title: Expression of the TGF-β-ALK-1 pathway in dura and the outer membrane of chronic subdural hematomas.
abstract: Neovascularization of the outer membrane plays a critical role in the development and enlargement of chronic subdural hematomas (CSHs) and vascular endothelial growth factor (VEGF) may promote their progression. However, the precise mechanisms remain to be determined. We focused on the signaling pathway upstream of VEGF, transforming growth factor β (TGF-β), and activin receptor-like kinase 1 (ALK-1) to identify the mechanisms underlying the neovascularization of the outer membrane of CSH. Retrospective comparative study was conducted on 15 consecutive patients diagnosed as CSH with burr-hole drainage. Dura and the outer membrane were collected. We immunohistochemically examined the expression of VEGF, integrin-α, TGF-β, and ALK-1 on the outer membrane and dura of CSH and compared our findings with control samples and the signal intensity of hematomas on computed tomography (CT) scans. VEGF and integrin-α expression was markedly up-regulated in both the dura and outer membrane of CSH, the expression of TGF-β and ALK-1 in the dura was slightly increased in the dura and markedly up-regulated in the outer membrane. There was no significant correlation between their expression and CT density. Here we first report the expression of TGF-β and ALK-1 in the outer membrane and dura mater of CSH. We suggest that the TGF-β-ALK-1 pathway and VEGF affect neovascularization and the progression of CSH.
authors.affiliation: Department of Neurosurgery, Aomori Prefectural Central Hospital.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Saito
authors.forename: Ayumi
authors.initials: A
authors.lastname: Narisawa
authors.forename: Hiroki
authors.initials: H
authors.lastname: Takasawa
authors.forename: Takahiro
authors.initials: T
authors.lastname: Morita
authors.forename: Seiya
authors.initials: S
authors.lastname: Sannohe
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Sasaki
authors.forename: Hidekachi
authors.initials: H
authors.lastname: Kurotaki
authors.forename: Michiharu
authors.initials: M
authors.lastname: Nishijima
mesh_terms: D030301:Activin Receptors, Type II / Q000096:biosynthesis* / Q000235:genetics; D000368:Aged; D000369:Aged, 80 and over; D006259:Craniocerebral Trauma / Q000150:complications; D056424:Decompressive Craniectomy; D018450:Disease Progression; D004388:Dura Mater / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation; D020200:Hematoma, Subdural, Chronic / Q000000981:diagnostic imaging / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D006801:Humans; D039001:Integrin alpha Chains / Q000096:biosynthesis / Q000235:genetics; D008297:Male; D008566:Membranes / Q000378:metabolism; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000209:etiology / Q000235:genetics / Q000378:metabolism*; D012189:Retrospective Studies; D015398:Signal Transduction; D013997:Time Factors; D014057:Tomography, X-Ray Computed; D016212:Transforming Growth Factor beta / Q000096:biosynthesis* / Q000235:genetics; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis / Q000235:genetics
chemical_list: D039001:Integrin alpha Chains; D016212:Transforming Growth Factor beta; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; C425364:ACVRL1 protein, human; D030301:Activin Receptors, Type II