A review on the relationship between mitochondrial dysfunction and white matter injury in preterm infants
LI Wen-Xing, QU Yi, MU De-Zhi, TANG Jun
Department of Pediatrics, West China Second Hospital, Sichuan University/Key Laboratory of Birth Defects and Related Diseases of Women and Children(Sichuan University), Ministry of Education, Chengdu 610041, China
Abstract White matter injury in preterm infants has a complex etiology and can lead to long-term neurocognitive and behavioral deficits, but there are still no specific treatment Methods for this disease at present. More and more studies have shown that mitochondrial dysfunction plays an important role in the pathogenesis of white matter injury in preterm infants and might be a common subcellular mechanism of white matter developmental disorder, which involves oxidative stress, reduced ATP synthesis, and disequilibrium of calcium homeostasis. This article reviews the role of mitochondria in brain development and the mechanism of mitochondrial dysfunction, with a hope to perform early intervention of white matter injury in preterm infants by protecting mitochondrial function, so as to provide a reference for improving the neurodevelopmental outcome of preterm infants who survive.
LI Wen-Xing,QU Yi,MU De-Zhi et al. A review on the relationship between mitochondrial dysfunction and white matter injury in preterm infants[J]. CJCP, 2018, 20(10): 864-869.
LI Wen-Xing,QU Yi,MU De-Zhi et al. A review on the relationship between mitochondrial dysfunction and white matter injury in preterm infants[J]. CJCP, 2018, 20(10): 864-869.
Back SA. White matter injury in the preterm infant:pathology and mechanisms[J]. Acta Neuropathol, 2017, 134(3):331-349.
[2]
Cree BAC, Niu J, Hoi KK, et al. Clemastine rescues myelination defects and promotes functional recovery in hypoxic brain injury[J]. Brain, 2018, 141(1):85-98.
[3]
Bonora M, De Marchi E, Patergnani S, et al. Tumor necrosis factor-α impairs oligodendroglial differentiation through a mitochondria-dependent process[J]. Cell Death Differ, 2014, 21(8):1198-1208.
[4]
Back SA, Luo NL, Borenstein NS, et al. Late oligodendrocyte progenitors coincide with the developmental window of vulnerability for human perinatal white matter injury[J]. J Neurosci, 2001, 21(4):1302-1312.
[5]
Kim HJ, Shaker MR, Cho B, et al. Dynamin-related protein 1 controls the migration and neuronal differentiation of subventricular zone-derived neural progenitor cells[J]. Sci Rep, 2015, 5:15962.
[6]
Erecinska M, Cherian S, Silver IA. Energy metabolism in mammalian brain during development[J]. Prog Neurobiol, 2004, 73(6):397-445.
[7]
Kostić MM, Zivković RV, Rapoport SM. Maturation-dependent changes of the rat reticulocyte energy metabolism and hormonal responsiveness[J]. Biomed Biochim Acta, 1990, 49(2-3):S178-S182.
[8]
Harris JJ, Attwell D. The energetics of CNS white matter[J]. J Neurosci, 2012, 32(1):356-371.
[9]
Bizzozero OA, Sanchez P, Tetzloff SU. Effect of ATP depletion on the palmitoylation of myelin proteolipid protein in young and adult rats[J]. J Neurochem, 1999, 72(6):2610-2616.
[10]
Rinholm JE, Vervaeke K, Tadross MR, et al. Movement and structure of mitochondria in oligodendrocytes and their myelin sheaths[J]. Glia, 2016, 64(5):810-825.
[11]
Leoni V, Caccia C. The impairment of cholesterol metabolism in Huntington disease[J]. Biochim Biophys Acta, 2015, 1851(8):1095-1105.
[12]
Voccoli V, Tonazzini I, Signore G, et al. Role of extracellular calcium and mitochondrial oxygen species in psychosineinduced oligodendrocyte cell death[J]. Cell Death Dis, 2014, 5:e1529.
[13]
Yagi M, Uchiumi T, Sagata N, et al. Neural-specific deletion of mitochondrial p32/C1qbp leads to leukoencephalopathy due to undifferentiated oligodendrocyte and axon degeneration[J]. Sci Rep, 2017, 7(1):15131.
[14]
Area-Gomez E, de Groof A, Bonilla E, et al. A key role for MAM in mediating mitochondrial dysfunction in Alzheimer disease[J]. Cell Death Dis, 2018, 9(3):335.
[15]
Bannwarth S, Ait-El-Mkadem S, Chaussenot A, et al. A mitochondrial origin for frontotemporal dementia and amyotrophic lateral sclerosis through CHCHD10 involvement[J]. Brain, 2014, 137(Pt 8):2329-2345.
[16]
Toldo I, Nosadini M, Boscardin C, et al. Neonatal mitochondrial leukoencephalopathy with brain and spinal involvement and high lactate:expanding the phenotype of ISCA2 gene mutations[J]. Metab Brain Dis, 2018, 33(3):805-812.
[17]
Vanopdenbosch L, Dubois B, D'Hooghe MB, et al. Mitochondrial mutations of Leber's hereditary optic neuropathy:a risk factor for multiple sclerosis[J]. J Neurol, 2000, 247(7):535-543.
[18]
Rezaee AR, Azadi A, Houshmand M, et al. Mitochondrial and nuclear genes as the cause of complex I deficiency[J]. Genet Mol Res, 2013, 12(3):3551-3554.
[19]
Yagi M, Uchiumi T, Sagata N, et al. Neural-specific deletion of mitochondrial p32/C1qbp leads to leukoencephalopathy due to undifferentiated oligodendrocyte and axon degeneration[J]. Sci Rep, 2017, 7(1):15131.
[20]
Graham EM, Burd I, Everett AD, et al. Blood biomarkers for evaluation of perinatal encephalopathy[J]. Front Pharmacol, 2016, 7:196.
[21]
Inder T, Mocatta T, Darlow B, et al. Elevated free radical products in the cerebrospinal fluid of VLBW infants with cerebral white matter injury[J]. Pediatr Res, 2002, 52(2):213-218.
[22]
González-Fernández E, Sánchez-Gómez MV, Pérez-Samartín A, et al. A3 Adenosine receptors mediate oligodendrocyte death and ischemic damage to optic nerve[J]. Glia, 2014, 62(2):199-216.
[23]
Kim JY, Lee EY, Sohn HJ, et al. Differential expression of αB-crystallin causes maturation-dependent susceptibility of oligodendrocytes to oxidative stress[J]. BMB Rep, 2013, 46(10):501-506.
[24]
Miyamoto N, Maki T, Pham LD, et al. Oxidative stress interferes with white matter renewal after prolonged cerebral hypoperfusion in mice[J]. Stroke, 2013, 44(12):3516-3521.
[25]
Takase H, Liang AC, Miyamoto N, et al. Protective effects of a radical scavenger edaravone on oligodendrocyte precursor cells against oxidative stress[J]. Neurosci Lett, 2018, 668:120-125.
[26]
O'Hare Doig RL, Bartlett CA, Maghzal GJ, et al. Reactive species and oxidative stress in optic nerve vulnerable to secondary degeneration[J]. Exp Neurol, 2014, 261:136-146.
[27]
Mendivil-Perez M, Soto-Mercado V, Guerra-Librero A, et al. Melatonin enhances neural stem cell differentiation and engraftment by increasing mitochondrial function[J]. J Pineal Res, 2017, 63:e12415.
[28]
Nuñez A, Benavente I, Blanco D, et al. Oxidative stress in perinatal asphyxia and hypoxic-ischaemic encephalopathy[J]. An Pediatr (Barc), 2018, 88(4):228.e1-228.e9.
[29]
Lee GH, Lee HY, Li B, et al. Bax Inhibitor-1-mediated inhibition of mitochondrial Ca2+ intake regulates mitochondrial permeability transition pore opening and cell death[J]. Sci Rep, 2014, 4:5194.
[30]
Milbourn HR, Toomey LM, Gavriel N, et al. Limiting oxidative stress following neurotrauma with a combination of ion channel inhibitors[J]. Discov Med, 2017, 23(129):361-369.
[31]
Schoenfeld R, Wong A, Silva J, et al. Oligodendroglial differentiation induces mitochondrial genes and inhibition of mitochondrial function represses oligodendroglial differentiation[J]. Mitochondrion, 2010, 10(2):143-150.
[32]
Wang Y, Zhang Y, He J, et al. Hyperforin promotes mitochondrial function and development of oligodendrocytes[J]. J Neurochem, 2011, 119(3):555-568.
[33]
Heidker RM, Emerson MR, Levine SM. Metabolic pathways as possible therapeutic targets for progressive multiple sclerosis[J]. Neural Regen Res, 2017, 12(8):1262-1267.
Juliano C, Sosunov S, Niatsetskaya Z, et al. Mild intermittent hypoxemia in neonatal mice causes permanent neurofunctional deficit and white matter hypomyelination[J]. Exp Neurol, 2015, 264:33-42.
[36]
Douglas RM, Ryu J, Kanaan A, et al. Neuronal death during combined intermittent hypoxia/hypercapnia is due to mitochondrial dysfunction[J]. Am J Physiol Cell Physiol, 2010, 298(6):C1594-C1602.
[37]
Rone MB, Cui QL, Fang J, et al. Oligodendrogliopathy in multiple sclerosis:low glycolytic metabolic rate promotes oligodendrocyte survival[J]. J Neurosci, 2016, 36(17):4698-4707.
[38]
Su X, Yuan H, Cui H, et al. Effect of T helper cell 1/T helper cell 2 balance and nuclear factor-κB on white matter injury in premature neonates[J]. Mol Med Rep, 2018, 17(4):5552-5556.
[39]
Elovitz MA, Mrinalini C, Sammel MD. Elucidating the early signal transduction pathways leading to fetal brain injury in preterm birth[J]. Pediatr Res, 2006, 59(1):50-55.
[40]
Bonora M, De Marchi E, Patergnani S, et al. Tumor necrosis factor-α impairs oligodendroglial differentiation through a mitochondria-dependent process[J]. Cell Death Differ, 2014, 21(8):1198-1208.
[41]
Chamberlain KA, Chapey KS, Nanescu SE, et al. Creatine enhances mitochondrial-mediated oligodendrocyte survival after demyelinating injury[J]. J Neurosci, 2017, 37(6):1479-1492.
Cavallucci V, Bisicchia E, Cencioni MT, et al. Acute focal brain damage alters mitochondrial dynamics and autophagy in axotomized neurons[J]. Cell Death Dis, 2014, 5:e1545.
[44]
Kim H, Lee JY, Park KJ, et al. A mitochondrial division inhibitor, Mdivi-1, inhibits mitochondrial fragmentation and attenuates kainic acid-induced hippocampal cell death[J]. BMC Neurosci, 2016, 17(1):33.
[45]
Yu S, Zheng S, Leng J, et al. Inhibition of mitochondrial calcium uniporter protects neurocytes from ischemia/reperfusion injury via the inhibition of excessive mitophagy[J]. Neurosci Lett, 2016, 628:24-29.