Neonatal hypoxic ischemic encephalopathy (HIE) is one of the main reasons of death and disability in neonatal, for lack of blood and oxygen during the time of birth. Progranulin (PGRN) as a neurotrophic factor is extensively expressed in the brain can regulate neurite growth and promote neuronal survival. The mutations of PGRN gene may contribute to frontotemporal dementia (FTD). However, the role of PGRN in neonatal HIE remains unclear. We designed this study to investigate the changes of PGRN expression in the brain of newborn mice at different time points after hypoxic -ischemic brain damage (HIBD). Postnatal 7day (P7) mouse pups were induced HIBD model by the method of Rice with some improvement. TTC was used to detect the ischemic lesion volume. The localization of PGRN brain cells was detected by immunofluorescence. We also used Western blotting to measure the expression level of PGRN at different days (1, 3, 7 days) following HIBD. The results showed that we established the HIIBD model successfully. PGRN was primarily expressed in neurons and microglia, but rarely in astrocytes. In addition, PGRN expression in the brain of HIBD mice markedly increased at 1 day and 3 days and was restored at 7 days after HIBD. The results indicated that increased PGRN levels may be involved in the pathological mechanism and neural repair process of HIBD.
| Published in | American Journal of Pediatrics (Volume 5, Issue 3) |
| DOI | 10.11648/j.ajp.20190503.23 |
| Page(s) | 152-158 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2019. Published by Science Publishing Group |
Progranulin, Hypoxia-Ischemic Brain Damage, Neonatal Mice
| [1] | Nguyen A D, Nguyen T A, Lauren Herl M, et al. Progranulin: at the interface of neurodegenerative and metabolic diseases [J]. Trends in Endocrinology & Metabolism Tem, 2013, 24 (12): 597-606. |
| [2] | Bellincanta N B, Aguiar S R, Forcellini P E, et al. Association between progranulin serum levels and dietary intake [J]. PLOS ONE, 2018, 13 (8): e0202149. |
| [3] | Cenik B, Sephton C F, Kutluk Cenik B, et al. Progranulin: A Proteolytically Processed Protein at the Crossroads of Inflammation and Neurodegeneration [J]. Journal of Biological Chemistry, 2012, 287 (39): 32298-32306. |
| [4] | Bateman A, Bennett H P J. The granulin gene family: From cancer to dementia [J]. BioEssays, 2009, 31 (11): 1245-1254. |
| [5] | Asakura R, Matsuwaki T, Shim J H, et al. Involvement of progranulin in the enhancement of hippocampal neurogenesis by voluntary exercise [J]. NeuroReport, 2011, 22 (17): 881-886. |
| [6] | Petkau T L, Leavitt B R. Progranulin in neurodegenerative disease [J]. Trends in Neurosciences, 2014, 37 (7): 388-398. |
| [7] | Van Damme P, Van Hoecke A, Lambrechts D, et al. Progranulin functions as a neurotrophic factor to regulate neurite outgrowth and enhance neuronal survival [J]. The Journal of Cell Biology, 2008, 181 (1): 37-41. |
| [8] | Wong R, Abussaud A, Leung J W, et al. Blockade of the swelling-induced chloride current attenuates the mouse neonatal hypoxic-ischemic brain injury in vivo [J]. Acta Pharmacologica Sinica, 2018, 39 (5): 858-865. |
| [9] | Vittorio F, Valerio V R, Raffaele L R, et al. A Controversial Medicolegal Issue: Timing the Onset of Perinatal Hypoxic-Ischemic Brain Injury [J]. Mediators of Inflammation, 2017, 2017: 1-11. |
| [10] | Zhou W H, Cheng G Q, Shao X M, et al. Selective Head Cooling with Mild Systemic Hypothermia after Neonatal Hypoxic-Ischemic Encephalopathy: A Multicenter Randomized Controlled Trial in China [J]. Journal of Pediatrics, 2010, 157 (3): 367-372000. |
| [11] | P Nar G, Funda, Tüzün, Seda O, et al. Effects of neotrofin on neonatal hypoxic ischemic brain injury [J]. Neuroscience Letters, 2011, 505 (2): 205-210. |
| [12] | Rice J 3. The influence of immaturity on hypoxic-ischemic brain damage in the rat [J]. Ann Neurol, 1981, 9. |
| [13] | Amara L, Donna F, Fernando G. Growth Factors for the Treatment of Ischemic Brain Injury (Growth Factor Treatment) [J]. Brain Sciences, 2015, 5 (2): 165-177. |
| [14] | Khatibi N H, Jadhav V, Charles S, et al. Capsaicin pre-treatment provides neurovascular protection against neonatal hypoxic-ischemic brain injury in rats. [J]. Acta Neurochirurgica Supplement, 2011, 111: 225. |
| [15] | Kaur C, Ling E A. Periventricular white matter damage in the hypoxic neonatal brain: Role of microglial cells [J]. Progress in Neurobiology, 2009, 87 (4): 0-280. |
| [16] | Hralová M, Plaňanská E, Angerová Y, et al, et al. Effects of a single dose of erythropoietin on motor function and cognition after focal brain ischemia in adult rats. [J]. Prague Med Rep, 2014, 115 (1-2): 5-15. |
| [17] | Johan Undén, Carin Sjölund, John-Kalle Länsberg, et al. Post-ischemic continuous infusion of erythropoeitin enhances recovery of lost memory function after global cerebral ischemia in the rat [J]. BMC Neuroscience, 2013, 14 (1): 27. |
| [18] | Liang, Lunan. Protective effects of VEGF treatment on focal cerebral ischemia in rats [J]. Molecular Medicine Reports, 2012, 6 (6): 1315-1318. |
| [19] | Van Velthoven C T J, Sheldon R A, Kavelaars A, et al. Mesenchymal Stem Cell Transplantation Attenuates Brain Injury After Neonatal Stroke [J]. Stroke, 2013, 44 (5): 1426-1432. |
| [20] | Ma Q, Zhang L. C-type natriuretic peptide functions as an innate neuroprotectant in neonatal hypoxic-ischemic brain injury in mouse, via, natriuretic peptide receptor 2 [J]. Experimental Neurology, 2018, 304: 58-66. |
| [21] | Xu, Jie. Progranulin expression in neural stem cells and their differentiated cell lineages: An immunocytochemical study [J]. Molecular Medicine Reports, 2013, 8 (5): 1359-1364. |
| [22] | Baker M, Mackenzie I R, Pickering-Brown S M, et al. Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17 [J]. Nature (London), 2006, 442 (7105): 916-919. |
| [23] | Baker M, Mackenzie I R, Pickering-Brown S M, et al. Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17 [J]. Nature (London), 2006, 442 (7105): 916-919. |
| [24] | Cruts M, Gijselinck I, Julie V D Z, et al. Null mutations in progranulin cause ubiquitin-positive frontotemporal dementia linked to chromosome 17q21 [J]. NATURE, 2006, 442 (7105): 920-924. |
| [25] | Daniel R, Daniels E, He Z, et al. Progranulin (acrogranin/PC cell-derived growth factor/granulin-epithelin precursor) is expressed in the placenta, epidermis, microvasculature, and brain during murine development [J]. Developmental Dynamics, 2003, 227 (4): 593-599. |
| [26] | Jackman K, Kahles T, Lane D, et al. Progranulin Deficiency Promotes Post-Ischemic Blood-Brain Barrier Disruption [J]. Journal of Neuroscience, 2013, 33 (50): 19579-19589. |
| [27] | Egashira Y, Suzuki Y, Azuma Y, et al. The growth factor progranulin attenuates neuronal injury induced by cerebral ischemia-reperfusion through the suppression of neutrophil recruitment [J]. Journal of Neuroinflammation, 2013, 10 (1): 884. |
| [28] | Yin F, Banerjee R, Thomas B, et al. Exaggerated inflammation, impaired host defense, and neuropathology in progranulin-deficient mice [J]. Journal of Experimental Medicine, 2010, 207 (1): 117-128. |
| [29] | Martens L H, Zhang J, Barmada S J, et al. Progranulin deficienc y promotes neuroinflammation and neuron loss following toxin-induced injury [J]. Journal of Clinical Investigation, 2012, 122 (11): 3955-3959. |
| [30] | Xu J, Xilouri M, Bruban J, et al. Extracellular progranulin protects cortical neurons from toxic insults by activating survival signaling [J]. Neurobiology of Aging, 2011, 32 (12): 2326. e5-2326. e16. |
| [31] | Gass J, Lee W C, Cook C, et al. Progranulin regulates neuronal outgrowth independent of Sortilin [J]. Molecular Neurodegeneration, 2012, 7 (1): 33. |
| [32] | De Muynck L, Herdewyn S, Beel S, et al. The neurotrophic properties of progranulin depend on the granulin E domain but do not require sortilin binding [J]. Neurobiology of Aging, 2013, 34 (11): 2541-2547. |
| [33] | Zhu J, Nathan C, Jin W, et al. Conversion of Proepithelin to Epithelins: Roles of SLPI and Elastase in Host Defense and Wound Repair [J]. Cell, 2002, 111 (6): 0-878. |
| [34] | Kessenbrock K, Leopold Fröhlich, Sixt M, et al. Proteinase 3 and neutrophil elastase enhance inflammation in mice by inactivating antiinflammatory progranulin [J]. Journal of Clinical Investigation, 2008, 118 (7): 2438-2447. |
| [35] | Tang W, Lu Y, Tian Q Y, et al. The Growth Factor Progranulin Binds to TNF Receptors and Is Therapeutic Against Inflammatory Arthritis in Mice [J]. Science, 2011, 332 (6028): 478-484. |
| [36] | Hyeon-Sook S, Namjong C, Leonid T, et al. Regulation of Progranulin Expression in Human Microglia and Proteolysis of Progranulin by Matrix Metalloproteinase-12 (MMP-12) [J]. PLoS ONE, 2012, 7 (4): e35115-. |
| [37] | Progranulin expression in the developing and adult murine brain [J]. Journal of Comparative Neurology, 2010, 518 (19): 3931-3947. |
| [38] | Tanaka Y, Matsuwaki T, Yamanouchi K, et al. Increased lysosomal biogenesis in activated microglia and exacerbated neuronal damage after traumatic brain injury in progranulin-deficient mice [J]. Neuroscience, 2013, 250: 8-19. |
| [39] | Naphade S B, Kigerl K A, Jakeman L B, et al. Progranulin expression is upregulated after spinal contusion in mice [J]. Acta Neuropathologica, 2010, 119 (1): 123-133. |
| [40] | Martens L H, Zhang J, Barmada S J, et al. Progranulin deficienc y promotes neuroinflammation and neuron loss following toxin-induced injury [J]. Journal of Clinical Investigation, 2012, 122 (11): 3955-3959. |
| [41] | Beel S, Herdewyn S, Fazal R, et al. Progranulin reduces insoluble TDP-43 levels, slows down axonal degeneration and prolongs survival in mutant TDP-43 mice [J]. Molecular Neurodegeneration, 2018, 13 (1). |
APA Style
Xuxin Ren, Qiaoli Ren, Yilin Liu, Wenyan Zhao, Wei Liu, et al. (2019). Expression of Progranulin in a Mouse Model of Newborn Hypoxic-ischemic Brain Damage. American Journal of Pediatrics, 5(3), 152-158. https://doi.org/10.11648/j.ajp.20190503.23
ACS Style
Xuxin Ren; Qiaoli Ren; Yilin Liu; Wenyan Zhao; Wei Liu, et al. Expression of Progranulin in a Mouse Model of Newborn Hypoxic-ischemic Brain Damage. Am. J. Pediatr. 2019, 5(3), 152-158. doi: 10.11648/j.ajp.20190503.23
AMA Style
Xuxin Ren, Qiaoli Ren, Yilin Liu, Wenyan Zhao, Wei Liu, et al. Expression of Progranulin in a Mouse Model of Newborn Hypoxic-ischemic Brain Damage. Am J Pediatr. 2019;5(3):152-158. doi: 10.11648/j.ajp.20190503.23
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Download@article{10.11648/j.ajp.20190503.23,
author = {Xuxin Ren and Qiaoli Ren and Yilin Liu and Wenyan Zhao and Wei Liu and Xing Tu and Junhua Yang and Jing Liu and Guoying Li and Mengxia Wang and Li Luo},
title = {Expression of Progranulin in a Mouse Model of Newborn Hypoxic-ischemic Brain Damage},
journal = {American Journal of Pediatrics},
volume = {5},
number = {3},
pages = {152-158},
doi = {10.11648/j.ajp.20190503.23},
url = {https://doi.org/10.11648/j.ajp.20190503.23},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajp.20190503.23},
abstract = {Neonatal hypoxic ischemic encephalopathy (HIE) is one of the main reasons of death and disability in neonatal, for lack of blood and oxygen during the time of birth. Progranulin (PGRN) as a neurotrophic factor is extensively expressed in the brain can regulate neurite growth and promote neuronal survival. The mutations of PGRN gene may contribute to frontotemporal dementia (FTD). However, the role of PGRN in neonatal HIE remains unclear. We designed this study to investigate the changes of PGRN expression in the brain of newborn mice at different time points after hypoxic -ischemic brain damage (HIBD). Postnatal 7day (P7) mouse pups were induced HIBD model by the method of Rice with some improvement. TTC was used to detect the ischemic lesion volume. The localization of PGRN brain cells was detected by immunofluorescence. We also used Western blotting to measure the expression level of PGRN at different days (1, 3, 7 days) following HIBD. The results showed that we established the HIIBD model successfully. PGRN was primarily expressed in neurons and microglia, but rarely in astrocytes. In addition, PGRN expression in the brain of HIBD mice markedly increased at 1 day and 3 days and was restored at 7 days after HIBD. The results indicated that increased PGRN levels may be involved in the pathological mechanism and neural repair process of HIBD.},
year = {2019}
}
TY - JOUR T1 - Expression of Progranulin in a Mouse Model of Newborn Hypoxic-ischemic Brain Damage AU - Xuxin Ren AU - Qiaoli Ren AU - Yilin Liu AU - Wenyan Zhao AU - Wei Liu AU - Xing Tu AU - Junhua Yang AU - Jing Liu AU - Guoying Li AU - Mengxia Wang AU - Li Luo Y1 - 2019/08/26 PY - 2019 N1 - https://doi.org/10.11648/j.ajp.20190503.23 DO - 10.11648/j.ajp.20190503.23 T2 - American Journal of Pediatrics JF - American Journal of Pediatrics JO - American Journal of Pediatrics SP - 152 EP - 158 PB - Science Publishing Group SN - 2472-0909 UR - https://doi.org/10.11648/j.ajp.20190503.23 AB - Neonatal hypoxic ischemic encephalopathy (HIE) is one of the main reasons of death and disability in neonatal, for lack of blood and oxygen during the time of birth. Progranulin (PGRN) as a neurotrophic factor is extensively expressed in the brain can regulate neurite growth and promote neuronal survival. The mutations of PGRN gene may contribute to frontotemporal dementia (FTD). However, the role of PGRN in neonatal HIE remains unclear. We designed this study to investigate the changes of PGRN expression in the brain of newborn mice at different time points after hypoxic -ischemic brain damage (HIBD). Postnatal 7day (P7) mouse pups were induced HIBD model by the method of Rice with some improvement. TTC was used to detect the ischemic lesion volume. The localization of PGRN brain cells was detected by immunofluorescence. We also used Western blotting to measure the expression level of PGRN at different days (1, 3, 7 days) following HIBD. The results showed that we established the HIIBD model successfully. PGRN was primarily expressed in neurons and microglia, but rarely in astrocytes. In addition, PGRN expression in the brain of HIBD mice markedly increased at 1 day and 3 days and was restored at 7 days after HIBD. The results indicated that increased PGRN levels may be involved in the pathological mechanism and neural repair process of HIBD. VL - 5 IS - 3 ER -
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