Seyed Mohammad Piri1,2, Zahra Ghodsi1, Sina Shool1,3, Ali Anjomshoa2, Amir Azarhomayoun1, Ehsan Jangholi4, Hamid Reza Dehghan5, Rasha Atlasi6,7, Alexander R Vaccaro8, Vafa Rahimi-Movaghar9,10,11. 1. Sina Trauma and Surgery Research Center, Sina Hospital, Tehran University of Medical Sciences, Hassan-Abad Square, Imam Khomeini Ave, 11365-3876, Tehran, Iran. 2. Student's Scientific Research Center (SSRC), Tehran University of Medical Sciences, Tehran, Iran. 3. Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. 4. Department of Neurosurgery, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran. 5. Research Center for Health Technology Assessment and Medical Informatics, School of Public Health, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. 6. Evidence Based Practice Research Center, Endocrinology and Metabolism Research Institute, Tehran University of Medical Sciences, Tehran, Iran. 7. Department of Medical Library and Information Science, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran. 8. Department of Orthopedics and Neurosurgery, Thomas Jefferson University and the Rothman Institute, Philadelphia, PA, USA. 9. Sina Trauma and Surgery Research Center, Sina Hospital, Tehran University of Medical Sciences, Hassan-Abad Square, Imam Khomeini Ave, 11365-3876, Tehran, Iran. v_rahimi@sina.tums.ac.ir. 10. Department of Neurosurgery, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran. v_rahimi@sina.tums.ac.ir. 11. Brain and Spinal Cord Injury Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. v_rahimi@sina.tums.ac.ir.
Abstract
PURPOSE: Macrophages play an important role in mediating damage after Spinal cord injury (SCI) by secreting macrophage migration inhibitory factor (MMIF) as a secondary injury mediator. We aimed to systematically review the role of MMIF as a therapeutic target after traumatic SCI. METHODS: Our systematic review has been performed according to the PRISMA 2009 Checklist. A systematic search in the scientific databases was carried out for studies published before 20 February 2019 from major databases. Two researchers independently screened titles. The risk of bias of eligible articles was assessed, and data were extracted. Finally, we systematically analyzed and interpreted related data. RESULTS: 785 papers were selected for the title and abstract screening. 12 papers were included for data extraction. Eight animal studies were of high quality and the remaining two were of medium quality. One of the two human studies was of poor quality and the other was of fair quality. MMIF as a pro-inflammatory mediator can cause increased susceptibility to glutamate-related neurotoxicity, increased nitrite production, increased ERK activation, and increased COX2/PGE2 signaling pathway activation and subsequent stimulation of CCL5-related chemotaxis. Two human studies and six animal studies demonstrated that MMIF level increases after SCI. MMIF inhibition might be a potential therapeutic target in SCI by multiple different mechanisms (6/12 studies). CONCLUSION: Most animal studies demonstrate significant neurologic improvement after administration of MMIF inhibitors, but these inhibitors have not been studied in humans yet. Further clinical trials are need to further understand MMIF inhibitor utility in acute or chronic SCI. LEVEL OF EVIDENCE I: Diagnostic: individual cross-sectional studies with the consistently applied reference standard and blinding.
PURPOSE: Macrophages play an important role in mediating damage after Spinal cord injury (SCI) by secreting macrophage migration inhibitory factor (MMIF) as a secondary injury mediator. We aimed to systematically review the role of MMIF as a therapeutic target after traumatic SCI. METHODS: Our systematic review has been performed according to the PRISMA 2009 Checklist. A systematic search in the scientific databases was carried out for studies published before 20 February 2019 from major databases. Two researchers independently screened titles. The risk of bias of eligible articles was assessed, and data were extracted. Finally, we systematically analyzed and interpreted related data. RESULTS: 785 papers were selected for the title and abstract screening. 12 papers were included for data extraction. Eight animal studies were of high quality and the remaining two were of medium quality. One of the two human studies was of poor quality and the other was of fair quality. MMIF as a pro-inflammatory mediator can cause increased susceptibility to glutamate-related neurotoxicity, increased nitrite production, increased ERK activation, and increased COX2/PGE2 signaling pathway activation and subsequent stimulation of CCL5-related chemotaxis. Two human studies and six animal studies demonstrated that MMIF level increases after SCI. MMIF inhibition might be a potential therapeutic target in SCI by multiple different mechanisms (6/12 studies). CONCLUSION: Most animal studies demonstrate significant neurologic improvement after administration of MMIF inhibitors, but these inhibitors have not been studied in humans yet. Further clinical trials are need to further understand MMIF inhibitor utility in acute or chronic SCI. LEVEL OF EVIDENCE I: Diagnostic: individual cross-sectional studies with the consistently applied reference standard and blinding.
Authors: Jennifer C Fleming; Michael D Norenberg; David A Ramsay; Gregory A Dekaban; Alexander E Marcillo; Alvaro D Saenz; Melissa Pasquale-Styles; W Dalton Dietrich; Lynne C Weaver Journal: Brain Date: 2006-10-28 Impact factor: 13.501
Authors: Adam Stein; Arti Panjwani; Cristina Sison; Lisa Rosen; Radhika Chugh; Christine Metz; Matthew Bank; Ona Bloom Journal: Arch Phys Med Rehabil Date: 2013-04-22 Impact factor: 3.966