Abstract All-trans retinoic acid (ATRA) is a vitamin A derivative and plays an important role in the regulation of cell aggregation, differentiation, apoptosis, proliferation, and inflammatory response. In recent years, some progress has been made in the role of ATRA in renal diseases, especially its protective effect on podocytes. This article reviews the research advances in podocyte injury, characteristics of ATRA, podocyte differentiation and regeneration induced by ATRA, and the protective effect of ATRA against proliferation, deposition of fibers, and apoptosis.
CHEN Xiu-Ping,QIN Yuan-Han. Research advances in the protective effect of all-trans retinoic acid against podocyte injury[J]. CJCP, 2017, 19(6): 719-723.
CHEN Xiu-Ping,QIN Yuan-Han. Research advances in the protective effect of all-trans retinoic acid against podocyte injury[J]. CJCP, 2017, 19(6): 719-723.
Scott RP, Quaggin SE. Review series:The cell biology of renal filtration[J]. J Cell Biol, 2015, 209(2):199-210.
[2]
Abrahamson DR. Steps on the Alport path to proteinuria[J]. Kidney Int, 2016, 90(2):242-244.
[3]
Hu W, Niu G, Li H, et al. The association between expression of IFIT1 in podocytes of MRL/lpr mice and the renal pathological changes it causes:An animal study[J]. Oncotarget, 2016, 7(47):76464-76470.
[4]
Nagata M. Podocyte injury and its consequences[J]. Kidney Int, 2016, 89(6):1221-1230.
[5]
Mo H, Wu Q, Miao J, et al. C-X-C chemokine receptor CXCR4 plays a crucial role in mediating oxidative stress-induced podocyte injury[J]. Antioxid Redox Signal, 2017 Mar 28. doi:10.1089/ars.2016.6758.[Epub ahead of print]
[6]
Kriz W, Shirato I, Nagata M, et al. The podocyte's response to stress:the enigma of foot process effacement[J]. Am J Physiol Renal Physiol, 2013, 304(4):F333-F347.
[7]
Zhang H, Wang Z, Dong LQ, et al. Children with steroid-resistant nephrotic syndrome:long-term outcomes of sequential steroid therapy[J]. Biomed Environ Sci, 2016, 29(9):650-655.
[8]
Neal CR, Crook H, Bell E, et al. Three-dimensional reconstruction of glomeruli by electron microscopy reveals a distinct restrictive urinary subpodocyte space[J]. J Am Soc Nephrol, 2005, 16(5):1223-1235.
[9]
Sachs N, Sonnenberg A. Cell-matrix adhesion of podocytes in physiology and disease[J]. Nat Rev Nephrol, 2013, 9(4):200-210.
[10]
Gu J, Yang M, Qi N, et al. Olmesartan prevents microalbuminuria in db/db diabetic mice through inhibition of angiotensin II/p38/SIRT1-induced podocyte apoptosis[J]. Kidney Blood Press Res, 2016, 41(6):848-864.
[11]
Neal CR. Podocytes... What's under yours? (Podocytes and foot processes and how they change in nephropathy)[J]. Front Endocrinol (Lausanne), 2015, 6:9.
[12]
Lohmann F, Sachs M, Meyer TN, et al. UCH-L1 induces podocyte hypertrophy in membranous nephropathy by protein accumulation[J]. Biochim Biophys Acta, 2014, 1842(7):945-958.
[13]
Comptour A, Rouzaire M, Belville C, et al. Nuclear retinoid receptors and pregnancy:placental transfer, functions, and pharmacological aspects[J]. Cell Mol Life Sci, 2016, 73(20):3823-3837.
[14]
Wang ZY, Chen Z. Acute promyelocytic leukemia:from highly fatal to highly curable[J]. Blood, 2008, 111(5):2505-2515.
[15]
Amann PM, Eichmuller SB, Schmidt J, et al. Regulation of gene expression by retinoids[J]. Curr Med Chem, 2011, 18(9):1405-1412.
[16]
Parrado A, Despouy G, Kraïba R, et al. Retinoic acid receptor alpha1 variants, RARalpha1DeltaB and RARalpha1DeltaBC, define a new class of nuclear receptor isoforms[J]. Nucleic Acids Res, 2001, 29(24):4901-4908.
[17]
di Masi A, Leboffe L, De Marinis E, et al. Retinoic acid receptors:from molecular mechanisms to cancer therapy[J]. Mol Aspects Med, 2015, 41:1-115.
[18]
Soprano DR, Qin P, Soprano KJ. Retinoic acid receptors and cancers[J]. Annu Rev Nutr, 2004, 24:201-221.
[19]
le Maire A, Bourguet W. Retinoic acid receptors:structural basis for coregulator interaction and exchange[J]. Subcell Biochem, 2014, 70:37-54.
[20]
He JC, Lu TC, Fleet M, et al. Retinoic acid inhibits HIV-1-induced podocyte proliferation through the cAMP pathway[J]. J Am Soc Nephrol, 2007, 18(1):93-102.
[21]
Qin YH, Lei FY, Hu P, et al. Effect of all-trans retinoic acid on renal expressions of matrix metalloproteinase-2, matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in rats with glomerulosclerosis[J]. Pediatr Nephrol, 2009, 24(8):1477-1486.
[22]
Chen XP, Lei FY, Qin YH, et al. The role of retinoic acid receptors in the signal pathway of all-trans retinoic acid-induced differentiation in adriamycin-induced podocyte injury[J]. J Recept Signal Transduct Res, 2014, 34(6):484-492.
[23]
Suzuki A, Ito T, Imai E, et al. Retinoids regulate the repairing process of the podocytes in puromycin aminonucleoside-induced nephrotic rats[J]. J Am Soc Nephrol, 2003, 14(4):981-991.
[24]
Romagnani P, Lasagni L, Remuzzi G. Renal progenitors:an evolutionary conserved strategy for kidney regeneration[J]. Nat Rev Nephrol, 2013, 9(3):137-146.
[25]
Ronconi E, Sagrinati C, Angelotti ML, et al. Regeneration of glomerular podocytes by human renal progenitors[J]. J Am Soc Nephrol, 2009, 20(2):322-332.
[26]
Zhang J, Pippin JW, Vaughan MR, et al. Retinoids augment the expression of podocyte proteins by glomerular parietal epithelial cells in experimental glomerular disease[J]. Nephron Exp Nephrol, 2012, 121(1-2):e23-e37.
[27]
Wanner N, Hartleben B, Herbach N, et al. Unraveling the role of podocyte turnover in glomerular aging and injury[J]. J Am Soc Nephrol, 2014, 25(4):707-716.
[28]
Peired A, Angelotti ML, Ronconi E, et al. Proteinuria impairs podocyte regeneration by sequestering retinoic acid[J]. J Am Soc Nephrol, 2013, 24(11):1756-1768.
[29]
Zhang L, Li K, Yan X, et al. MicroRNA-498 inhibition enhances the differentiation of human adipose-derived mesenchymal stem cells into podocyte-like cells[J]. Stem Cells Dev, 2015, 24(24):2841-2852.
[30]
Lazzeri E, Peired AJ, Lasagni L, et al. Retinoids and glomerular regeneration[J]. Semin Nephrol, 2014, 34(4):429-436.
[31]
Ratnam KK, Feng X, Chuang PY, et al. Role of the retinoic acid receptor-alpha in HIV-associated nephropathy[J]. Kidney Int, 2011, 79(6):624-634.
[32]
Zhong Y, Wu Y, Liu R, et al. Roflumilast enhances the renal protective effects of retinoids in an HIV-1 transgenic mouse model of rapidly progressive renal failure[J]. Kidney Int, 2012, 81(9):856-864.
[33]
Khurana S, Chakraborty S, Lam M, et al. Familial focal segmental glomerulosclerosis (FSGS)-linked alpha-actinin 4(ACTN4) protein mutants lose ability to activate transcription by nuclear hormone receptors[J]. J Biol Chem, 2012, 287(15):12027-12035.
[34]
Lu TC, Wang Z, Feng X, et al. Retinoic acid utilizes CREB and USF1 in a transcriptional feed-forward loop in order to stimulate MKP1 expression in human immunodeficiency virus-infected podocytes[J]. Mol Cell Biol, 2008, 28(18):5785-5794.
[35]
McConnell BB, Yang VW. Mammalian Krüppel-like factors in health and diseases[J]. Physiol Rev, 2010, 90(4):1337-1381.
[36]
Mallipattu SK, Liu R, Zheng F, et al. Krüppel-like factor 15(KLF15) is a key regulator of podocyte differentiation[J]. J Biol Chem, 2012, 287(23):19122-19135.
[37]
Ivy JR, Drechsler M, Catterson JH, et al. Klf15 is critical for the development and differentiation of drosophila nephrocytes[J]. PLoS One, 2015, 10(8):e0134620.
[38]
Mallipattu SK, Guo Y, Revelo MP, et al. Krüppel-Like factor 15 mediates glucocorticoid-induced restoration of podocyte differentiation markers[J]. J Am Soc Nephrol, 2017, 28(1):166-184.
[39]
Mallipattu SK, He JC. The podocyte as a direct target for treatment of glomerular disease[J]. Am J Physiol Renal Physiol, 2016, 311(1):F46-F51.
[40]
Hu P, Qin YH, Pei J, et al. Beneficial effect of all-trans retinoic acid (ATRA) on glomerulosclerosis rats via the down-regulation of the expression of alpha-smooth muscle actin:a comparative study between ATRA and benazepril[J]. Exp Mol Pathol, 2010, 89(1):51-57.
[41]
Dechow C, Morath C, Peters J, et al. Effects of all-trans retinoic acid on renin-angiotensin system in rats with experimental nephritis[J]. Am J Physiol Renal Physiol, 2001, 281(15):F909-F919.
[42]
Wagner J, Dechow C, Morath C, et al. Retinoic acid reduces glomerular injury in a rat model of glomerular damage[J]. J Am Soc Nephrol, 2000, 11(8):1479-1487.
[43]
Lei FY, Zhou TB, Qin YH, et al. Potential signal pathway of all-trans retinoic acid for MMP-2 and MMP-9 expression in injury podocyte induced by adriamycin[J]. J Recept Signal Transduct Res, 2014, 34(5):378-385.
[44]
Han SY, So GA, Jee YH, et al. Effect of retinoic acid in experimental diabetic nephropathy[J]. Immunol Cell Biol, 2004, 82(6):568-576.
[45]
Oseto S, Moriyama T, Kawada N, et al. Therapeutic effect of all-trans retinoic acid on rats with anti-GBM antibody glomerulonephritis[J]. Kidney Int, 2003, 64(4):1241-1252.
[46]
Moreno-Manzano V, Mampaso F, Sepulveda-Munoz JC, et al. Retinoids as a potential treatment for experimental puromycin-induced nephrosis[J]. Br J Pharmacol, 2003, 139(4):823-831.
[47]
Moreno-Manzano V, Ishikawa Y, Lucio-Cazana J, et al. Suppression of apoptosis by all-trans-retinoic acid. Dual intervention in the c-Jun n-terminal kinase-AP-1 pathway[J]. J Biol Chem, 1999, 274(29):20251-20258.
[48]
Lo-Coco F, Avvisati G, Vignetti M, et al. Retinoic acid and arsenic trioxide for acute promyelocytic leukemia[J]. N Engl J Med, 2013, 369(2):111-121.
[49]
Elsayed AM, Abdelghany TM, Akool el-S, et al. All-trans retinoic acid potentiates cisplatin-induced kidney injury in rats:impact of retinoic acid signaling pathway[J]. Naunyn Schmiedebergs Arch Pharmacol, 2016, 389(3):327-337.