Transforming growth factor-β2 increases NMDA receptor-mediated excitotoxicity in rat cerebral cortical neurons independently of glia

1996 ◽  
Vol 204 (1-2) ◽  
pp. 93-96 ◽  
Author(s):  
Cynthia J.M. Kane ◽  
Ginger J. Brown ◽  
Kevin D. Phelan
Keyword(s):  
Nmda Receptor ◽  
Growth Factor ◽  
Cortical Neurons ◽  
Transforming Growth Factor ◽  
Cerebral Cortical Neurons ◽  
Transforming Growth Factor Β2

scholarly journals Transforming Growth Factor β2 Is a Neuronal Death-Inducing Ligand for Amyloid-β Precursor Protein

2005 ◽  
Vol 25 (21) ◽  
pp. 9304-9317 ◽  
Author(s):  
Yuichi Hashimoto ◽  
Tomohiro Chiba ◽  
Marina Yamada ◽  
Mikiro Nawa ◽  
Kohsuke Kanekura ◽  
...  
Keyword(s):  
Growth Factor ◽  
Binding Affinity ◽  
Neuronal Death ◽  
Cortical Neurons ◽  
Transforming Growth Factor ◽  
Neuronal Cell Death ◽  
Amyloid Β ◽  
Neuronal Cell ◽  
Precursor Protein ◽  
Transforming Growth Factor Β2

ABSTRACT APP, amyloid β precursor protein, is linked to the onset of Alzheimer's disease (AD). We have here found that transforming growth factor β2 (TGFβ2), but not TGFβ1, binds to APP. The binding affinity of TGFβ2 to APP is lower than the binding affinity of TGFβ2 to the TGFβ receptor. On binding to APP, TGFβ2 activates an APP-mediated death pathway via heterotrimeric G protein Go, c-Jun N-terminal kinase, NADPH oxidase, and caspase 3 and/or related caspases. Overall degrees of TGFβ2-induced death are larger in cells expressing a familial AD-related mutant APP than in those expressing wild-type APP. Consequently, superphysiological concentrations of TGFβ2 induce neuronal death in primary cortical neurons, whose one allele of the APP gene is knocked in with the V642I mutation. Combined with the finding indicated by several earlier reports that both neural and glial expression of TGFβ2 was upregulated in AD brains, it is speculated that TGFβ2 may contribute to the development of AD-related neuronal cell death.

Expression of transforming growth factor-β2 and β3 mRNAs and proteins in the developing chicken embryo

1994 ◽  
Vol 55 (2) ◽  
pp. 105-118 ◽  
Author(s):  
Sonia B. Jakowlew ◽  
Gary Ciment ◽  
Rocky S. Tuan ◽  
Michael B. Sporn ◽  
Anita B. Roberts
Keyword(s):  
Growth Factor ◽  
Chicken Embryo ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β2

Increased transforming growth factor-β2 expression in the glomerular arteriole of the juxtaglomerular apparatus in a bartter's-like syndrome

1999 ◽  
Vol 30 (8) ◽  
pp. 992-995 ◽  
Author(s):  
Tatsuo Yamamoto ◽  
Tosiyuki Takahashi ◽  
Katsuhiko Yonemura ◽  
Katsuyuki Matsui ◽  
Mitsumasa Nagase ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Juxtaglomerular Apparatus ◽  
Transforming Growth Factor Β2

Elevated transforming growth factor β2 enhances apoptosis and contributes to abnormal outflow tract and aortic sac development in retinoic X receptor α knockout embryos

Development ◽  
2002 ◽  
Vol 129 (3) ◽  
pp. 733-746
Author(s):  
Steven W. Kubalak ◽  
D. Reneé Hutson ◽  
Karen K. Scott ◽  
Rebecca A. Shannon
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Qualitative Difference ◽  
Outflow Tract ◽  
Brdu Incorporation ◽  
Wild Type ◽  
Endocardial Cushions ◽  
Precise Integration ◽  
Partial Restoration ◽  
Transforming Growth Factor Β2

Septation of the single tubular embryonic outflow tract into two outlet segments in the heart requires the precise integration of proliferation, differentiation and apoptosis during remodeling. Lack of proper coordination between these processes would result in a variety of congenital cardiac defects such as those seen in the retinoid X receptor α knockout (Rxra–/–) mouse. Rxra–/– embryos exhibit lethality between embryonic day (E) 13.5 and 15.5 and harbor a variety of conotruncal and aortic sac defects making it an excellent system to investigate the molecular and morphogenic causes of these cardiac malformations. At E12.5, before the embryonic lethality, we found no qualitative difference between wild type and Rxra–/– proliferation (BrdU incorporation) in outflow tract cushion tissue but a significant increase in apoptosis as assessed by both TUNEL labeling in paraffin sections and caspase activity in trypsin-dispersed hearts. Additionally, E12.5 embryos demonstrated elevated levels of transforming growth factor β2 (TGFβ2) protein in multiple cell lineages in the heart. Using a whole-mouse-embryo culture system, wild-type E11.5 embryos treated with TGFβ2 protein for 24 hours displayed enhanced apoptosis in both the sinistroventralconal cushion and dextrodorsalconal cushion in a manner analogous to that observed in the Rxra–/–. TGFβ2 protein treatment also led to malformations in both the outflow tract and aortic sac. Importantly, Rxra–/– embryos that were heterozygous for a null mutation in the Tgfb2 allele exhibited a partial restoration of the elevated apoptosis and of the malformations. This was evident at both E12.5 and E13.5. The data suggests that elevated levels of TGFβ2 can (1) contribute to abnormal outflow tract morphogenesis by enhancing apoptosis in the endocardial cushions and (2) promote aortic sac malformations by interfering with the normal development of the aorticopulmonary septum.

Transforming growth factor-β2 levels in aqueous humor of glaucomatous eyes

2001 ◽  
Vol 239 (2) ◽  
pp. 109-113 ◽  
Author(s):  
Masaru Inatani ◽  
Hidenobu Tanihara ◽  
Hideto Katsuta ◽  
Megumi Honjo ◽  
Noriaki Kido ◽  
...  
Keyword(s):  
Growth Factor ◽  
Aqueous Humor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β2
Sign in / Sign up

Export Citation Format

Share Document