2013 Fiscal Year Final Research Report
Pathological Investigation of the Pathogenesis and Development of Preventive and Therapeutic Procedures for Amyloidosis
| Project/Area Number |
23390093
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Experimental pathology
|
|---|
| Research Institution | Shinshu University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MORI Masayuki 信州大学, 医学系研究科, 准教授 (60273190)
SAWASHITA Jinko 信州大学, 医学系研究科, 助教 (40359732)
KAMETANI Fuyuki 公益財団法人東京都医学総合研究所・認知症, 高次脳機能研究分野, 主席研究員 (70186013)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
HIROSE Masamichi 岩手医科大学, 薬学部, 教授 (40273081)
KAKUTA Sigeru 東京大学, 農学生命科学研究科, 准教授 (80345032)
|
|---|
| Project Period (FY) |
2011-04-01 – 2014-03-31
|
| Keywords | 疾患モデル動物 / アミロイドーシス / 伝播 / 線維形成 / Apolipoprotein A-II / 治療 / マウス / SAA |
|---|
| Research Abstract |
Amyloidosis refers to a group of protein folding disorders characterized by accumulation of fine amyloid fibrils. The patients of amyloidoses are increasing and it has been longing for the development of new therapeutic and preventive procedures.
We used animal models of amyloidosis including mouse AApoAII and AA amyloidosis and revealed that 1) Amyloidosis may be transmitted by prion-like infectious process. We found that amyloid fibrils in the feces and blood/blood cells could serve as self-propagating agents for the instigation and progression of amyloidosis. 2) Activated endoplasmic reticulum (ER) stress signals play an important role both in protecting and damaging tissues associated with amyloid deposition. 3) Deficiency of apoliporptein A-I accelerated amyloidosis.
We succeeded in suppressing amyloid deposition in mice by treatment with the C-terminal peptide of type F ApoA-II protein which blocks the active ends of premature amyloid fibrils for self-propagation.
|
Research Products
(51 results)
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
[Presentation] Heat shock factor 1 (Hsf1) plays a key role in AApoAII cardiac amyloidosis in mice2012
Author(s)
Qian J, Hirose M, Zhang B, Wang Y, Tian G, Luo H, Liu Y, Fu X, Ge F, Sawashita J, Mori M, Fujimoto M, Nakai A, Higuchi K
Place of Presentation
Groningen, The Netherlands
Year and Date
20120506-10
-
-
-
-
-
-
-
-
-
-
-
-
-
[Presentation] アミロイドーシスの伝播に対する提言-どこまでわかっているのか? どう対処すべきか?2011
Author(s)
樋口 京一, 張 蓓茹, 銭 金澤, 王 耀勇, 田 耕, 澤下 仁子, 森 政之, 池田 修一, 宇根 有美, 内木 宏延, 安東 由喜雄
Organizer
アミロイドーシス夏のワークショップ 2011
Place of Presentation
熊本市
Year and Date
2011-07-29
Invited
-
-
-
-
-
-
-
-
-
[Book] Heat shock factor 1 (Hsf1) plays a key role in AApoAII cardiac amyloidosis in mice, Hazenberg B.P.C & Bijzet J eds2013
Author(s)
Qian J, Hirose M, Zhang B, Wang Y, Tian G, Luo H, Liu Y, Fu X, Ge F, Sawashita J, Mori M, Fujimoto M, Nakai A, Higuchi K
Total Pages
122-125
Publisher
XIIIth International Symposium on Amyloidosis From Molecular Mechanisms Towards the Cure of Systemic Amyloidosis, Zalsman, Groningen B.V, The Netherlands
-
-
[Book] Mouse Models to Study Systemic Amyloidoses: Is Prion-Like transmission a common pathogenic mechanism? Saranstseva S. ed, "Amyloidosis-Mechanism and Prospects for Therapy"2011
Author(s)
Higuchi K, Fu X, Zhang P, Sawashita J, Zhang Z, Qian J, Wang Y, Mori M
Total Pages
163-180
Publisher
INTEC, Rijeka, Croatia
-
-
