J. Neurosci. 30, 1512-1522.
  • Zong N. C., Li H., Li H., Lam M. P., Jimenez R. C., Kim C. S., Deng N., Kim A. K., Choi J. H., Zelaya I., Liem D., Meyer D., Odeberg J., Fang C., Lu H. J., Xu T., Weiss J., Duan H., Uhlen M., Yates J. R. Apweiler R., Ge J., Hermjakob H., Ping P., 2013. Integration of cardiac proteome biology and medicine by a specialized knowledgebase. Circ. Res. 113, 1043-1053.
Document Type
Publication order reference
Identifiers
YADDA identifier
bwmeta1.element.bwnjournal-article-ksv64p11kz
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.