scholarly journals Overexpression of p63 Protein in Patients with Seborrheic Keratosis in the Setting of Carbohydrate Metabolism Disorders

2019 ◽  
Vol 26 (4) ◽  
pp. 18-25
Author(s):  
A. К. Alexandrova ◽  
V. A. Smolyannikova
Keyword(s):  
Monoclonal Antibodies ◽  
Carbohydrate Metabolism ◽  
Histological Study ◽  
Tumour Cells ◽  
Nuclear Staining ◽  
Seborrheic Keratosis ◽  
Chronic Hyperglycemia ◽  
Weak Staining ◽  
P63 Isoforms

Aim. The paper studies p63 expression in patients with seborrheic keratosis in the presence or absence of carbohydrate metabolism disorders.Materials and methods. The study involved 130 patients with seborrheic keratosis. Following the endocrinologist’s consultation, the patients were divided into two groups. The fi rst group comprised 68 people: 44 patients with type 2 diabetes and 24 patients with impaired glucose tolerance. The second group was composed of patients without carbohydrate metabolism disorders (62 people). The authors performed a histological study and an immunohistochemical (IHC) test using monoclonal antibodies to р63. The results of the IHC test were analysed according to the number of stained tumour cells: 0 — no response or weak staining of less than 10% of the cells, 1 — from 10% to 30% of tumour cells are stained, 2 — staining of more than 30% of tumor cells; as well as according to the colour intensity: weak (+) and marked (++).Results. The IHC test using monoclonal antibodies to р63 produced a positive reaction in 82.3% of cases. Sixty-fi ve seborrheic keratomas (SK) (50%) exhibited a diffuse pronounced expression of p63. Weak nuclear staining (10%–30% of cells) was recorded in 42 SKs (32.3%). The study revealed a high correlation dependence of p63 expression in SK on the presence of carbohydrate metabolism disorders in patients (R = 0.82, p = 0.0000001). Thus, in patients with carbohydrate metabolism disorders, overexpression of p63 in SKs was found to be signifi cantly higher — 89.7%, as compared to 6.4% in patients without impaired carbohydrate metabolism (p = 0.00001).Conclusion. P63 overexpression in seborrheic keratosis correlates with the presence of chronic hyperglycemia in patients. Disruption of cellular metabolism leads to changes in the balance between p63 isoforms and plays an important role in the pathogenesis of seborrheic keratosis.

Wogonin Alleviates Hyperglycemia Through Increased Glucose Entry into Cells Via AKT/GLUT4 Pathway

2019 ◽  
Vol 25 (23) ◽  
pp. 2602-2606 ◽  
Author(s):  
Shahzad Khan ◽  
Mohammad A. Kamal
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Modern World ◽  
Major Health Problem ◽  
Major Health ◽  
Chronic Hyperglycemia ◽  
Main Factor

: Insulin resistance and type 2 Diabetes mellitus resulting in chronic hyperglycemia is a major health problem in the modern world. Many drugs have been tested to control hyperglycemia which is believed to be the main factor behind many of the diabetes-related late-term complications. Wogonin is a famous herbal medicine which has been shown to be effective in controlling diabetes and its complications. In our previous work, we showed that wogonin is beneficial in many ways in controlling diabetic cardiomyopathy. In this review, we mainly explained wogonin anti-hyperglycemic property through AKT/GLUT4 pathway. Here we briefly discussed that wogonin increases Glut4 trafficking to plasma membrane which allows increased entry of glucose and thus alleviates hyperglycemia. Conclusion: Wogonin can be used as an anti-diabetic and anti-hyperglycemic drug and works via AKT/GLUT4 pathway.

Identification of tumour cells in CSF using monoclonal antibodies

Pathology ◽  
1984 ◽  
Vol 16 (4) ◽  
pp. 480
Author(s):  
W.W. Hancock ◽  
R.C. Atkins ◽  
G. Medley ◽  
M. Drake
Keyword(s):  
Monoclonal Antibodies ◽  
Tumour Cells

Detection of fos protein during osteogenesis by monoclonal antibodies

1988 ◽  
Vol 8 (5) ◽  
pp. 2251-2256
Author(s):  
P De Togni ◽  
H Niman ◽  
V Raymond ◽  
P Sawchenko ◽  
I M Verma
Keyword(s):  
Monoclonal Antibodies ◽  
Amino Acid ◽  
Indirect Immunofluorescence ◽  
Protein Complex ◽  
Synthetic Peptide ◽  
Immunohistochemical Staining ◽  
Nuclear Staining ◽  
Rat Embryos ◽  
Fos Protein ◽  
Modified Forms

We have generated monoclonal antibodies by using a synthetic peptide corresponding to amino acid positions 4 to 17 of the human fos protein. The antibodies detected both v- and c-fos proteins by immunoprecipitation, immunoblotting, and indirect immunofluorescence. The monoclonal antibodies not only identified the fos protein complex with the cellular 39-kilodalton protein, but also recognized the modified forms of the mouse, rat, and human fos proteins. In day-17 rat embryos, nuclear-staining fos protein could be identified in the cartilage by immunohistochemical staining.

Secreted modular calcium-binding protein 1 binds and activates thrombin to account for platelet hyperreactivity in diabetes

Blood ◽  
2021 ◽  
Vol 137 (12) ◽  
pp. 1641-1651
Author(s):  
Fredy Delgado Lagos ◽  
Amro Elgheznawy ◽  
Anastasia Kyselova ◽  
Dagmar Meyer zu Heringdorf ◽  
Corina Ratiu ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Monoclonal Antibodies ◽  
Platelet Function ◽  
Calcium Binding ◽  
Transforming Growth Factor ◽  
Binding Protein ◽  
Calcium Binding Protein ◽  
Matricellular Protein

Abstract Secreted modular calcium-binding protein 1 (SMOC1) is an osteonectin/SPARC-related matricellular protein, whose expression is regulated by microRNA-223 (miR-223). Given that platelets are rich in miR-223, this study investigated the expression of SMOC1 and its contribution to platelet function. Human and murine platelets expressed SMOC1, whereas platelets from SMOC1+/− mice did not present detectable mature SMOC1 protein. Platelets from SMOC1+/− mice demonstrated attenuated responsiveness to thrombin (platelet neutrophil aggregate formation, aggregation, clot formation, Ca2+ increase, and β3 integrin phosphorylation), whereas responses to other platelet agonists were unaffected. SMOC1 has been implicated in transforming growth factor-β signaling, but no link to this pathway was detected in platelets. Rather, the SMOC1 Kazal domain directly bound thrombin to potentiate its activity in vitro, as well as its actions on isolated platelets. The latter effects were prevented by monoclonal antibodies against SMOC1. Platelets from miR-223–deficient mice expressed high levels of SMOC1 and exhibited hyperreactivity to thrombin that was also reversed by preincubation with monoclonal antibodies against SMOC1. Similarly, SMOC1 levels were markedly upregulated in platelets from individuals with type 2 diabetes, and the SMOC1 antibody abrogated platelet hyperresponsiveness to thrombin. Taken together, we have identified SMOC1 as a novel thrombin-activating protein that makes a significant contribution to the pathophysiological changes in platelet function associated with type 2 diabetes. Thus, strategies that target SMOC1 or its interaction with thrombin may be attractive therapeutic approaches to normalize platelet function in diabetes.

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