Cognitive Impairment, P300, and Transforming Growth Factor β1 in Different Forms of Dementia

2020 ◽  
Vol 78 (2) ◽  
pp. 837-845
Author(s):  
Eman M. Khedr ◽  
Asmaa M.S. Gomaa ◽  
Omyma G. Ahmed ◽  
Hanaa M.M. Sayed ◽  
Ayman Gamea
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Serum Levels ◽  
Transforming Growth Factor Β1 ◽  
Control Group ◽  
P300 Latency ◽  
Memory Assessment ◽  
Diagnostic And Statistical Manual ◽  
Dementia Patients ◽  
Tgf Β1

Background: There are currently few biomarkers to assist in early diagnosis of dementias. Objective: To distinguish between different dementias: Alzheimer’s disease (AD), vascular dementia (VaD), and Parkinson’s disease dementia (PDD) using simple neurophysiologic (P300) and laboratory markers (transforming growth factor β1 “TGF-β1”). Methods: The study included 15 patients for each type of dementia and 25 age- and sex-matched control subjects. Dementia patients were diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders 4th edition-revised (DSM-IV-R). Modified Mini-Mental State Examination (3MS), Memory Assessment Scale (MAS), P300, and TGF-β1 were examined for each participant. Results: There were no significant differences between groups as regard to age, sex, and education, social, and economic levels. Significant differences between groups were observed in registration and naming variables of the 3MS. Compared with the control group, P300 latency was prolonged in all groups, although to a greater extent in AD and PDD than in VaD. A serum level of TGF-β1 was significantly elevated in all groups but was significantly higher in AD and VaD than in PDD. 3MS tended to correlate with P300 more than TGF-β1, and to be stronger in AD than the other groups. Conclusion: Measurements of P300 latency and serum levels of TGF-β1 can help distinguish AD, PDD, and VaD. P300 was more prolonged in AD and PDD than VaD whereas TGF-β1 was significantly higher in AD and VaD than PDD. Thus P300 and TGF-β1 may be useful biomarkers for detection and evaluation of the extent of cognitive dysfunction.

scholarly journals Study Of Coleus Amboinicus Extract in Increasing of Transforming Growth Factor-β1 (TGF-β1) Concentration and Docking Prediction Quercetin Derivatives in 4X0M Receptor on Uric Acid-Induced in Rats

2020 ◽  
Vol 17 ◽  
Author(s):  
Rondius Solfaine ◽  
Lailatul Muniroh ◽  
Iwan Sahrial Hamid
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Uric Acid ◽  
Growth Factor ◽  
Serum Creatinine ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Control Group ◽  
Tgf Β1 ◽  
Coleus Amboinicus

Background: Coleus amboinicus extracts are known to have anti-oxidant activity, anti-platelet aggregations, antibacterial, anticancer and anti-inflammation. Objective: To evaluate Coleus amboinicus (CA) extracts in increasing of transforming growth factor-β1 concentration and molecular docking prediction of quercetin on receptor 4X0M (TGF-β1), measuring the levels of BUN, serum creatinine and Glutathione Peroxidase (GPx) on uric acid-induced rats. Method: Fourty-two male Wistar rats (Rattus norvegicus), 3 months, 150-200 g were allocated into 3 groups (n=14). The control group received placebo (U-0), treatment group were administered orally with uric acid 1,5% and oxonic acid 2% (U1) and received 500 mg/kg bw of the CA extracts (U-2) respectively for 30 days. Blood serums collected for analysis of creatinine and BUN concentrations. All groups were sacrificed to collect kidney for measuring of GPx activity and TGF-β1 concentration was conducted by avidin-horseradish peroxidase (HRP) sandwich-Elisa. Kidney organ was collected to histopathological analyzed by HE and PAS staining. Results: CA extract analyzed by TLC has a relative fraction of flavonoids, terpenes, saponins, polyphenols and alkaloids. Induction with uric acid has proven to causes acute renal failure with indicated of elevated BUN, serum creatinine concentration and necrotic lesions of tubular membrane in treatment groups. Treatment of CA extract at a dose of 500 mg/kg bw could increase of GPx and of TGF-β1 concentration significantly (p≤0.05). Quercetin as a marker compound of CA extract has stronger bind to the TGF-β1receptor (PDB code: 4X0M) than its of 3WA_601 ligand by in silico. Conclusion: CA extract is proven to inhibit acute renal failure by increasing of TGF-β1concentration and has strong binding of its receptor.

scholarly journals Glutathione S-Transferase Omega-2 and Transforming Growth Factor-β1 Polymorphisms in Iranian Glaucoma Patients

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Shahram Bamdad ◽  
Fatemeh Sanie-Jahromi ◽  
Marzieh Alamolhoda ◽  
Nasrin Masihpour ◽  
Mohammad-Hossein Karimi
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Open Angle Glaucoma ◽  
Transforming Growth Factor Β1 ◽  
Angle Closure ◽  
Control Group ◽  
Glutathione S Transferase ◽  
Significant Difference ◽  
And Control ◽  
Tgf Β1

Background. To investigate the association of glutathione s-transferase omega 2 (GSTO2) (142N > D) and transforming growth factor-β1 (TGF-β1) (869T > C) gene polymorphisms on the pathogenesis of two common types of glaucoma (including primary open-angle glaucoma (POAG) and chronic angle-closure glaucoma (CACG)) in the Iranian population. Methods. A total of 100 glaucoma patients (60% males and 40% females with an age mean ± SD of 34.66 ± 14.25 years; 56 cases of POAG and 44 cases of CACG) were enrolled in this study. GSTO2 (142N > D) and TGF-β1 (869T > C) polymorphisms were evaluated by PCR-based methods in patients and controls. Results. At locus GSTO2 (142N > D), the odds of ND genotype with respect to DD and NN genotypes were 1.55 and 2.08 times higher in POAG and CACG patients compared to those of patients in the control group (95% CI1: 0.80–2.98; 95% CI2: 1.00–4.33) which was statistically significant in CACG patients. However, the odds of DD and NN genotypes against the reference genotype in two patients group were not statistically significant as compared to those of patients in the control group. There was a significant association between the ND genotype and male patients (OR = 2.28, 95% CI: 1.06–4.92). The analysis of TGF-β1 (869T > C) polymorphisms showed no significant difference between the genotypes of TGF-β1 (869T > C) polymorphisms in patients and control groups; however, the CT genotype of TGF-β1 significantly differed between female controls and patients (OR = 0.42, 95% CI: 0.18–0.96). Conclusion. The presented results revealed that there was a significant association between the ND genotype of GSTO2 and the pathogenesis of glaucoma. Furthermore, this genotype can be considered as a sex-dependent genetic risk factor for the development of glaucoma. In contrast, the CT genotype of TGF-β1 is suggested to be a protective genetic factor against the pathogenesis of glaucoma.

scholarly journals Clinical parameters of inflammatory bowel disease in children do not correlate with four common polymorphisms of the transforming growth factor β1 gene.

2011 ◽  
Vol 58 (4) ◽  
Author(s):  
Anna Liberek ◽  
Joanna Jakóbkiewicz-Banecka ◽  
Anna Kloska ◽  
Joanna Świderska ◽  
Zbigniew Kmieć ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Growth Factor ◽  
Intestinal Mucosa ◽  
Bowel Disease ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Control Group ◽  
Clinical Parameters ◽  
Inflammatory Bowel ◽  
Tgf Β1

Transforming growth factor β1 (TGF-β1) is a cytokine affecting cell proliferation and development, which also has an immunomodulatory activity. Correlations between polymorphisms of the TGF-β1 gene and clinical parameters of inflammatory bowel disease (IBD) were reported previously in adults. Here, we tested whether such correlations occur in pediatric patients suffering from IBD. One hundred and four pediatric IBD patients were involved in this study. Among them, 36 were diagnosed with Crohn's Disease (CD) and 68 were diagnosed with ulcerative colitis (UC). The control group consisted of 103 children, in which IBD was excluded. TGF-β1 levels were determined in plasma and intestinal mucosa samples. The presence of the TGF β1 protein and the amount of TGF β1 mRNA were estimated in intestinal mucosa by immunohistochemistry and reverse transcription Real-Time PCR, respectively. Four common polymorphisms of the TGF-β1 gene were investigated: -800G/A, -509C/T, 869T/C and 915G/C. No significant correlation between TGF-β1 genotypes and (i) TGF-β1 levels in plasma and tissue samples, (ii) TGF-β1 gene expression efficiency in intestinal mucosa, (iii) IBD clinical parameters and (iv) inflammatory activity could be detected in children suffering from IBD. We conclude that, contrary to previous suggestions, the four common polymorphisms of the TGF-β1 gene do not influence the susceptibility to or clinical parameters of IBD in the tested population of children.

Pyrrolidine dithiocarbamate attenuates paraquat-induced acute pulmonary poisoning in vivo via transforming growth factor β1 and nuclear factor κB pathway interaction

2016 ◽  
Vol 35 (12) ◽  
pp. 1312-1318 ◽  
Author(s):  
M Huang ◽  
D Lou ◽  
H-H Li ◽  
Q Cai ◽  
Y-P Wang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Pulmonary Fibrosis ◽  
Protein Expression ◽  
Transforming Growth Factor ◽  
Serum Levels ◽  
Nuclear Factor Κb ◽  
Transforming Growth Factor Β1 ◽  
Pyrrolidine Dithiocarbamate ◽  
Nuclear Factor ◽  
Tgf Β1

Paraquat (PQ) exposure could cause pulmonary fibrosis. The aim of this study was to investigate the protective effect of pyrrolidine dithiocarbamate (PDTC) in an acute PQ poison model. One hundred and forty-four Sprague Dawley rats were equally divided into three experimental groups: control group, PQ group, and PQ + PDTC group. At days 1, 3, 7, 14, 28, and 56 of treatment, the serum levels of transforming growth factor β1 (TGF-β1), the levels of hydroxyproline, the protein expression of nuclear factor κB (NF-κB) pathway, and histopathological change in lung tissue were assessed. The survival rate of rats treated with PQ + PDTC was increased compared with that of rats treated only with PQ ( p < 0.05), and the occurrence of pathological changes was dramatically attenuated in the PQ + PDTC group. The serum levels of TGF-β1 and the hydroxyproline levels in the PQ group were significantly increased in a time-dependent manner compared with those in the control and PQ + PDTC groups on days 7, 14, 28, and 56 ( p < 0.05). Additionally, the protein levels of NF-κB proteins p65, inhibitor of κB (IκB) kinase (IKKβ, and IκB-α were significantly downregulated in the PQ + PDTC group as determined by array analysis. The present findings suggest that overexpression of TGF-β1 may play an important role in PQ-induced lung injury and that PDTC, a strong NF-κB inhibitor, can rescue PQ-induced pulmonary fibrosis by influencing the protein expression of NF-κB pathway.

Stress, Peer Affiliation, and Transforming Growth Factor-β1 in Differentially Reared Primates

CNS Spectrums ◽  
2001 ◽  
Vol 6 (7) ◽  
pp. 573-578 ◽  
Author(s):  
Eric L.P. Smith ◽  
Olcay A. Batuman ◽  
Jeremy D. Coplan ◽  
Leonard A. Rosenblum
Keyword(s):  
Growth Factor ◽  
Hpa Axis ◽  
Transforming Growth Factor ◽  
Serum Levels ◽  
Transforming Growth Factor Β1 ◽  
Peer Affiliation ◽  
Fear Stimulus ◽  
Highly Correlated ◽  
The Relationship ◽  
Tgf Β1

AbstractA bidirectional regulatory interaction between the central nervous system and the immune system is largely provided by cytokines and their specific receptors, which are expressed by cells of both systems. Transforming growth factor-β1 (TGF-β1), produced by glial cells and lymphocytes and regulated by steroid hormones, is one such cytokine. In the current study, we examined the relationship between TGF-β1 and peer affiliation in bonnet macaques (Macaca radiata) either reared normally or exposed as infants to conditions in which their mothers faced fluctuating requirements for food procurement (variable foraging demand [VFD]). Rearing under VFD conditions has been previously shown to produce dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis in these animals. Serum levels of TGF-β1 after exposure to a moderate stressor had no correlation with peer affiliation under baseline conditions (r=.07), but were highly correlated with affiliation after subsequent challenge with a fear stimulus (r=.62). Affiliation after the fear stimulus also was inversely correlated with baseline levels of affiliation (r=−.71). These data suggest that changes in peripheral TGF-β1 may be reflective of latent behavioral and biochemical propensities possibly related to affect. Further examination of the effects of early adversity will improve our understanding of the relationship between the HPA axis and immune function.

scholarly journals JNK and p38 Inhibitors Prevent Transforming Growth Factor-β1-Induced Myofibroblast Transdifferentiation in Human Graves’ Orbital Fibroblasts

2021 ◽  
Vol 22 (6) ◽  
pp. 2952
Author(s):  
Tzu-Yu Hou ◽  
Shi-Bei Wu ◽  
Hui-Chuan Kau ◽  
Chieh-Chih Tsai
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Mapk Pathway ◽  
Transforming Growth Factor Β1 ◽  
Tissue Growth ◽  
Mitogen Activated Protein Kinase ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Western Blots ◽  
Orbital Fibroblasts ◽  
Tgf Β1

Transforming growth factor-β1 (TGF-β1)-induced myofibroblast transdifferentiation from orbital fibroblasts is known to dominate tissue remodeling and fibrosis in Graves’ ophthalmopathy (GO). However, the signaling pathways through which TGF-β1 activates Graves’ orbital fibroblasts remain unclear. This study investigated the role of the mitogen-activated protein kinase (MAPK) pathway in TGF-β1-induced myofibroblast transdifferentiation in human Graves’ orbital fibroblasts. The MAPK pathway was assessed by measuring the phosphorylation of p38, c-Jun N-terminal kinase (JNK), and extracellular-signal-regulated kinase (ERK) by Western blots. The expression of connective tissue growth factor (CTGF), α-smooth muscle actin (α-SMA), and fibronectin representing fibrogenesis was estimated. The activities of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) responsible for extracellular matrix (ECM) metabolism were analyzed. Specific pharmacologic kinase inhibitors were used to confirm the involvement of the MAPK pathway. After treatment with TGF-β1, the phosphorylation levels of p38 and JNK, but not ERK, were increased. CTGF, α-SMA, and fibronectin, as well as TIMP-1 and TIMP-3, were upregulated, whereas the activities of MMP-2/-9 were inhibited. The effects of TGF-β1 on the expression of these factors were eliminated by p38 and JNK inhibitors. The results suggested that TGF-β1 could induce myofibroblast transdifferentiation in human Graves’ orbital fibroblasts through the p38 and JNK pathways.

scholarly journals Transforming growth factor-β1-induced N-cadherin drives cell–cell communication through connexin43 in osteoblast lineage

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Yueyi Yang ◽  
Wenjing Liu ◽  
JieYa Wei ◽  
Yujia Cui ◽  
Demao Zhang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Gap Junction ◽  
Cell Line ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Cx43 Expression ◽  
Mc3t3 Cell ◽  
Primary Osteoblasts ◽  
Tgf Β1 ◽  
Cell Cell

AbstractGap junction (GJ) has been indicated to have an intimate correlation with adhesion junction. However, the direct interaction between them partially remains elusive. In the current study, we aimed to elucidate the role of N-cadherin, one of the core components in adhesion junction, in mediating connexin 43, one of the functional constituents in gap junction, via transforming growth factor-β1(TGF-β1) induction in osteoblasts. We first elucidated the expressions of N-cadherin induced by TGF-β1 and also confirmed the upregulation of Cx43, and the enhancement of functional gap junctional intercellular communication (GJIC) triggered by TGF-β1 in both primary osteoblasts and MC3T3 cell line. Colocalization analysis and Co-IP experimentation showed that N-cadherin interacts with Cx43 at the site of cell–cell contact. Knockdown of N-cadherin by siRNA interference decreased the Cx43 expression and abolished the promoting effect of TGF-β1 on Cx43. Functional GJICs in living primary osteoblasts and MC3T3 cell line were also reduced. TGF-β1-induced increase in N-cadherin and Cx43 was via Smad3 activation, whereas knockdown of Smad3 signaling by using siRNA decreased the expressions of both N-cadherin and Cx43. Overall, these data indicate the direct interactions between N-cadherin and Cx43, and reveal the intervention of adhesion junction in functional gap junction in living osteoblasts.

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