Pathogenicity of lncRNA MALAT1 in diabetic microangiopathy

doi:10.3877/cma.j.issn.2095-8757.2017.01.005

Abstract

Abstract:

With the continued increase in the prevalence of type 2 diabetes, diabetes-induced microvascular and macrovascular diseases have attracted much attention. Vascular complications and diabetes mortality are directly related. Microvascular disease is an important complication of diabetic vascular complications. At present, the pathogenesis of diabetes mellitus is still unclear. Diabetic microvascular disease is mainly related to the formation of hyperglycemia-related glucoside toxicity products and its interference with cell signaling pathway, which causes endothelial dysfunction. The human genome contains abundant RNA sequences that are highly transcribed but not translated into proteins, which help to control and regulate cell function through different mechanisms. A class of non-coding RNA-lncRNA (long non-coding RNA) with length> 200 nucleotides gradually entered the line of sight. Among them, MALAT1 (lung adenocarcinoma-associated transcript 1) was initially found as a tumor-associated lncRNA, also known as noncoding nuclear-enriched abundant transcript 2 (NEAT2), involved in the regulation of gene expression splicing and controlling epigenetics. Recent studies have found that MALAT1 is also involved in the pathogenesis of diabetic microangiopathy. Further study may provide the appropriate strategy for the prevention and treatment of diabetic complications.

Key words: lncRNA, MALAT1, Diabetes mellitus, Microvascular complication

Jingyi Xu, Hua Li, Ming Feng, Sujun Li, Tianyi Li, Tao Feng. Pathogenicity of lncRNA MALAT1 in diabetic microangiopathy[J]. Chinese Journal of Geriatrics Research(Electronic Edition), 2017, 04(01): 19-23.

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References 39

[1]	Ogurtsova K, da Rocha Fernandes JD, Huang Y, et al. IDF diabetes atlas: global estimates for the prevalence of diabetes for 2015 and 2040[J].Diabetes Res Clin Pract, 2017, 128: 40-50.
[2]	Ma RC, Lin X, Jia W, et al. Causes of type 2 diabetes in China[J]. Lancet Diabetes Endocrinol, 2014, 2(12): 980-991.
[3]	Garrido-Castro A. Prevalencia de la diabetes entre hombres y mujeres en China[J]. Revista Clínica Española, 2010, 210(9): 469-470.
[4]	Sena CM, Pereira AM, Seiça R. Endothelial dysfunction - a major mediator of diabetic vascular disease[J]. Biochim Biophys Acta, 2013, 1832(12): 2216-2231.
[5]	Fadini GP, Ferraro F, Quaini F, et al. Concise review: diabetes, the bone marrow niche, and impaired vascular regeneration[J]. Stem Cells Transl Med, 2014, 3(8): 949-957.
[6]	Madonna R, De Caterina R. Cellular and molecular mechanisms of vascular injury in diabetes--part II: cellular mechanisms and therapeutic targets[J]. Vascul Pharmacol, 2011, 54(3-6): 75-79.
[7]	Psaltis PJ, Simari RD. Vascular wall progenitor cells in health and disease[J]. Circ Res, 2015, 116(8): 1392-1412.
[8]	Xu J, Zou MH. Molecular insights and therapeutic targets for diabetic endothelial dysfunction[J]. Circulation, 2009, 120(13): 1266-1286.
[9]	Tabit CE, Chung WB, Hamburg NM, et al. Endothelial dysfunction in diabetes mellitus: molecular mechanisms and clinical implications[J]. Rev Endocr Metab Disord, 2010, 11(1): 61-74.
[10]	Hammes HP, Feng Y, Pfister F, et al. Diabetic retinopathy: targeting vasoregression[J]. Diabetes, 2011, 60(1): 9-16.
[11]	International Human Genome Sequencing Consortium. Finishing the euchromatic sequence of the human genome[J]. Nature, 2004, 431(7011): 931-945.
[12]	Wilusz JE, Sunwoo H, Spector DL. Long noncoding RNAs: functional surprises from the RNA world[J]. Genes Dev, 2009, 23(13): 1494-1504.
[13]	Guo X, Gao L, Wang Y, et al. Advances in long noncoding RNAs: identification, structure prediction and function annotation[J]. Brief Funct Genomics, 2016, 15(1): 38-46.
[14]	Mercer TR, Mattick JS. Structure and function of long noncoding RNAs in epigenetic regulation[J]. Nat Struct Mol Biol, 2013, 20(3): 300-307.
[15]	Ponting CP, Oliver PL, Reik W. Evolution and functions of long noncoding RNAs[J]. Cell, 2009, 136(4): 629-641.
[16]	Yang F, Yi F, Zheng Z, et al. Characterization of a carcinogenesis-associated long non-coding RNA[J]. RNA Biol, 2012, 9(1): 110-116.
[17]	Sánchez Y, Huarte M. Long non-coding RNAs: challenges for diagnosis and therapies[J]. Nucleic Acid Ther, 2013, 23(1): 15-20.
[18]	Rayner KJ, Liu PP. Long noncoding RNAs in the heart: the regulatory roadmap of cardiovascular development and disease[J]. Circ Cardiovasc Genet, 2016, 9(2): 101-103.
[19]	Huang M, Hou J, Wang Y, et al. Long noncoding RNA LINC00673 is activated by SP1 and exerts oncogenic properties by interacting with LSD1 and EZH2 in gastric cancer[J]. Mol Ther, 2017, 25(4): 1014-1026.
[20]	Pullen TJ, Rutter GA. Could lncRNAs contribute toβ-cell identity and its loss in Type 2 diabetes [J]? Biochem Soc Trans, 2013, 41(3): 797-801.
[21]	Arnes L, Akerman I, Balderes DA, et al.βlinc1 encodes a long noncoding RNA that regulates isletβ-cell formation and function[J]. Genes Dev, 2016, 30(5): 502-507.
[22]	Liu Y, Zheng L, Wang Q, et al. Emerging roles and mechanisms of long noncoding RNAs in atherosclerosis[J]. Int J Cardiol, 2017, 228: 570-582.
[23]	Qiu GZ, Tian W, Fu HT, et al. Long noncoding RNA-MEG3 is involved in diabetes mellitus-related microvascular dysfunction[J]. Biochem Biophys Res Commun, 2016, 471(1): 135-141.
[24]	Li CP, Wang SH, Wang WQ, et al. Long noncoding RNA-Sox2OT knockdown alleviates diabetes mellitus-induced retinal ganglion cell (RGC) injury[J]. Cell Mol Neurobiol, 2017, 37(2): 361-369.
[25]	Ji P, Diederichs S, Wang W, et al. MALAT-1, a novel noncoding RNA, and thymosin beta4 predict metastasis and survival in early-stage non-small cell lung cancer[J]. Oncogene, 2003, 22(39): 8031-8041.
[26]	Gutschner T, Hämmerle M, Eissmann M, et al. The noncoding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells[J]. Cancer Res, 2013, 73(3): 1180-1189.
[27]	Zhang M, Gu H, Xu W, et al. Down-regulation of lncRNA MALAT1 reduces cardiomyocyte apoptosis and improves left ventricular function in diabetic rats[J]. Int J Cardiol, 2016, 203: 214-216.
[28]	Bugger H, Abel ED. Molecular mechanisms of diabetic cardiomyopathy[J].Diabetologia, 2014, 57(4): 660-671.
[29]	Kern TS. Contributions of inflammatory processes to the development of the early stages of diabetic retinopathy[J]. Exp Diabetes Res, 2007, 2007: 95103.
[30]	Gutschner T, Hämmerle M, Diederichs S. MALAT1 -- a paradigm for long noncoding RNA function in cancer[J]. J Mol Med (Berl), 2013, 91(7): 791-801.
[31]	Han CY, Subramanian S, Chan CK, et al. Adipocyte-derived serum amyloid A3 and hyaluronan play a role in monocyte recruitment and adhesion[J]. Diabetes, 2007, 56(9): 2260-2273.
[32]	Zhang B, Arun G, Mao YS, et al. The lncRNA Malat1 is dispensable for mouse development but its transcription plays a cis-regulatory role in the adult[J]. Cell Rep, 2012, 2(1): 111-123.
[33]	Puthanveetil P, Chen S, Feng B, et al. Long non-coding RNA MALAT1 regulates hyperglycaemia induced inflammatory process in the endothelial cells[J]. J Cell Mol Med, 2015, 19(6): 1418-1425.
[34]	Cao Z, Cooper ME. Pathogenesis of diabetic nephropathy[J]. J Diabetes Investig, 2011, 2(4): 243-247.
[35]	Forbes JM, Coughlan MT, Cooper ME. Oxidative stress as a major culprit in kidney disease in diabetes[J]. Diabetes, 2008, 57(6): 1446-1454.
[36]	Kroemer G, Galluzzi L, Vandenabeele P, et al. Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009[J]. Cell Death Differ, 2009, 16(1): 3-11.
[37]	Li X, Zeng L, Cao C, et al. Long noncoding RNA MALAT1 regulates renal tubular epithelial pyroptosis by modulated miR-23c targeting of ELAVL1 in diabetic nephropathy[J]. Experimental Cell Research, 2017, 350(2): 327-335.
[38]	Liu JY, Yao J, Li XM, et al. Pathogenic role of lncRNA-MALAT1 in endothelial cell dysfunction in diabetes mellitus[J]. Cell Death Dis, 2014, 5: e1506.
[39]	Zhang M, Gu H, Chen J, et al. Involvement of long noncoding RNA MALAT1 in the pathogenesis of diabetic cardiomyopathy[J]. Int J Cardiol, 2016, 202: 753-755.

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