Mohammed Abdul Muneer, PhD
Associate Professor
Research Interests: Neuroinflammation and neurodegeneration in traumatic brain injury (TBI), blood-brain barrier (BBB) disruption and transmigration of immune cells in TBI, neurovascular dysfunction in alcohol use disorder (AUD), gene and peptide-based therapeutic strategies for TBI and AUD, and survival surgeries and rodent behavioral assessments.Research Advancements: neuronal and neurovascular dysfunction in TBI and chronic alcohol exposure using advanced molecular biology tools, high-resolution microscopy and imaging, cerebral blood flow analysis, optogenetics, and electrophysiology. The research integrates gene and peptide therapies to promote neurovascular repair and cognitive recovery. Using in vivo and in vitro injury models, the lab applies viral gene transfer, CRISPR/Cas9 editing, conditional knockouts, pharmacological interventions, survival surgeries, and behavioral assays.
Research Area: molecular and cellular mechanisms underlying axonal regeneration, neuronal repair, and survival following traumatic brain injury (TBI), aiming to develop effective therapeutic strategies for neurological recovery. His research explores signaling pathways that limit neuronal regeneration in central nervous system (CNS) injury. Additionally, Dr. Muneer investigates blood-brain barrier disruption and its role in neurovascular inflammation and neurological disorders such as stroke linked to alcohol use disorder.
Lab: The Laboratory of CNS Injury and Molecular Therapy
Website: https://bme.fiu.edu/people/faculty-instructors/mohammed-abdul-muneer-phd/
Biography
Dr. Mohammed Abdul Muneer is an Associate Professor with a Ph.D. in Molecular Biology and extensive experience in translational neuroscience, focusing on neuroimmunology of traumatic brain injury (TBI), and alcohol-induced neurovascular dysfunction. His research explores the cellular and molecular mechanisms of neuroinflammation, neurodegeneration, and blood-brain barrier disruption in TBI and alcohol use disorder. Dr. Muneer’s research has been published in more than 50 high-impact peer-reviewed journals, including The Journal of Neuroscience, Molecular Neurodegeneration, Brain Behavior and Immunity, eNeuro etc. His work is supported by multiple extramural grants, notably: an NIH R01 grant ($2.21M; awarded in 2024), an NIH R21 grant ($470,000; awarded in 2023), and three grants from the New Jersey Department of Health (in 2016, 2018, and 2019). He has mentored several postdoctoral fellows, graduate and undergraduate students, and trainees at various academic levels, and advised seven master’s theses. Dr. Muneer serves on grant review panels for the NIH, Department of Defense (DoD), and national funding agencies of Israel and Poland. He is an active peer reviewer for more than 20 scientific journals and has evaluated Ph.D. theses for various universities. In addition, he holds roles as a Research Council Member and Advisory Board Member at multiple academic institutions, and he has served as an IACUC committee member for 9 years. has served as a IACUC committee member for 9 years. He is also an Editorial Board member in different journals such as the Journal of Spinal Cord Medicine, Antioxidants, Frontiers in Genetics, Trauma Cases and Reviews, JSM Brain Science; and Topical Advisory Panel in ‘Antioxidants’.
Lab Website: https://pmamuneer.wixsite.com/muneer-lab
Research
Dr. Muneer’s current research focuses on developing peptide and gene therapeutic strategies for traumatic brain injury, and alcohol-induced brain damage. For more details, visit https://pmamuneer.wixsite.com/muneer-lab. His current projects are
1) Peptide therapeutic study for blocking the formation of neutrophil extracellular traps (NET) in TBI: Leukocyte adhesion is key to immune cell migration into injured tissue. In TBI, neutrophil activation may lead to the formation of neutrophil extracellular traps (NETs), but their role in thrombosis remains unclear. This project explores whether inhibiting NET formation via PAD4 antagonistic peptide (PAP) can reduce NET-induced thrombosis, enhance neovascularization, and improve recovery after TBI.
2) ICAM-1 antagonistic peptide for TBI treatment: The lab investigates the role of intercellular adhesion molecule-1 (ICAM-1) in mediating leukocyte transmigration, vascular permeability, and neuroinflammation after TBI. ICAM-1 interacts with LFA-1 and Mac-1 on immune cells to facilitate their migration into the injured brain, triggering inflammatory cascades via paxillin and focal adhesion pathways. These mechanisms contribute to neurodegeneration and cognitive deficits. The lab is exploring whether genetic or pharmacological inhibition of ICAM-1 can reduce neuroinflammation and improve functional outcomes following TBI.
3) Role of piRNA in the pathogenesis of mild TBI: PIWI-interacting RNAs (piRNAs), a class of small non-coding RNAs, are emerging as regulators of gene expression in the brain, particularly under pathological conditions. In traumatic brain injury (TBI), dysregulated piRNA expression may contribute to neuroinflammation, neuronal death, and blood-brain barrier disruption by targeting key disease-associated genes. Therapeutically modulating piRNA pathways could offer a novel strategy to silence pathogenic gene expression and promote neuroprotection and recovery after TBI.
4) Therapeutic strategy for neurovascular remodeling in alcohol use disorder: Peptide-based therapies are a promising strategy for CNS injury and alcohol-induced damage due to their low toxicity and strong efficacy. This project uses a synthetic peptide (NP, EMD Millipore) linked to a TAT sequence to activate Nrf2 by disrupting its interaction with Keap1, thereby enhancing antioxidant gene expression through ARE activation.
List of Publications
1. Muneer PMA*, Poovanthodi Y, Saikia BB, Kassim Z, Alikunju S (2025). Nrf2 activator peptide protects the brain from cerebral vascular dysfunction in alcohol ingestion. Journal of Clinical Investigation Insights (In revision). *Corresponding author.
2. Saikia BB, Bhowmick S, Malat A, Preetha Rani MR, Thaha A, Muneer PMA* (2024). ICAM-1 deletion using CRISPR/Cas9 protects the brain from traumatic brain injury-induced inflammatory leukocyte adhesion and transmigration cascades by attenuating the paxillin/FAK-dependent Rho GTPase pathway. Journal of Neuroscience, e1742232024; DOI: https://doi.org/10.1523/JNEUROSCI.1742-23.2024. This article is selected for JNeurosci’s highlight “This Week in the Journal” and one of our Figure images is selected for the Journal’s cover image. *Corresponding author.
3. Bhowmick S, Preetha Rani MR, Singh S, Muneer PMA* (2023). Discovery of novel microRNAs and their pathogenic responsive target genes in mild traumatic brain injury. Experimental Brain Research, 241(8): p. 2107-2123. *Corresponding author.
4. Muneer PMA*, Saikia BB, Bhowmick S (2022). Synergistic effect of mild traumatic brain injury and alcohol exacerbates neuroinflammation, amyloidogenesis, tau pathology, neurodegeneration, and blood-brain barrier alterations: impact on psychological stress. Experimental Neurology; 358:114222. doi: 10.1016/j.expneurol.2022.114222. *Corresponding author.
5. Bhowmick S, Alikunju S, Muneer PMA* (2022). NADPH oxidase-induced activation of transforming growth factor-beta-1 causes neuropathy by suppressing antioxidant signaling pathways in alcohol use disorder. Neuropharmacology; DOI: 10.1016/j.neuropharm.2022.109136. *Corresponding author.
6. Bhowmick S, Malat A, Caruso D, Ponery N, D’Mello V, Finn C, Muneer PMA* (2021). Intercellular adhesion molecule-1-induced post-traumatic brain injury neuropathology in the prefrontal cortex and hippocampus leads to sensorimotor function deficits and psychological stress. eNeuro, ENEURO.0242-21.2021. *Corresponding author.
7. Bhowmick S, D’Mello V, Caruso D, Muneer PMA* (2019). Traumatic brain injury-induced downregulation of Nrf2 activates inflammatory response and apoptotic cell death. Journal of Molecular Medicine (Berl). 2019 Dec;97(12):1627-1641. *Corresponding author.
8. Bhowmick S, D’Mello V, Wallerstein A, Caruso D, Muneer PMA* (2019). Impairment of endothelial cell-pericyte cross-talk leads to blood-brain barrier damage following traumatic brain injury. Experimental Neurology, 317: 260-270. *Corresponding author.
9. Bhowmick S, D’Mello V, Muneer PMA* (2018). Synergistic Inhibition of ERK1/2 and JNK, Not p38, Phosphorylation Ameliorates Neuronal Damages after Traumatic Brain Injury. Molecular Neurobiology, DOI: 10.1007/s12035-018-1132-7. *Corresponding author.
10. Bhowmick S, D’Mello V, Muneer PMA* (2017). Neurodegeneration and sensorimotor deficits in the mouse model of traumatic brain injury. Brain Sciences, Jan 6; 8(1). Pii:E11. doi 10.3390/brainsci8010011. *Corresponding author.
11. Patel RK, Prasad N, Kuwar R, Haldar D, Muneer PMA* (2017). Transforming growth factor-beta 1 signaling regulates neuroinflammation and apoptosis in mild traumatic brain injury. Brain, Behavior, and Immunity; 64:244-258. doi: 10.1016/j.bbi.2017.04.012. *Corresponding author
12. Muneer PMA*, Bhowmick S, Briski N (2017). Angiotensin II causes neuronal damage in stretch injured neurons: protective effects of losartan, an angiotensin II type 1 receptor antagonist. Molecular Neurobiology, doi: 10.1007/s12035-017-0812-z. *Corresponding author.
13. Muneer PMA, Alikunju S, Schuetz H, Szlachetka AM, Ma X, and Haorah J* (2017). Impairment of Thiamine Transport at the GUT-BBB-axis Contributes to Wernicke Encephalopathy. Molecular Neurobiology; doi: 10.1007/s12035-017-0811-0.
14. Muneer PMA, Alikunju S, Mishra V, Szlachetka AM, and Haorah J* (2017). Activation of NLRP3 inflammasome by cholesterol crystals in alcohol intake induces atherosclerotic lesions. Brain, behavior and Immunity, 62:291-305. doi: 10.1016/j.bbi.2017.02.014.
15. Muneer PMA*, Conte AA, Haldar D, Long M, Santhakumar V, Overall CM, Pfister BJ (2016). Traumatic brain injury-induced matrix metalloproteinase-2 cleaves CXCL12α (stromal cell derived factor 1α) and causes neurodegeneration. Brain, Behavior and Immunity, 59:190-199. http://dx.doi.org/10.1016/j.bbi.2016.09.002. *Corresponding author.
16. Muneer PMA*, Long M, Conte AA, Santhakumar V, Pfister BJ (2015). High Ca2+ influx during traumatic brain injury leads to caspase-1 dependent neuroinflammation and cell death. Molecular Neurobiology. DOI: 10.1007/s12035-016-9949-4. *Corresponding author.
17. Muneer PMA*, Pfister BJ, Haorah J, Chandra N (2015). Role of matrix metalloproteinases in the pathogenesis of traumatic brain injury and other neurological diseases. Molecular Neurobiology, 53(9):6106-6123. DOI: 10.1007/s12035-015-9520-8. Review manuscript. *Corresponding author.
18. Muneer PMA*, Chandra N, Haorah J (2014). Interactions of oxidative stress and neurovascular inflammation in the pathogenesis of secondary mild traumatic brain injury. Molecular Neurobiology, 51(3):966-979. Review manuscript. *Corresponding author.
19. Otake Y, Park D, Muneer PMA, Li H, Xu B, Sharma K, Smith GM, Selzer ME and Li S (2014). The effect of systemic PTEN antagonist peptides on axon growth and functional recovery after spinal cord injury. Biomaterials, 35(16):4610-4626.
20. Muneer PMA, Schueltz H, Wang F, Skotak M, Jones J, Gorantla S, Zimmerman MC, Chandra N and Haorah J (2013). Induction of Oxidative and Nitrosative damage leads to Cerebrovascular Inflammation in Animal Model of Mild Traumatic Brain Injury Induced by Primary Blast. Free Radical Biology and Medicine; 60(2013)282–291.
21. Muneer PMA, Alikunju S, Szlachetka AM, and Haorah J (2012). The Mechanisms of Cerebral Vascular Dysfunction and Neuroinflammation by MMP-mediated Degradation of VEGFR-2 in Alcohol Ingestion. Arteriosclerosis, Thrombosis and Vascular Biology; 32: 1167-1177.
22. Alikunju S*, Muneer PMA*, Zhang Y, Szlachetka AM, and Haorah J (2011). The inflammatory footprints of alcohol-induced oxidative damage in neurovascular components. Brain Behavior and Immunity, 25 Suppl 1:S129-36. *Joint-first authors.
23. Muneer PMA*, Alikunju S*, Szlachetka AM, and Haorah J (2011). Methamphetamine Inhibits Glucose Uptake by Human Astrocytes and Neurons: Stabilization by Acetyl-L-carnitine. PLoS ONE, 6(4): e19258. *Joint-first authors.
24. Muneer PMA, Alikunju S, Szlachetka AM, Murrin CL, and Haorah J (2011). Impairment of brain endothelial glucose transporter by methamphetamine causes blood-brain barrier dysfunction. Molecular Neurodegeneration, 6:23. Highly accessed.
25. Muneer PMA, Alikunju S, Szlachetka AM, and Haorah J (2011). Inhibitory effects of alcohol on glucose transport across the blood–brain barrier leads to neurodegeneration: preventive role of acetyl-L-carnitine. Psychopharmacology. 214(3): 707-718.