NDLI: Integrin β8 Deletion Enhances Vascular Dysplasia and Hemorrhage in the Brain of Adult Alk1 Heterozygous Mice

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Integrin β8 Deletion Enhances Vascular Dysplasia and Hemorrhage in the Brain of Adult Alk1 Heterozygous Mice

Content Provider	Springer Nature Link
Author	Ma, Li Shen, Fanxia Jun, Kristine Bao, Chen Kuo, Robert Young, William L. Nishimura, Stephen L. Su, Hua
Copyright Year	2016
Abstract	Brain arteriovenous malformation (bAVM), characterized by tangled dysplastic vessels, is an important cause of intracranial hemorrhage in young adults, and its pathogenesis and progression are not fully understood. Patients with haploinsufficiency of transforming growth factor-β (TGF-β) receptors, activin receptor-like kinase 1 (ALK1) or endoglin (ENG) have a higher incidence of bAVM than the general population. However, bAVM does not develop effectively in mice with the same haploinsufficiency. The expression of integrin β8 subunit (ITGB8), another member in the TGF-β superfamily, is reduced in sporadic human bAVM. Brain angiogenic stimulation results at the capillary level of vascular malformation in adult Alk1 haploinsufficient (Alk1 $^{+/− }$) mice. We hypothesized that deletion of Itgb8 enhances bAVM development in adult Alk1 $^{+/−}$ mice. An adenoviral vector expressing Cre recombinase (Ad-Cre) was co-injected with an adeno-associated viral vector expressing vascular endothelial growth factor (AAV-VEGF) into the brain of Alk1 $^{+/−}$;Itgb8-floxed mice to induce focal Itgb8 gene deletion and angiogenesis. We showed that compared with Alk $^{+/− }$ mice (4.75 ± 1.38/mm$^{2}$), the Alk1 $^{+/−}$;Itgb8-deficient mice had more dysplastic vessels in the angiogenic foci (7.14 ± 0.68/mm$^{2}$, P = 0.003). More severe hemorrhage was associated with dysplastic vessels in the brain of Itgb8-deleted Alk1 $^{+/− }$, as evidenced by larger Prussian blue-positive areas (1278 ± 373 pixels/mm$^{2}$ vs. Alk1 $^{+/− }$ : 320 ± 104 pixels/mm$^{2}$; P = 0.028). These data indicate that both Itgb8 and Alk1 are important in maintaining normal cerebral angiogenesis in response to VEGF. Itgb8 deficiency enhances the formation of dysplastic vessels and hemorrhage in Alk1 $^{+/−}$ mice.
Starting Page	488
Ending Page	496
Page Count	9
File Format	PDF
ISSN	18684483
Journal	Translational Stroke Research
Volume Number	7
Issue Number	6
e-ISSN	1868601X
Language	English
Publisher	Springer US
Publisher Date	2016-06-29
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Activin receptor-like kinase 1 Brain arteriovenous malformations Brain hemorrhage Integrin β8 Mouse model Neurosciences Neurology Cardiology Neurosurgery Vascular Surgery
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine Neuroscience Neurology (clinical)

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Integrin β8 Deletion Enhances Vascular Dysplasia and Hemorrhage in the Brain of Adult Alk1 Heterozygous Mice.

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