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In molecular biology mir-210 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.
mir-210 has been strongly linked with the hypoxia pathway, and is upregulated in response to Hypoxia-inducible factors. It is also overexpressed in cells affected by cardiac disease and tumours. MiRNA-210 in particular, has been studied for its effects in rescuing cardiac function after myocardial infarcts via the up-regulation of angiogenesis and inhibition of cardiomyocyte apoptosis.
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In molecular biology mir-210 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.
mir-210 has been strongly linked with the hypoxia pathway, and is upregulated in response to Hypoxia-inducible factors.[1] It is also overexpressed in cells affected by cardiac disease and tumours.[2] MiRNA-210 in particular, has been studied for its effects in rescuing cardiac function after myocardial infarcts via the up-regulation of angiogenesis and inhibition of cardiomyocyte apoptosis.[3]
[edit] Myocardial Infarction Therapy
Myocardial infarction is cardiac tissue necrosis that results from occlusion of blood supply via coronary arteries, thereby starving cells of oxygen and nutrients (termed ischemia). Prolong ischemia will eventually kill the cells and the destruction of cardiac cells leads to tissue death, which can lead to heart failure.
Delivery of miRNA-210 to an ischemic heart improves heart function, possibly by promoting the release of angiogenic factors like interleukin-1α (IL-1α), tumor necrosis factor-α (TNF-α) and leptin, as seen in HL-1 cardiomyocytes injected with miRNA-210.[3] However, miRNA-210 also targets the Efna3 and Ptp1b genes, which are genes which endogenously regulate angiogenesis and apoptosis, respectively.[3]
Ephrin-A3 (Efna3) is a gene that is involved in the inhibition of angiogenesis. Although it is known that Efna3 inhibits the formation of new blood vessels, its specific role is still unknown.[4] MiRNA-210 suppresses Efna3 at the mRNA level, thereby allowing angiogenesis to occur in cardiac tissue post-infarct.[3]
The second target gene, protein tyrosine phosphatase-1B (Ptp1b) is involved in the induction of apoptosis. Ptp1b gene protein has been known to regulate apoptosis by regulating the phosphorylation status of apoptotic proteins such as caspase-3 and caspase-8.[5] MiRNA-210 inhibits the effects of Ptp1b protein, which suppresses its pro-apoptotic functions.[3] Therefore, suppression of these two particular genes may contribute to the improvement of cardiac tissue and function by up-regulating angiogenesis and inhibiting apoptosis of cardiomyocytes after myocardial infarct.
[edit] See also
[edit] References
- ^ Huang, X; Le, QT, Giaccia, AJ (2010 May). "MiR-210--micromanager of the hypoxia pathway.". Trends in molecular medicine 16 (5): 230–7. doi:10.1016/j.molmed.2010.03.004. PMID 20434954.
- ^ Devlin, C; Greco, S, Martelli, F, Ivan, M (2011 Feb). "miR-210: More than a silent player in hypoxia.". IUBMB life 63 (2): 94–100. doi:10.1002/iub.427. PMID 21360638.
- ^ a b c d e Hu et al. “MicroRNA-210 as a Novel Therapy for treatment of Ischemic Heart Disease.” Journal of the American Heart Association. (2010) 122: S124 – S131
- ^ Fasanaro et al. “MicroRNA-210 Modulates Endothelial Cell Response to Hypoxia and Inhibits the Receptor Tyrosine Kinase Ligand Ephrin-A3.” The Journal of Biological Chemistry. (2008) 283.23: 15878 – 15883
- ^ Song et al. “Small interference RNA against PTP-1B reduces hypoxia/reoxygenation induced apoptosis of rat cardiomyocytes.” Apoptosis. (2008) 13: 383 – 393
[edit] Further reading
- ^ Tsuchiya S, Fujiwara T, Sato F, Shimada Y, Tanaka E, Sakai Y, Shimizu K, Tsujimoto G (2010). "MicroRNA-210 regulates cancer cell proliferation through targeting fibroblast growth factor receptor-like 1 (FGFRL1).". J Biol Chem 286 (1): 420–8. doi:10.1074/jbc.M110.170852. PMC 3013001. PMID 21044961.
- ^ Li T, Cao H, Zhuang J, Wan J, Guan M, Yu B, Li X, Zhang W (2010). "Identification of miR-130a, miR-27b and miR-210 as serum biomarkers for atherosclerosis obliterans". Clin Chim Acta 412 (1–2): 66–70. doi:10.1016/j.cca.2010.09.029. PMID 20888330.
- ^ Puisségur MP, Mazure NM, Bertero T, Pradelli L, Grosso S, Robbe-Sermesant K, Maurin T, Lebrigand K, Cardinaud B, Hofman V, Fourre S, Magnone V, Ricci JE, Pouysségur J, Gounon P, Hofman P, Barbry P, Mari B (2010). "miR-210 is overexpressed in late stages of lung cancer and mediates mitochondrial alterations associated with modulation of HIF-1 activity". Cell Death Differ 18 (3): 465–478. doi:10.1038/cdd.2010.119. PMID 20885442.
- ^ Hu S, Huang M, Li Z, Jia F, Ghosh Z, Lijkwan MA, Fasanaro P, Sun N, Wang X, Martelli F, Robbins RC, Wu JC (2010). "MicroRNA-210 as a novel therapy for treatment of ischemic heart disease". Circulation 122 (11 Suppl): S124–31. doi:10.1161/CIRCULATIONAHA.109.928424. PMC 2952325. PMID 20837903.
- ^ Zhang GL, Li YX, Zheng SQ, Liu M, Li X, Tang H (2010). "Suppression of hepatitis B virus replication by microRNA-199a-3p and microRNA-210". Antiviral Res 88 (2): 169–75. doi:10.1016/j.antiviral.2010.08.008. PMID 20728471.
- ^ Chen Z, Li Y, Zhang H, Huang P, Luthra R (2010). "Hypoxia-regulated microRNA-210 modulates mitochondrial function and decreases ISCU and COX10 expression". Oncogene 29 (30): 4362–8. doi:10.1038/onc.2010.193. PMID 20498629.
- ^ Favaro E, Ramachandran A, McCormick R, Gee H, Blancher C, Crosby M, Devlin C, Blick C, Buffa F, Li JL, Vojnovic B, Pires das Neves R, Glazer P, Iborra F, Ivan M, Ragoussis J, Harris AL (2010). "MicroRNA-210 regulates mitochondrial free radical response to hypoxia and krebs cycle in cancer cells by targeting iron sulfur cluster protein ISCU". In Gartel, Andrei L. PLoS ONE 5 (4): e10345. doi:10.1371/journal.pone.0010345. PMC 2859946. PMID 20436681.
- ^ Ho AS, Huang X, Cao H, Christman-Skieller C, Bennewith K, Le QT, Koong AC (2010). "Circulating miR-210 as a Novel Hypoxia Marker in Pancreatic Cancer". Transl Oncol 3 (2): 109–13. PMC 2847318. PMID 20360935.
- ^ Chan SY, Loscalzo J (2010). "MicroRNA-210: A unique and pleiotropic hypoxamir". Cell Cycle 9 (6): 1072–83. PMC 2912143. PMID 20237418.
- ^ Gee HE, Camps C, Buffa FM, Patiar S, Winter SC, Betts G, Homer J, Corbridge R, Cox G, West CM, Ragoussis J, Harris AL (2010). "hsa-mir-210 is a marker of tumor hypoxia and a prognostic factor in head and neck cancer". Cancer 116 (9): 2148–58. doi:10.1002/cncr.25009. PMID 20187102.
- ^ Kushibiki T (2010). "Photodynamic therapy induces microRNA-210 and -296 expression in HeLa cells". J Biophotonics 3 (5–6): 368–72. doi:10.1002/jbio.200900082. PMID 19953537.
- ^ Fasanaro P, Greco S, Lorenzi M, Pescatori M, Brioschi M, Kulshreshtha R, Banfi C, Stubbs A, Calin GA, Ivan M, Capogrossi MC, Martelli F (2009). "An integrated approach for experimental target identification of hypoxia-induced miR-210". J Biol Chem 284 (50): 35134–43. doi:10.1074/jbc.M109.052779. PMC 2787374. PMID 19826008.
- ^ Chan SY, Zhang YY, Hemann C, Mahoney CE, Zweier JL, Loscalzo J (2009). "MicroRNA-210 controls mitochondrial metabolism during hypoxia by repressing the iron-sulfur cluster assembly proteins ISCU1/2". Cell Metab 10 (4): 273–84. doi:10.1016/j.cmet.2009.08.015. PMC 2759401. PMID 19808020.
- ^ Huang X, Ding L, Bennewith KL, Tong RT, Welford SM, Ang KK, Story M, Le QT, Giaccia AJ (2009). "Hypoxia-inducible mir-210 regulates normoxic gene expression involved in tumor initiation". Mol Cell 35 (6): 856–67. doi:10.1016/j.molcel.2009.09.006. PMC 2782615. PMID 19782034.
- ^ Mathew LK, Simon MC (2009). "mir-210: a sensor for hypoxic stress during tumorigenesis". Mol Cell 35 (6): 737–8. doi:10.1016/j.molcel.2009.09.008. PMC 2869244. PMID 19782023.
- ^ Kim HW, Haider HK, Jiang S, Ashraf M (2009). "Ischemic preconditioning augments survival of stem cells via miR-210 expression by targeting caspase-8-associated protein 2". J Biol Chem 284 (48): 33161–8. doi:10.1074/jbc.M109.020925. PMC 2785158. PMID 19721136.
- ^ Bianchi N, Zuccato C, Lampronti I, Borgatti M, Gambari R (2009). "Expression of miR-210 during erythroid differentiation and induction of gamma-globin gene expression". BMB Rep 42 (8): 493–9. PMID 19712585.
- ^ Zhang Z, Sun H, Dai H, Walsh RM, Imakura M, Schelter J, Burchard J, Dai X, Chang AN, Diaz RL, Marszalek JR, Bartz SR, Carleton M, Cleary MA, Linsley PS, Grandori C (2009). "MicroRNA miR-210 modulates cellular response to hypoxia through the MYC antagonist MNT". Cell Cycle 8 (17): 2756–68. doi:10.4161/cc.8.17.9387. PMID 19652553.
- ^ Mizuno Y, Tokuzawa Y, Ninomiya Y, Yagi K, Yatsuka-Kanesaki Y, Suda T, Fukuda T, Katagiri T, Kondoh Y, Amemiya T, Tashiro H, Okazaki Y (2009). "miR-210 promotes osteoblastic differentiation through inhibition of AcvR1b". FEBS Lett 583 (13): 2263–8. doi:10.1016/j.febslet.2009.06.006. PMID 19520079.
- ^ Pulkkinen K, Malm T, Turunen M, Koistinaho J, Ylä-Herttuala S (2008). "Hypoxia induces microRNA miR-210 in vitro and in vivo ephrin-A3 and neuronal pentraxin 1 are potentially regulated by miR-210". FEBS Lett 582 (16): 2397–401. doi:10.1016/j.febslet.2008.05.048. PMID 18539147.
- ^ Fasanaro P, D'Alessandra Y, Di Stefano V, Melchionna R, Romani S, Pompilio G, Capogrossi MC, Martelli F (2008). "MicroRNA-210 modulates endothelial cell response to hypoxia and inhibits the receptor tyrosine kinase ligand Ephrin-A3". J Biol Chem 283 (23): 15878–83. doi:10.1074/jbc.M800731200. PMID 18417479.
- ^ Corn PG (2008). "Hypoxic regulation of miR-210: shrinking targets expand HIF-1's influence". Cancer Biol Ther 7 (2): 265–7. doi:10.4161/cbt.7.2.5745. PMID 18347426.
- ^ Camps C, Buffa FM, Colella S, Moore J, Sotiriou C, Sheldon H, Harris AL, Gleadle JM, Ragoussis J (2008). "hsa-miR-210 Is induced by hypoxia and is an independent prognostic factor in breast cancer". Clin Cancer Res 14 (5): 1340–8. doi:10.1158/1078-0432.CCR-07-1755. PMID 18316553.
- ^ Giannakakis A, Sandaltzopoulos R, Greshock J, Liang S, Huang J, Hasegawa K, Li C, O'Brien-Jenkins A, Katsaros D, Weber BL, Simon C, Coukos G, Zhang L (2008). "miR-210 links hypoxia with cell cycle regulation and is deleted in human epithelial ovarian cancer". Cancer Biol Ther 7 (2): 255–64. doi:10.4161/cbt.7.2.5297. PMID 18059191.
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