2005 Fiscal Year Final Research Report Summary
Analysis of extracellular matrix-binding proteins that regulate angiogenesis.
| Project/Area Number |
16590327
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Experimental pathology
|
|---|
| Research Institution | Aichi Medical University |
|---|
Principal Investigator |
SAGA Shinsuke Aichi Medical School, School of Medicine, Professor, 医学部, 教授 (40144141)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
YOSHIKAWA Kazuhiro Aichi Medical School, School of Medicine, Professor, 医学部, 講師 (60109759)
|
|---|
| Project Period (FY) |
2004 – 2005
|
| Keywords | caspin / PEDF / angiogenesis / endothelial cells / apoptosis / endochondral ossification / in situ hybridization |
|---|
| Research Abstract |
Previously we isolated and characterized caspin, a unique member of serpin family, which possesses the nature to bind specifically to type I collagen with high affinity and to type III collagen with lower affinity. Pigment epithelium-derived factor (PEDF), human counterparts of caspin, was reported to act as an antiangiogenic factor as well as an inducer of neurite outgrowth in cultured retinoblastoma cell line. However, the mechanism how caspin/PEDF inhibits the angiogenesis has not been well understood.
In this study we have intended to isolate candidates of the receptor for caspin/PEDF in order to elucidate the mechanism of endothelial apoptosis induced by caspin/PEDF and the proteins that bind to extracellular matrix (ECM) and regulate angiogenesis in relation to caspin/PEDF. However, the caspin fraction prepared from recombinant E. coli without denaturant was found to contain LPS, which injures the endothelial cells and confuse the apoptosis induced by caspin/PEDF.
We also investigated the role of caspin/PEDF in the differentiation and the embryonic morphogenesis of cartilage tissue. The expression and distribution of caspin molecules in 15.5 day mouse embryos was analyzed by in situ hybridization in addition of the immunohistochemical method. Both the immature mesenchymal cells and the mature cartilage cells expressed caspin mRNA, and the expression was reduced and disappeared during transformation to the hypertrophic cartilage. Prominent deposition of caspin was detected in the region surrounding hypertrophic cartilage cells. It seems to behave as the inhibitor of vascular invasion into cartilage tissue.
|
