scholarly journals TGFα preserves oligodendrocyte lineage cells and improves white matter integrity after cerebral ischemia

2019 ◽  
Vol 40 (3) ◽  
pp. 639-655 ◽  
Author(s):  
Xuejiao Dai ◽  
Jie Chen ◽  
Fei Xu ◽  
Jingyan Zhao ◽  
Wei Cai ◽  
...  
Keyword(s):  
Cell Death ◽  
White Matter ◽  
Cerebral Ischemia ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Glucose Deprivation ◽  
White Matter Integrity ◽  
Functional Impairments ◽  
Transforming Growth Factor Α

Transforming growth factor α (TGF-α) has been reported to play important roles in neurogenesis and angiogenesis in the injured brain. The present study characterizes a novel role for TGFα in oligodendrocyte lineage cell survival and white matter integrity after ischemic stroke. Three days after transient (60 min) middle cerebral artery occlusion (tMCAO), TGFα expression was significantly increased in microglia/macrophages and neurons. Expression of the receptor of TGFα—epidermal growth factor receptor (EGFR)—was increased in glial cells after ischemia, including in oligodendrocyte lineage cells. TGFα knockout enlarged brain infarct volumes and exacerbated cell death in oligodendrocyte precursor cells (OPCs) and oligodendrocytes three days after tMCAO. TGFα-deficient mice displayed long-term exacerbation of sensorimotor deficits after tMCAO, and these functional impairments were accompanied by loss of white matter integrity and impaired oligodendrocyte replacement. In vitro studies confirmed that 5 or 10 ng/mL TGFα directly protected OPCs and oligodendrocytes against oxygen and glucose deprivation (OGD)-induced cell death, but exerted no effects on OPC differentiation. Further studies identified STAT3 as a key transcription factor mediating the effects of TGFα on OPCs and oligodendrocytes. In conclusion, TGFα provides potent oligodendrocyte protection against cerebral ischemia, thereby maintaining white matter integrity and improving neurological recovery after stroke.

scholarly journals The Activity of Differentiation Factors Induces Apoptosis in Polyomavirus Large T-Expressing Myoblasts

1998 ◽  
Vol 9 (6) ◽  
pp. 1449-1463 ◽  
Author(s):  
Gian Maria Fimia ◽  
Vanesa Gottifredi ◽  
Barbara Bellei ◽  
Maria Rosaria Ricciardi ◽  
Agostino Tafuri ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Growth Factor ◽  
Cell Cycle Progression ◽  
Transforming Growth Factor ◽  
Myogenic Differentiation ◽  
Transforming Growth Factor Β ◽  
Large Tumor ◽  
Cycle Progression

It is commonly accepted that pathways that regulate proliferation/differentiation processes, if altered in their normal interplay, can lead to the induction of programmed cell death. In a previous work we reported that Polyoma virus Large Tumor antigen (PyLT) interferes with in vitro terminal differentiation of skeletal myoblasts by binding and inactivating the retinoblastoma antioncogene product. This inhibition occurs after the activation of some early steps of the myogenic program. In the present work we report that myoblasts expressing wild-type PyLT, when subjected to differentiation stimuli, undergo cell death and that this cell death can be defined as apoptosis. Apoptosis in PyLT-expressing myoblasts starts after growth factors removal, is promoted by cell confluence, and is temporally correlated with the expression of early markers of myogenic differentiation. The block of the initial events of myogenesis by transforming growth factor β or basic fibroblast growth factor prevents PyLT-induced apoptosis, while the acceleration of this process by the overexpression of the muscle-regulatory factor MyoD further increases cell death in this system. MyoD can induce PyLT-expressing myoblasts to accumulate RB, p21, and muscle- specific genes but is unable to induce G00arrest. Several markers of different phases of the cell cycle, such as cyclin A, cdk-2, and cdc-2, fail to be down-regulated, indicating the occurrence of cell cycle progression. It has been frequently suggested that apoptosis can result from an unbalanced cell cycle progression in the presence of a contrasting signal, such as growth factor deprivation. Our data involve differentiation pathways, as a further contrasting signal, in the generation of this conflict during myoblast cell apoptosis.

Transforming growth factor-α directly augments histidine decarboxylase and vesicular monoamine transporter 2 production in rat enterochromaffin-like cells

2004 ◽  
Vol 286 (3) ◽  
pp. G508-G514 ◽  
Author(s):  
Hideaki Kazumori ◽  
Shunji Ishihara ◽  
Mohammad A. K. Rumi ◽  
Cesar F. Ortega-Cava ◽  
Yasunori Kadowaki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Histidine Decarboxylase ◽  
Vesicular Monoamine Transporter ◽  
Vesicular Monoamine Transporter 2 ◽  
Transforming Growth Factor Α ◽  
Ecl Cells ◽  
Factor Α

For the production and vesicle storage of histamine, Enterochromaffin-like (ECL) cells express histidine decarboxylase (HDC) and vesicular monoamine transporter 2 (VMAT2). Although HDC and VMAT2 show dynamic changes during gastric ulcer healing, the control system of their expression has not been fully investigated. In the present study, we investigated the effect of transforming growth factor-α (TGF-α) and proinflammatory cytokines on HDC and VMAT2 expression in rat ECL cells. Time course changes in the expression of TGF-α during the healing of acetic acid-induced ulcers were studied. EGF receptor (EGFR) expression was also examined in ECL cells, whereas the direct effects of TGF-α and proinflammatory cytokines on HDC and VMAT2 expression in ECL cells were investigated using in vivo and in vitro models. During the process of ulcer healing, expression of TGF-α mRNA was markedly augmented. Furthermore, EGFR was identified in isolated ECL cells. TGF-α stimulated HDC and VMAT2 mRNA expression and protein production and also increased histamine release from ECL cells. Selective EGFR tyrosine kinase inhibitor tyrphostin AG1478 almost completely inhibited HDC and VMAT2 gene expression induced by TGF-α in vivo and in vitro. During gastric mucosal injury, TGF-α was found to stimulate ECL cell functions by increasing HDC and VMAT2 expression.

scholarly journals Immune factors in human embryo culture and their significance

Medicina ◽  
2010 ◽  
Vol 46 (4) ◽  
pp. 233 ◽  
Author(s):  
Živilė Čerkienė ◽  
Audronė Eidukaitė ◽  
Audronė Usonienė
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Platelet Activating Factor ◽  
Human Leukocyte ◽  
Preimplantation Embryos ◽  
Embryonic Cells ◽  
Embryo Viability ◽  
Transforming Growth Factor Α

There is increasing evidence that human development before implantation is regulated by embryonically and maternally derived growth factors. The “regulators” of embryonic origin such as soluble human leukocyte antigen G, platelet-activating factor, Th1/Th2 cytokines, insulinlike growth factor, epidermal growth factor, transforming growth factor α, colony-stimulating factor, platelet-derived growth factor may be used as indicators of embryo viability and implantation potential. The data prove the infl uence of growth factors on the development and growth of preimplantation embryos. Though there is a lot of research in the field of biomarkers during folliculogenesis and maternal-fetal interface, only few of them deal with regulators derived from embryonic cells to the cultivation medium. The aim of our study was to summarize the research dealing with immune markers produced by embryos in vitro and to estimate their impact on the cell growth, viability and implantation potential.

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