Roles of HtrA1 in non-hypertensive arteriosclerosis
Penulis/Author
Dr. apt. Muthi' Ikawati, M.Sc. (1); Antono Pangestu Hadi (2); Masashi Kawaichi (3); Chio Oka (4)
Tanggal/Date
2013
Kata Kunci/Keyword
Abstrak/Abstract
Loss-of-function mutations of human HtrA1 cause a non-hypertensive ischemic cerebral small-vessel disease called CARASIL, which is characterized by severe arteriosclerosis. We have generated HtrA1 knock- out (KO) mice to understand the roles of HtrA1 in maintenance of normal arteries. The KO mice develop normally to adulthood. The brain arteries of KO mice are normal even 52 weeks after birth. Interestingly the aorta is larger and smooth muscle cells (SMC) are decreased in KO mice at 38-42 and 52 weeks of age than wild type (WT) littermates. Moreover, 52-weeks old KO mice show increase in local intimal proliferation. We hypothesize that HtrA1 is involved in vascular SMC differentiation.
Rumpun Ilmu
Biologi (dan Bioteknologi Umum)
Level
Internasional
Status
Dokumen Karya
No
Judul
Tipe Dokumen
Aksi
1
20131013-ICCAD 2013.pdf
[PAK] Sertifikat Seminar
2
2013-ICCAD-Editorial.pdf
[PAK] Informasi Dewan Redaksi/Editor/Steering Committee