CD36 is a highly glycosylated integral membrane protein that belongs to the scavenger receptor class B family and regulates the pathological progress of metabolic diseases.CD36 was recently found to be widely expresse...CD36 is a highly glycosylated integral membrane protein that belongs to the scavenger receptor class B family and regulates the pathological progress of metabolic diseases.CD36 was recently found to be widely expressed in various cell types in the nervous system,including endothelial cells,pericytes,astrocytes,and microglia.CD36 mediates a number of regulatory processes,such as endothelial dysfunction,oxidative stress,mitochondrial dysfunction,and inflammatory responses,which are involved in many central nervous system diseases,such as stroke,Alzheimer’s disease,Parkinson’s disease,and spinal cord injury.CD36 antagonists can suppress CD36 expression or prevent CD36 binding to its ligand,thereby achieving inhibition of CD36-mediated pathways or functions.Here,we reviewed the mechanisms of action of CD36 antagonists,such as Salvianolic acid B,tanshinone IIA,curcumin,sulfosuccinimidyl oleate,antioxidants,and small-molecule compounds.Moreover,we predicted the structures of binding sites between CD36 and antagonists.These sites can provide targets for more efficient and safer CD36 antagonists for the treatment of central nervous system diseases.展开更多
Background: Diabetes mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia. DM-related dyslipidemia are associated with complications resulting from progressive damage of various organs. CD36 is...Background: Diabetes mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia. DM-related dyslipidemia are associated with complications resulting from progressive damage of various organs. CD36 is 88-kD, class B scavenger receptor, expressed on different types of cells. In diabetic patients, LDL particles are glycated with strong level;this increases CD36 expression, initiates foam cell formation and accelerates atherosclerosis. Objective: This study aimed to determine the correlation between serum CD36 level and lipid profile among patients with type 2 diabetes mellitus in Zeenam Specialized center, Khartoum State, Sudan, in a period between 2019 and 2022. Methodology: Hundred participants at different ages were included in this study;70 were type 2 diabetic patients (cases) and 30 apparently healthy individual (control). 3 ml of venous blood were collected from the participants by using a sterile needle and syringe into a labeled plain container. Each sample was stood until complete clot occurs. Clotted blood sample was then centrifuged to obtain the serum. Then they were used for measurement of total cholesterol, LDL cholesterol, HDL cholesterol, triglyceride and soluble CD36 levels. Total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides were measured using Biosystem chemistry analyzer BTS-302. Serum CD36 was measured using Microplate Reader (URIT-660). Results: The results revealed that serum total cholesterol, LDL cholesterol, HDL cholesterol, and triglyceride levels were significantly higher in patients with type 2 diabetes mellitus compared with control (P = 0.03, P = 0.031, P = 0.000, P = 0.000) respectively, while there is no statistically significant differences in serum CD36 level between cases and control (P = 0.129). Also this study showed that there is no statistically significant correlation between serum CD36 level and total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, age and body mass index. Conclusion: This study concluded that there is no statistically significant difference in serum CD36 level between cases and control. And sCD36 level was not correlated with total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, body mass index, and age.展开更多
The 8th International Workshop on Human Leucocyte Differentiation Antigens (chaired by Zola H and managed by Swart B) was run over a 4-year period and culminated in a conference in December 2004. Here we review the ac...The 8th International Workshop on Human Leucocyte Differentiation Antigens (chaired by Zola H and managed by Swart B) was run over a 4-year period and culminated in a conference in December 2004. Here we review the achieve- ments of the HLDA Workshops and provide links to information on CD molecules and antibodies against them, including the 93 new CDs assigned in the 8th Workshop. We consider what remains to be achieved (including an estimate of the number of leucocyte surface molecules still to be discovered), and how the field can best move forward.展开更多
Objective:To isolate and characterize RNA aptamers that are specific to human CD36 protein using systematic evolution of ligands by exponential enrichment(SELEX)technology to identify candidates for adjunct therapy to...Objective:To isolate and characterize RNA aptamers that are specific to human CD36 protein using systematic evolution of ligands by exponential enrichment(SELEX)technology to identify candidates for adjunct therapy to reverse the binding of Plasmodiuminfected erythrocytes.Methods:RNA aptamers were isolated using nitrocellulose membrane-based SELEX and binding analysis was screened using an electrophoretic mobility shift assay and enzyme-linked oligonucleotide assay.Results:Thirteen cycles of nitrocellulose membrane-based SELEX yielded three aptamers(RC60,RC25,RC04)exhibiting high binding against CD36 protein as shown on electrophoretic mobility shift assay.The sequence analysis revealed a G-quadruplex sequence within all the isolated aptamers that might contribute to aptamer binding and thermodynamic stability.The specificity assay further showed that RC60 and RC25 were highly specific to CD36.The competitive inhibition assay demonstrated that RC60 and RC25 shared a similar binding epitope recognized by m Ab FA6-152,a specific monoclonal antibody against CD36.Conclusions:RC60 and RC25 are promising candidates as anticytoadherence for severe malaria adjunct therapy.展开更多
In this article, we report the changes in serum triglyceride (TG) levels that occurred during repeated tail blood sampling using a mouse restrainer. We used three groups of mice, namely, “PBS-restrained” “PBS-unres...In this article, we report the changes in serum triglyceride (TG) levels that occurred during repeated tail blood sampling using a mouse restrainer. We used three groups of mice, namely, “PBS-restrained” “PBS-unrestrained” and “mock-restrained”. The mice in the PBS-restrained and PBS-unrestrained groups were intraperitoneally (i.p.) injected with 100 mL PBS and tail blood sampling was performed at 1, 5, 8, 24, and 48 h after i.p. injection. For the mock-restrained group, no i.p. injection was performed whereas the subsequent tail blood sampling was similarly performed. During the tail blood sampling, the mice of the two “restrained” groups were placed inside the restrainer designed from an open-ended 50 mL conical tube. The blood from the mice in the PBS-unrestrained group mice was sampled from the tail held by the operator’s hands while being allowed to move on a stage. Strikingly, in all of the three groups, the serum TG level initially decreased to remarkably low levels (approximately 30 mg/dL) after several blood samplings were performed over 8 h. This decrease was followed by a 2 - 3-fold increase in the levels relative to that in the control mice in the subsequent 24 - 48 h time period. We concluded that the acute stress associated with blood sampling caused alterations in TG levels. Serum levels of free fatty acid showed only modest changes. Changes in TG levels were not associated with serum corticosterone levels but with a dramatic increase in CD36 transcript levels in the liver. The relevance of this finding to the previously reported release of lipoprotein lipase (LPL) from white fatty tissue into the plasma during acute stress is also discussed.展开更多
Subretinal inflammation plays a critical role in retinal degenerative diseases.Although activated macrophages have been shown to play a key role in the progression of retinopathies and specifically in age-related macu...Subretinal inflammation plays a critical role in retinal degenerative diseases.Although activated macrophages have been shown to play a key role in the progression of retinopathies and specifically in age-related macular degeneration,little is known about the mechanisms involved in the loss of photoreceptors leading to vision impairment.In our study on retinal damages induced by photo-oxidative stress,we have observed that CD36-deficient mice featured less subretinal macrophage accumulation with attenuated photoreceptor degeneration compared to wild-type(WT)mice.Treatment with CD36-selective azapeptide ligand(labelled MPE-001)as modulator of the inflammatory environment of the retina reduced subretinal macrophage/activated microglia accumulation with preservation of photoreceptor layers and function assessed by ERG in WT,in a CD36-dependent manner.The azapeptide modulated the transcriptome of subretinal macrophage/activated microglia by reducing pro-inflammatory markers.In isolated macrophages,the CD36-selective azapeptide induced dissociation of the CD36-TLR2/6 heterodimer complex(using FRET)altering the TLR2 signaling pathway,thus decreasing NF-κB activation and inflammasome activity.The azapeptide also incurred cytoprotection against photoreceptor apoptosis elicited by activated macrophages.These findings suggest that the azapeptide as ligand of co-receptor CD36 decreases the inflammatory response by modulating CD36-TLR2/6 complex signaling pathway in macrophages,and suggests its potential application in the treatment of retinal degenerative diseases.展开更多
基金supported by the National Major Project of Research and Development,No.2022YFA1105500(to SZ)the National Natural Science Foundation of China,No.81870975(to SZ)Innovation Program for Graduate Students in Jiangsu Province of China,No.KYCX223335(to MZ)。
文摘CD36 is a highly glycosylated integral membrane protein that belongs to the scavenger receptor class B family and regulates the pathological progress of metabolic diseases.CD36 was recently found to be widely expressed in various cell types in the nervous system,including endothelial cells,pericytes,astrocytes,and microglia.CD36 mediates a number of regulatory processes,such as endothelial dysfunction,oxidative stress,mitochondrial dysfunction,and inflammatory responses,which are involved in many central nervous system diseases,such as stroke,Alzheimer’s disease,Parkinson’s disease,and spinal cord injury.CD36 antagonists can suppress CD36 expression or prevent CD36 binding to its ligand,thereby achieving inhibition of CD36-mediated pathways or functions.Here,we reviewed the mechanisms of action of CD36 antagonists,such as Salvianolic acid B,tanshinone IIA,curcumin,sulfosuccinimidyl oleate,antioxidants,and small-molecule compounds.Moreover,we predicted the structures of binding sites between CD36 and antagonists.These sites can provide targets for more efficient and safer CD36 antagonists for the treatment of central nervous system diseases.
文摘Background: Diabetes mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia. DM-related dyslipidemia are associated with complications resulting from progressive damage of various organs. CD36 is 88-kD, class B scavenger receptor, expressed on different types of cells. In diabetic patients, LDL particles are glycated with strong level;this increases CD36 expression, initiates foam cell formation and accelerates atherosclerosis. Objective: This study aimed to determine the correlation between serum CD36 level and lipid profile among patients with type 2 diabetes mellitus in Zeenam Specialized center, Khartoum State, Sudan, in a period between 2019 and 2022. Methodology: Hundred participants at different ages were included in this study;70 were type 2 diabetic patients (cases) and 30 apparently healthy individual (control). 3 ml of venous blood were collected from the participants by using a sterile needle and syringe into a labeled plain container. Each sample was stood until complete clot occurs. Clotted blood sample was then centrifuged to obtain the serum. Then they were used for measurement of total cholesterol, LDL cholesterol, HDL cholesterol, triglyceride and soluble CD36 levels. Total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides were measured using Biosystem chemistry analyzer BTS-302. Serum CD36 was measured using Microplate Reader (URIT-660). Results: The results revealed that serum total cholesterol, LDL cholesterol, HDL cholesterol, and triglyceride levels were significantly higher in patients with type 2 diabetes mellitus compared with control (P = 0.03, P = 0.031, P = 0.000, P = 0.000) respectively, while there is no statistically significant differences in serum CD36 level between cases and control (P = 0.129). Also this study showed that there is no statistically significant correlation between serum CD36 level and total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, age and body mass index. Conclusion: This study concluded that there is no statistically significant difference in serum CD36 level between cases and control. And sCD36 level was not correlated with total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, body mass index, and age.
文摘The 8th International Workshop on Human Leucocyte Differentiation Antigens (chaired by Zola H and managed by Swart B) was run over a 4-year period and culminated in a conference in December 2004. Here we review the achieve- ments of the HLDA Workshops and provide links to information on CD molecules and antibodies against them, including the 93 new CDs assigned in the 8th Workshop. We consider what remains to be achieved (including an estimate of the number of leucocyte surface molecules still to be discovered), and how the field can best move forward.
基金supported by an Exploratory Research Grant Scheme(ERGS203/CIPPM/6730106)+2 种基金Higher Institution Centre of Excellent(HICo E311/CIPPM/4401005)from the Malaysian,Ministry of Higher EducationUniversiti Sains Malaysia Fellowship Scheme.
文摘Objective:To isolate and characterize RNA aptamers that are specific to human CD36 protein using systematic evolution of ligands by exponential enrichment(SELEX)technology to identify candidates for adjunct therapy to reverse the binding of Plasmodiuminfected erythrocytes.Methods:RNA aptamers were isolated using nitrocellulose membrane-based SELEX and binding analysis was screened using an electrophoretic mobility shift assay and enzyme-linked oligonucleotide assay.Results:Thirteen cycles of nitrocellulose membrane-based SELEX yielded three aptamers(RC60,RC25,RC04)exhibiting high binding against CD36 protein as shown on electrophoretic mobility shift assay.The sequence analysis revealed a G-quadruplex sequence within all the isolated aptamers that might contribute to aptamer binding and thermodynamic stability.The specificity assay further showed that RC60 and RC25 were highly specific to CD36.The competitive inhibition assay demonstrated that RC60 and RC25 shared a similar binding epitope recognized by m Ab FA6-152,a specific monoclonal antibody against CD36.Conclusions:RC60 and RC25 are promising candidates as anticytoadherence for severe malaria adjunct therapy.
文摘In this article, we report the changes in serum triglyceride (TG) levels that occurred during repeated tail blood sampling using a mouse restrainer. We used three groups of mice, namely, “PBS-restrained” “PBS-unrestrained” and “mock-restrained”. The mice in the PBS-restrained and PBS-unrestrained groups were intraperitoneally (i.p.) injected with 100 mL PBS and tail blood sampling was performed at 1, 5, 8, 24, and 48 h after i.p. injection. For the mock-restrained group, no i.p. injection was performed whereas the subsequent tail blood sampling was similarly performed. During the tail blood sampling, the mice of the two “restrained” groups were placed inside the restrainer designed from an open-ended 50 mL conical tube. The blood from the mice in the PBS-unrestrained group mice was sampled from the tail held by the operator’s hands while being allowed to move on a stage. Strikingly, in all of the three groups, the serum TG level initially decreased to remarkably low levels (approximately 30 mg/dL) after several blood samplings were performed over 8 h. This decrease was followed by a 2 - 3-fold increase in the levels relative to that in the control mice in the subsequent 24 - 48 h time period. We concluded that the acute stress associated with blood sampling caused alterations in TG levels. Serum levels of free fatty acid showed only modest changes. Changes in TG levels were not associated with serum corticosterone levels but with a dramatic increase in CD36 transcript levels in the liver. The relevance of this finding to the previously reported release of lipoprotein lipase (LPL) from white fatty tissue into the plasma during acute stress is also discussed.
文摘Subretinal inflammation plays a critical role in retinal degenerative diseases.Although activated macrophages have been shown to play a key role in the progression of retinopathies and specifically in age-related macular degeneration,little is known about the mechanisms involved in the loss of photoreceptors leading to vision impairment.In our study on retinal damages induced by photo-oxidative stress,we have observed that CD36-deficient mice featured less subretinal macrophage accumulation with attenuated photoreceptor degeneration compared to wild-type(WT)mice.Treatment with CD36-selective azapeptide ligand(labelled MPE-001)as modulator of the inflammatory environment of the retina reduced subretinal macrophage/activated microglia accumulation with preservation of photoreceptor layers and function assessed by ERG in WT,in a CD36-dependent manner.The azapeptide modulated the transcriptome of subretinal macrophage/activated microglia by reducing pro-inflammatory markers.In isolated macrophages,the CD36-selective azapeptide induced dissociation of the CD36-TLR2/6 heterodimer complex(using FRET)altering the TLR2 signaling pathway,thus decreasing NF-κB activation and inflammasome activity.The azapeptide also incurred cytoprotection against photoreceptor apoptosis elicited by activated macrophages.These findings suggest that the azapeptide as ligand of co-receptor CD36 decreases the inflammatory response by modulating CD36-TLR2/6 complex signaling pathway in macrophages,and suggests its potential application in the treatment of retinal degenerative diseases.
文摘目的为HLA和CD36复合抗体所致血小板输注无效(PTR)患者寻求相合或相容的供者血小板输注。方法采用ELISA方法检测PTR患者的血小板抗体及HLA⁃Ⅰ类抗体特异性;运用MATCH IT!和HLA Matchmaker软件,分析患者HLA⁃Ⅰ类抗体特异性及相应抗原决定簇(epitopes);采用HLA⁃SSO分型技术,获得供、患者的HLA基因型;根据HLA⁃I类抗原交叉反应组(CREG)或HLA表位配型(Eplet)策略,寻找与PTR患者相合或相容的供者血小板;通过血小板抗原单克隆抗体特异性免疫固定检测技术(MAIPA)和血小板免疫荧光流式检测(PIFT)鉴定匹配程度;最后,通过血小板计数纠正增加指数(CCI)评估血小板输注效果。结果2名PTR患者体内检测到针对HLA⁃Ⅰ类和CD36的复合抗体,且CD36流式表型为Ⅰ型缺失;抗体特异性检测结果显示,患者1和患者2的血清中存在高频的HLA⁃Ⅰ类抗体,PRA分别为56%(54/96)和53%(51/96);运用HLA的CREG和Eplet配型策略,在CD36缺失供者库分别筛选到与患者1匹配等级C的供者1名,与患者2匹配等级D的供者1名,且选择的供者均规避患者HLA⁃Ⅰ类抗体表位所针对的抗原;MAIPA和PIFT结果亦证实患者与供者血小板无免疫反应,且患者2输注相容血小板24 h CCI>4.5。结论针对HLA和CD36复合抗体所致PTR患者,可联合运用血清学交叉配型、HLA⁃CREG及Eplet配型策略,选择CD36缺失,规避HLA⁃Ⅰ类抗体对应抗原且HLA表位匹配的供者血小板。
