title: Vascular ligation response is independent of p107: stressing the role of the related p130.
abstract: Recent studies have revealed the role of the pRb family members pRb and p130 in the response to vascular injury. We evaluated the arterial injury response in the absence of p107, a protein that shares a high degree of homology with the injury-controlling p130. Carotid artery ligation and perivascular electric injury of the femoral artery were applied to p107 knockout (p107 -/-) mice, and morphometric analysis was performed 3 wk after ligation and electric injury. Arterial vessels of p107 -/- mice were indistinguishable from controls under basal conditions. After carotid artery ligation the p107 -/- mice (n = 7) did not display an enhanced ligation response compared with controls (n = 9), which was studied over a distance of approximately 450 microm proximal and approximately 200 microm distal from the ligation site, with regard to vessel wall area, neointima area, and lumen area. Corresponding with this, morphometric data obtained from the perivascular electric injury of the femoral artery confirmed the lack of enhanced ligation and injury response in the absence of p107. We conclude that the pRb family member p107 is not a key regulator in vascular injury response. These data, in conjunction with previously reported results, indicate that the control of vascular injury response is not a redundant feature of pRb proteins but primarily specific for p130. Further studies on functional domains of p130 and p107 will help to resolve the pathways in vascular injury response.
authors.affiliation: Krannert Institute of Cardiology and Indiana Center for Vascular Biology and Medicine, Indiana University Medical Center, Indianapolis, IN 46202, USA. sinderm@uni-muenster.de
authors.forename: Jürgen R
authors.initials: JR
authors.lastname: Sindermann
authors.forename: Christiane
authors.initials: C
authors.lastname: Köbbert
authors.forename: Florian
authors.initials: F
authors.lastname: Bauer
authors.forename: Adriane
authors.initials: A
authors.lastname: Skaletz-Rorowski
authors.forename: Helge
authors.initials: H
authors.lastname: Hohage
authors.forename: Gabriele
authors.initials: G
authors.lastname: Plenz
authors.forename: Günter
authors.initials: G
authors.lastname: Breithardt
authors.forename: Keith L
authors.initials: KL
authors.lastname: March
mesh_terms: D000818:Animals; D002339:Carotid Arteries / Q000378:metabolism / Q000473:pathology; D020212:Carotid Artery Injuries / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D004558:Electric Stimulation; D008026:Ligation; D051379:Mice; D008811:Mice, Inbred DBA; D018345:Mice, Knockout; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism*; D010750:Phosphoproteins / Q000378:metabolism*; D011506:Proteins; D050720:Retinoblastoma-Like Protein p107; D050717:Retinoblastoma-Like Protein p130
chemical_list: D009687:Nuclear Proteins; D010750:Phosphoproteins; D011506:Proteins; C489485:Rbl1 protein, mouse; C493838:Rbl2 protein, mouse; D050720:Retinoblastoma-Like Protein p107; D050717:Retinoblastoma-Like Protein p130