Abstract:
:Oxygen tension is critical for proliferation of human and murine midbrain-derived neural precursor cells (mNPCs). Lack of hypoxia-inducible factor-1α (HIF1α) impairs midbrain dopaminergic neurogenesis which could be rescued by vascular endothelial growth factor (VEGF) via VEGFR-2 signaling. Here, we conditionally inactivated the VEGFR-2, encoded by the fetal liver kinase 1 (Flk1) gene, in murine NPCs to determine its role in proliferation and survival in vitro as well as survival of dopaminergic neurons in vivo. Flk1 conditional knock-out (Flk1 CKO) mice showed no general brain phenotype. There was no midbrain-specific impairment of NPC proliferation as seen in HIF1α CKO mice. In the substantia nigra (SN) of adult Flk1 CKO mice, nonbiased stereological cell counts revealed no reduction of TH-positive neurons of Flk1 CKO mice compared with control Cre/wt mice (in which the wild-type Flk1 allele is expressed in parallel with the Cre recombinase allele). In conclusion, VEGF receptor signaling seems not to be relevant to the development and survival of substantia nigra dopaminergic neurons within the hypoxia-HIF1α signaling pathway.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Hermann A,Loewenbrück KF,Boldt Ä,Fiedler C,Maisel M,Kalucka J,Schwarz J,Breier G,Storch Adoi
10.1016/j.neulet.2013.08.031subject
Has Abstractpub_date
2013-10-11 00:00:00pages
142-7eissn
0304-3940issn
1872-7972pii
S0304-3940(13)00764-7journal_volume
553pub_type
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