Dedicator of Cytokinesis 2 in Cell Signaling Regulation and Disease Development

2017 ◽  
Vol 232 (8) ◽  
pp. 1931-1940 ◽  
Author(s):  
Xia Guo ◽  
Shi-You Chen
2021 ◽  
Vol 17 (15) ◽  
pp. 4223-4237
Author(s):  
Mengyuan Qu ◽  
Xuan Zhou ◽  
Xiaotong Wang ◽  
Honggang Li

2022 ◽  
Vol 8 ◽  
Author(s):  
Chih-Ru Lin ◽  
Karim Bahmed ◽  
Beata Kosmider

Pulmonary emphysema is characterized by the destruction of alveolar septa and irreversible airflow limitation. Cigarette smoking is the primary cause of this disease development. It induces oxidative stress and disturbs lung physiology and tissue homeostasis. Alveolar type II (ATII) cells have stem cell potential and can repair the denuded epithelium after injury; however, their dysfunction is evident in emphysema. There is no effective treatment available for this disease. Challenges in this field involve the large complexity of lung pathophysiological processes and gaps in our knowledge on the mechanisms of emphysema progression. It implicates dysregulation of various signaling pathways, including aberrant inflammatory and oxidative responses, defective antioxidant defense system, surfactant dysfunction, altered proteostasis, disrupted circadian rhythms, mitochondrial damage, increased cell senescence, apoptosis, and abnormal proliferation and differentiation. Also, genetic predispositions are involved in this disease development. Here, we comprehensively review studies regarding dysregulated cell signaling, especially in ATII cells, and their contribution to alveolar wall destruction in emphysema. Relevant preclinical and clinical interventions are also described.


2017 ◽  
Vol 89 (3) ◽  
pp. 43-47 ◽  
Author(s):  
L N Sorokina ◽  
V N Mineev ◽  
V V Lim

Aim. To conduct a comprehensive study of the components of negative cell signaling regulation in different types of asthma. Subjects and methods. A total of 171 people, including 80 patients with allergic asthma (AA), 60 patients with non-allergic asthma (NAA), and 31 apparently healthy individuals, were examined. SOCS5 mRNA expression was assessed by reverse-transcription polymerase chain reaction. The expression of SOCS1 and SOCS3 proteins was investigated by immunoblotting. The concentration of total serum IgE was determined by enzyme immunoassay; the level of cytokines was measured according to the standard protocol using a Bio-Plex fluorometer. Results. The findings show that the patients with AA generally display more marked changes in the expression of all three investigated SOCSes (SOCS1, SOCS3, and SOCS5) at baseline and when interleukin 4 (IL-4) acts. In NAA, there are pronounced changes in the expression of SOCS3 only and, to a lesser extent, SOCS5. The results of investigating the concentrations of IL-4 in the examined groups demonstrate its significant decrease in the AA group, whereas in the NAA group, it is similar to those in healthy individuals. On the contrary, IL-10 concentrations in AA tend towards those in the control group, but much exceed in NAA. Conclusion. The findings allow one to consider the complexity of regulatory disorders arising at various levels of cell signaling in the context of the multifunctional nature of the molecules from the family of negative regulators of transcription of the SOCS1, SOCS3, and SOCS5 genes, which provide the comprehensive control of cytokine signaling simultaneously in different signal pathways.


2010 ◽  
Vol 285 (53) ◽  
pp. 41781-41794 ◽  
Author(s):  
Águeda Martínez-Barriocanal ◽  
Emma Comas-Casellas ◽  
Simo Schwartz ◽  
Margarita Martín ◽  
Joan Sayós

2012 ◽  
Vol 40 (18) ◽  
pp. 9369-9378 ◽  
Author(s):  
Shunnichi Kashida ◽  
Tan Inoue ◽  
Hirohide Saito

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