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Objective:To investigate the relationship between the concentration of soluble platelet-derived growth factor receptor β (sPDGFRβ) in the cerebrospinal fluid (CSF) of patients with Alzheimer′s disease (AD) and the degree of cognitive impairment and cerebrospinal fluid biomarkers.Methods:A total of 50 patients with AD in the Department of Neurology of Provincial Hospital Affiliated to Anhui Medical University from September 2018 to August 2020 were selected as AD group, and 33 patients with normal cognition who had no significant difference in age and gender in the same period served as control group. The neuropsychological evaluation was conducted. According to the Clinical Dementia Rating scale scores, the AD patients were divided into mild AD group and moderate to severe AD group.The clinical data and cognitive function of the three groups were compared. And the level of CSF sPDGFRβ, CSF amyloid-β (Aβ) 1-40, CSF Aβ 1-42, CSF total tau protein (T-tau), CSF phosphorylated tau protein (P-tau) were measured by enzyme linked immunosorbent assay in each group. According to whether apolipoprotein E4 (ApoE4) gene was carried, the patients with AD were divided into ApoE4 + group and ApoE4 - group. Differences among the three groups were compared and the correlation analysis was carried out. Results:The levels of sPDGFRβ in the CSF of the mild AD group [(219.301±69.711) pg/ml] and the moderate to severe AD group [(235.358±86.187) pg/ml] were significantly higher than that of the control group [(184.878±52.944) pg/ml, F=3.90, P=0.024], while there was no significant difference in the level of CSF sPDGFRβ between the ApoE4 + group [(219.493±76.745) pg/ml] and the ApoE4 - group [(222.802±81.665) pg/ml, t=-0.13, P=0.900]. And the level of sPDGFRβ in the CSF in the mild AD group was positively correlated with the level of CSF P-tau ( r=0.43, P=0.019), but not correlated with Aβ 1-42, T-tau, Mini-Mental State Examination scores or Montreal Cognitive Assessment scores, whereas no significant correlation was found in the control group and the moderate to severe AD group. Conclusions:Expression of sPDGFRβ in CSF of AD patients is increased, and may relate to P-tau. Pericyte injury may be involved in the phosphorylation of tau protein in the brain of AD patients.
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Objective To investigate the blood-brain barrier permeability of platelet-derived growth factor receptor-β + (pdgfi-β +) vascular wall cells at 2h,24h,3 d,7 d,14 d and 21 d after lithium-pilocarpine-inducedstatus epilepticus.Methods One hundred and thirty-five clean male Sprague-Dawley rats were randomly divided into control group (n =15) and model group (n =120).The model group was divided into 2h,24h,3d,7d,14d and21d after SE.We evaluated the permeability of blood-brain barrier in hippocampus of rats in each group after status epilepticus by Evans blue method and wet and dry weight method.We observed the ultrastructural changes of pericytes and blood-brain barriers at different stages after onset by electron microscopy.We used Western Blot to detect the expression of pericyte marker pdgfr-β and α-SMA in hippocampus at different stages after onset.Results (1) The blood-brain barrier permeability increased after epileptic seizures (P ＜ 0.05),and the permeability was the highest at 24h after onset (P ＜ 0.01),and gradually returned to normal after 3d and later.(2) Transmission electron microscopy showed that the ultrastructure of cerebral microvascular pericytes and their basement membranes were degenerated after SE.(3) Western blot showed that the expression level of pdgfr-β and α-SMA at 24 h after SE was significantly higher than that of the control group (P ＜0.05),and gradually became stable after 3d and later.Conclusion Pdgfr-β + microvascular wall cells in brain microvessels may be involved in the opening of blood-brain barrier after status epilepticus,and may be dedicated to the conversion of disease into refractory epilepsy.
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Objective To investigate the effects of PDGF-D/PDGFR-β signaling on interstitial collagen hyperplasia and fibroplasia of myocardium following cardiopulmonary resuscitation (CPR)in rats.Methods A total of 90 male Sprague-Dawley (SD) rats were randomly (random number) assigned into 5 groups:sham,control,Imatinib,Ad-GFP and Ad-PDGFR groups.Each group was further subdivided into post-resuscitation (PR) 4 h and PR 72 h groups.The ventricular fibrillation cardiopulmonary resuscitation (CPR) model was used.Cardiac collagen volume fraction (CVF) was measured with Sirius red staining.Platelet derived growth factor D (PDGF-D) was detected by enzyme-linked immunosorbent assay (ELISA).Collagen Ⅰ,α smooth muscle actin (α-SMA),vimentin and PDGF receptor β (PDGFRβ) were detected by Western blot.The data were analyzed by a two-way ANOVA and Bonferroni test.P ＜0.05 was considered statistically significant.Results (1) At PR 72 h,the CVF value in the control group was significantly higher than that in the sham group [(11.24 ± 0.31) vs (1.65 ± 0.19),t =10.81,P ＜0.05] and in the Ad-PDGFR group significantly higher than that in Ad-GFP group [(25.60 ±4.09) vs (10.73 ± 2.42),t =16.77,P ＜0.05],respectively.Compared to the control group,the level of CVF in the Imatinib group significantly decreased [(5.11 ± 0.29)vs (11.24 ± 0.31),t =3.892,P ＜0.05].(2) At PR 4 h,compared with the sham group,the expression of serum PDGF-D was greatly increased in the control,Imatinib,Ad-GFP and Ad-PDGFR groups (all P＜0.05).At PR 72 h,serum PDGF-D was continuously significantly higher in the Ad-PDGFR group when compared with the sham group [(296.46± 30.82) pg/mL vs (93.74 ± 5.43) pg/mL,t =7.755,P ＜0.05].(3) At PR 72 h,the expression of Collagen I,α-SMA,Vimentin and PDGFR-β in the control and Ad-PDGFR groups were significantly increased than those in the sham and Ad-GFP groups,respectively (all P＜0.05).However,compared with the control group,Imatinib significantly decreased the expressions of the above proteins (all P＜0.05).Conclusions The interstitial collagen hyperplasia and fibroplasia of myocardium at 72 h following CPR in rats might be related to the increased levels of PDGF-D in serum and PDGFR-β in myocardium.
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As the second cause of cancer relative deaths,gastric cancer's different biological characteristics lead to obviously different treatment results and prognosis.The mechanism to determine the initiation,lead to obviously different development and the biological characreristics of gastric cancer is doctors' interest.Recently,platelet-de-rived growth factor receptor-β (PDGFR-β) become one of hot research fields,its excessive activation and abnormal expression can induce tumor angiogenesis,and promote tumor growth,and can also degrade extracellular matrix,reduce the number of cell adhesion molecular.Through these,PDGFR-β was directly or indirectly involved in tumor invasion and metastasis.PDZK1 can bind with PDGFR-β specifically and futher affect the downstream of PDGFR-β signaling pathway (Ras-MAPK signaling pathway,the PI3K-Akt signaling pathway,PLC signaling pathway),and then affect cell proliferation,differentiation and migration.