Astrocyte-derived fatty acid-binding protein 7 protects blood-brain barrier integrity through a caveolin-1/MMP signaling pathway following traumatic brain injury

Qin, Rui; Ni, Haibo; Lin, Xiaohui; Zhu, Xiaojue; Li, Di; Liu, Huixiang; Chen, Gang

doi:10.1016/j.expneurol.2019.113044

Cited by 43 publications

(28 citation statements)

References 47 publications

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“…The modified Garcia test and Beam Balance test (Garcia et al, 1995 ; Rui et al, 2019 ) were used to evaluate the neurological deficits of animals after TBI and drug treatment. The neurological functions of each group were double-blindly evaluated at 72 h after TBI.…”

Section: Methodsmentioning

confidence: 99%

HIF-1α Mediates TRAIL-Induced Neuronal Apoptosis via Regulating DcR1 Expression Following Traumatic Brain Injury

Fang

Wang

et al. 2020

Front. Cell. Neurosci.

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Background: Neuronal apoptosis involved in secondary injury following traumatic brain injury (TBI) significantly contributes to the poor outcomes of patients with TBI. The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can selectively induce apoptosis of tumor cells. Hypoxia factor (HIF) 1α is a controversial factor that mediates the neuronal apoptotic pathway. Herein, we hypothesize that HIF-1α may mediate the TRAIL-induced neuronal apoptosis after TBI. Methods: We used Western blots and immunofluorescence to study the expression and cell localization of TRAIL and death receptor 5 (DR5) after TBI in rats. Soluble DR5 (sDR5) administration was used to block the TRAIL-induced neuronal death and neural deficits. HIF-1α inhibitor 2ME and agonist DMOG were used to study the role of HIF-1α in TRAILinduced neuronal death. Meanwhile, HIF-1α siRNA was used to investigate the role of HIF-1α in TRAIL-induced neuronal death in vitro. Results: The expressions of microglia-located TRAIL and neuron-located DR5 were significantly upregulated after TBI. sDR5 significantly attenuated TRAIL-induced neuronal apoptosis and neurological deficits. 2ME decreased neuronal apoptosis, lesion area, and brain edema and improved neurological function via increased expression of TRAIL decoy receptor 1 (DcR1), which inhibited TRAIL-induced apoptosis after TBI. The administration of DMOG produced the opposite effect than did 2ME. Similarly, HIF-1α siRNA attenuated TRAIL-induced neuronal death via increased DcR1 expression in vitro. Conclusion: Our findings suggested that the TRAIL/DR5 signaling pathway plays an important role after neuronal apoptosis after TBI. HIF-1α mediates TRAIL-induced neuronal apoptosis by regulating DcR1 expression following TBI.

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Section: Methodsmentioning

confidence: 99%

HIF-1α Mediates TRAIL-Induced Neuronal Apoptosis via Regulating DcR1 Expression Following Traumatic Brain Injury

Fang

Wang

et al. 2020

Front. Cell. Neurosci.

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“…Matrix metalloproteinases (MMPs) are most commonly associated with protease degradation [76], where the protease-degradable cross-linker can be tailored to be more susceptible to certain MMPs and less sensitive to others [77]. For CNS applications, MMP-2 and MMP-9 are of interest due to higher levels of these MMPs after CNS damage [78][79][80][81]. Several MMP-cleavable peptide sequences have been reported for MMP-2 and MMP-9 [77].…”

Section: Covalent Cross-linking Mechanismsmentioning

confidence: 99%

Hyaluronic Acid Biomaterials for Central Nervous System Regenerative Medicine

Jensen

Holloway

Stabenfeldt

2020

Cells

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Hyaluronic acid (HA) is a primary component of the brain extracellular matrix and functions through cellular receptors to regulate cell behavior within the central nervous system (CNS). These behaviors, such as migration, proliferation, differentiation, and inflammation contribute to maintenance and homeostasis of the CNS. However, such equilibrium is disrupted following injury or disease leading to significantly altered extracellular matrix milieu and cell functions. This imbalance thereby inhibits inherent homeostatic processes that support critical tissue health and functionality in the CNS. To mitigate the damage sustained by injury/disease, HA-based tissue engineering constructs have been investigated for CNS regenerative medicine applications. HA’s effectiveness in tissue healing and regeneration is primarily attributed to its impact on cell signaling and the ease of customizing chemical and mechanical properties. This review focuses on recent findings to highlight the applications of HA-based materials in CNS regenerative medicine.

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“…5) Zhang et al 2019 ; Nagao et al 2018 FABP7 ; MRG; BLBP; FABPB; B-FABP Brain, neurons, glia, skin, salivary gland, fat Transport of FA; plays a fundamental role in the formation of radial fiber in the developing brain ↑Tumorigenesis (breast cancer, melanoma, renal carcinoma, cystic carcinoma, and invasive glioma) ↓Neurodegenerative and neuropsychiatric disorders ↑Protective response to BBB disruption 132 aa (Chr. 6) Liu et al 2010 ; Nagao et al 2018 ; Matsumata et al 2016 ; Pelsers and Glatz 2005 ; Teunissen et al 2011 ; Ebrahimi et al 2016 ; Rui et al 2019 FABP8 ; PMP2; P2; MP2; CMT1G; M-FABP Brain (myelin sheaths of the peripheral nervous system) Transport of FA; stabilizes the myelin sheath ↓Dominant demyelinating Charcot-Marie-Tooth neuropathy 132 aa (Chr. 8) Hong et al 2016 FABP9 ; PERF; TLBP; PERF15; T-FABP Testis, spleen, fat brain, endometrium Transport of FA, fertility (?)…”

Section: Fabps In Health and Diseasementioning

confidence: 99%

“…These results suggest that astrocytic FABP7 is important for the growth of the dendritic arbor, the formation of neuronal excitatory synapses, and synaptic transmission, providing new insights that link FABP7-dependent lipid homeostasis and neuropsychiatric disorders (Ebrahimi et al 2016 ). Furthermore, astrocyte-FABP7 may function as a modulator of blood-brain barrier (BBB) permeability, after traumatic brain injury (TBI) (Rui et al 2019 ). Consequently, the overexpression of FABP7 in conjunction with the upregulation of endothelial Cav-1 may be an endogenous protective response to BBB disruption (Rui et al 2019 ).…”

Section: Fabp Chaperonopathiesmentioning

confidence: 99%

“…Furthermore, astrocyte-FABP7 may function as a modulator of blood-brain barrier (BBB) permeability, after traumatic brain injury (TBI) (Rui et al 2019 ). Consequently, the overexpression of FABP7 in conjunction with the upregulation of endothelial Cav-1 may be an endogenous protective response to BBB disruption (Rui et al 2019 ).…”

Section: Fabp Chaperonopathiesmentioning

confidence: 99%

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Lipid chaperones and associated diseases: a group of chaperonopathies defining a new nosological entity with implications for medical research and practice

D’Anneo

Bavisotto

Gammazza

et al. 2020

Cell Stress and Chaperones

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Fatty acid–binding proteins (FABPs) are lipid chaperones assisting in the trafficking of long-chain fatty acids with functions in various cell compartments, including oxidation, signaling, gene-transcription regulation, and storage. The various known FABP isoforms display distinctive tissue distribution, but some are active in more than one tissue. Quantitative and/or qualitative changes of FABPs are associated with pathological conditions. Increased circulating levels of FABPs are biomarkers of disorders such as obesity, insulin resistance, cardiovascular disease, and cancer. Deregulated expression and malfunction of FABPs can result from genetic alterations or posttranslational modifications and can be pathogenic. We have assembled the disorders with abnormal FABPs as chaperonopathies in a distinct nosological entity. This entity is similar but separate from that encompassing the chaperonopathies pertaining to protein chaperones. In this review, we discuss the role of FABPs in the pathogenesis of metabolic syndrome, cancer, and neurological diseases. We highlight the opportunities for improving diagnosis and treatment that open by encompassing all these pathological conditions within of a coherent nosological group, focusing on abnormal lipid chaperones as biomarkers of disease and etiological-pathogenic factors.

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Astrocyte-derived fatty acid-binding protein 7 protects blood-brain barrier integrity through a caveolin-1/MMP signaling pathway following traumatic brain injury

Cited by 43 publications

References 47 publications

HIF-1α Mediates TRAIL-Induced Neuronal Apoptosis via Regulating DcR1 Expression Following Traumatic Brain Injury

HIF-1α Mediates TRAIL-Induced Neuronal Apoptosis via Regulating DcR1 Expression Following Traumatic Brain Injury

Hyaluronic Acid Biomaterials for Central Nervous System Regenerative Medicine

Lipid chaperones and associated diseases: a group of chaperonopathies defining a new nosological entity with implications for medical research and practice

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