Role of CD36 in central nervous system diseases

Feng, Ming; Zhang, Qiang; Xie, Huimin; Liu, Chang; Zheng, Mengru; Zhang, Shuyu; Zhou, Songlin; Zhao, Jun

doi:10.4103/1673-5374.380821

Cited by 8 publications

(3 citation statements)

References 132 publications

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“…This is in alignment with Scott et al‘s findings, which indicated enhanced neurological recovery in CD36 knockout mice following spinal cord injury [ 48 ]. CD36 is predominantly expressed in microglia and astrocytes within the brain [ 49 ], as confirmed by our experiments, and is known to modulate inflammatory responses and glial scarring [ 44 , 45 , 50 , 51 ]. Furthermore, CD36 expression in vascular endothelial cells has been implicated in fatty acid transport [ 52 ] and the regulation of angiogenesis [ 13 ].…”

Section: Discussionsupporting

confidence: 77%

CD36 deletion prevents white matter injury by modulating microglia polarization through the Traf5-MAPK signal pathway

Hou,

Qu,

Chen

et al. 2024

J Neuroinflammation

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Background White matter injury (WMI) represents a significant etiological factor contributing to neurological impairment subsequent to Traumatic Brain Injury (TBI). CD36 receptors are recognized as pivotal participants in the pathogenesis of neurological disorders, including stroke and spinal cord injury. Furthermore, dynamic fluctuations in the phenotypic polarization of microglial cells have been intimately associated with the regenerative processes within the injured tissue following TBI. Nevertheless, there is a paucity of research addressing the impact of CD36 receptors on WMI and microglial polarization. This investigation aims to elucidate the functional role and mechanistic underpinnings of CD36 in modulating microglial polarization and WMI following TBI. Methods TBI models were induced in murine subjects via controlled cortical impact (CCI). The spatiotemporal patterns of CD36 expression were examined through quantitative polymerase chain reaction (qPCR), Western blot analysis, and immunofluorescence staining. The extent of white matter injury was assessed via transmission electron microscopy, Luxol Fast Blue (LFB) staining, and immunofluorescence staining. Transcriptome sequencing was employed to dissect the molecular mechanisms underlying CD36 down-regulation and its influence on white matter damage. Microglial polarization status was ascertained using qPCR, Western blot analysis, and immunofluorescence staining. In vitro, a Transwell co-culture system was employed to investigate the impact of CD36-dependent microglial polarization on oligodendrocytes subjected to oxygen-glucose deprivation (OGD). Results Western blot and qPCR analyses revealed that CD36 expression reached its zenith at 7 days post-TBI and remained sustained at this level thereafter. Immunofluorescence staining exhibited robust CD36 expression in astrocytes and microglia following TBI. Genetic deletion of CD36 ameliorated TBI-induced white matter injury, as evidenced by a reduced SMI-32/MBP ratio and G-ratio. Transcriptome sequencing unveiled differentially expressed genes enriched in processes linked to microglial activation, regulation of neuroinflammation, and the TNF signaling pathway. Additionally, bioinformatics analysis pinpointed the Traf5-p38 axis as a critical signaling pathway. In vivo and in vitro experiments indicated that inhibition of the CD36-Traf5-MAPK axis curtailed microglial polarization toward the pro-inflammatory phenotype. In a Transwell co-culture system, BV2 cells treated with LPS + IFN-γ exacerbated the damage of post-OGD oligodendrocytes, which could be rectified through CD36 knockdown in BV2 cells. Conclusions This study illuminates that the suppression of CD36 mitigates WMI by constraining microglial polarization towards the pro-inflammatory phenotype through the down-regulation of the Traf5-MAPK signaling pathway. Our findings present a potential therapeutic strategy for averting neuroinflammatory responses and ensuing WMI damage resulting from TBI. Graphical Abstract

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Section: Discussionsupporting

confidence: 77%

CD36 deletion prevents white matter injury by modulating microglia polarization through the Traf5-MAPK signal pathway

Hou,

Qu,

Chen

et al. 2024

J Neuroinflammation

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“…The emphasis is on the fatty acid transport function of CD36 within the cardiovascular system, as it has been most extensively studied in this context. We do not discuss the role of CD36 in other tissues but refer the reader to more comprehensive reviews on CD36 in platelet biology (8), in atherosclerosis (9,10), in intestine (11), in liver and nonalcoholic fatty liver disease (12,13), in the central nervous system (14), and in cancer (15)(16)(17)(18)(19).…”

Section: Clinical Highlightsmentioning

confidence: 99%

CD36 as a gatekeeper of myocardial lipid metabolism and therapeutic target for metabolic disease

Glatz,

Heather,

Luiken

2024

Physiological Reviews

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The multifunctional membrane glycoprotein CD36 is expressed in different types of cells and plays a key regulatory role in cellular lipid metabolism. CD36 facilitates the cellular uptake of long-chain fatty acids, mediates lipid signaling, and regulates storage and oxidation of lipids in various tissues with active lipid metabolism. CD36 deficiency leads to marked impairments in peripheral lipid metabolism, which consequently impacts on the cellular utilization of multiple different fuels, due to the integrated nature of metabolism. The functional presence of CD36 at the plasma membrane is regulated by its reversible subcellular recycling from and to endosomes, and is under the control of mechanical, hormonal and nutritional factors. Aberrations in this dynamic role of CD36 are causally associated with various metabolic diseases, in particular insulin resistance, diabetic cardiomyopathy, and cardiac hypertrophy. Recent research in cardiac muscle has disclosed the endosomal proton pump v-ATPase as a key enzyme regulating subcellular CD36 recycling and being the site of interaction between various substrates to determine cellular substrate preference. In addition, evidence is accumulating that interventions targeting CD36 directly or modulating its subcellular recycling are effective for the treatment of metabolic diseases. In conclusion, subcellular CD36 localization is the major adaptive regulator of cellular uptake and metabolism of long-chain fatty acids, and appears a suitable target for metabolic modulation therapy to mend failing hearts.

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“…Numerous life-threatening diseases demand the advancement of efficient, reliable, and noninvasive methods for early diagnosis and the precise identification of key biomarkers such as those embodied within small extracellular vesicles (sEVs) [1][2][3]. Surface-enhanced Raman spectroscopy (SERS) has emerged as a powerful technique for biosensing applications, leveraging the plasmonic resonance of metallic nanostructures such as gold and silver.…”

Section: Introductionmentioning

confidence: 99%

Controlling the Nucleation and Growth of Salt from Bodily Fluid for Enhanced Biosensing Applications

Srivastava,

Terai,

Liu

et al. 2023

Biosensors

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Surface-enhanced Raman spectroscopy (SERS) represents a transformative tool in medical diagnostics, particularly for the early detection of key biomarkers such as small extracellular vesicles (sEVs). Its unparalleled sensitivity and compatibility with intricate biological samples make it an ideal candidate for revolutionizing noninvasive diagnostic methods. However, a significant challenge that mars its efficacy is the throughput limitation, primarily anchored in the prerequisite of hotspot and sEV colocalization within a minuscule range. This paper delves deep into this issue, introducing a never-attempted-before approach which harnesses the principles of crystallization—nucleation and growth. By synergistically coupling lasers with plasmonic resonances, we navigate the challenges associated with the analyte droplet drying method and the notorious coffee ring effect. Our method, rooted in a profound understanding of crystallization’s materials science, exhibits the potential to significantly increase the areal density of accessible plasmonic hotspots and efficiently guide exosomes to defined regions. In doing so, we not only overcome the throughput challenge but also promise a paradigm shift in the arena of minimally invasive biosensing, ushering in advanced diagnostic capabilities for life-threatening diseases.

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Role of CD36 in central nervous system diseases

Cited by 8 publications

References 132 publications

CD36 deletion prevents white matter injury by modulating microglia polarization through the Traf5-MAPK signal pathway

CD36 deletion prevents white matter injury by modulating microglia polarization through the Traf5-MAPK signal pathway

CD36 as a gatekeeper of myocardial lipid metabolism and therapeutic target for metabolic disease

Controlling the Nucleation and Growth of Salt from Bodily Fluid for Enhanced Biosensing Applications

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