1991 Fiscal Year Final Research Report Summary
The control mechanism of cell-cell junctions in normal and diseased Keratinocytes
| Project/Area Number |
01480267
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Dermatology
|
|---|
| Research Institution | Jichi Medical School |
|---|
Principal Investigator |
KITAJIMA Yasuo Dept. of Dermatol. Jichi Med. Sch Associate Professor, 医学部, 助教授 (70111797)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
KANAZAWA Kazuya Dept. of Dermatol. Jichi Med. Sch. Joshu, 医学部, 助手 (20169543)
|
|---|
| Project Period (FY) |
1989 – 1991
|
| Keywords | Keratinocytes / desmosome / hemidesmosome / protein kinase C / lipocortin / bullous disease / cell-cell contact / 80 Kd acidic protein |
|---|
| Research Abstract |
The purpose of this study is to elucidate the control mechanisms of lthe formation and disintegration of cell-cell junctions and that in diseased cells. As an experimental system. we empployed Ca^<2+>-induced cell-cell junction formation using normal keratinocytes and a cancer cell line (DJM-l). DJM-L cells grown in low Ca^<2+> medium did not form cell-cell junctions ; desmosomeKIF. When they were shifted to normal (high) Ca^<2+> medium. a rapid translocation of desnoplakins from the cytosol to the plasma membrane to fors desmosomes and reorganization of 180 kd-hesidesmosome proteins were induced almost simultaneously. In correlation with these morphological responses, the Ca^<2+> shift caused a breakdown of inositol phospholipids, a formation of diacylglycerol and IP_3. protein kinase C (PKC) activation. and Ca^<2+> influx. TPA-treatment of low Ca^<2+>-grown DJM-L cells also caused desmosome formation in association with PKC activation. Treatment with other PKC-activating a gents PDBU and DOG also induced desmosome formation. TPAtreatment of normal Ca^<2+>-grown cells collapsed the organized distribution of the 180 kd-hemidesmosome protein and appeared to detach this protein from the cell-ECM adhering sites. From this result, it may be speculated, -that the attachment force of the cells to ECM may be reduced. These results suggest that PKC activation plays important roles in upregulation of cell-cell junctions and downregulation of cell-ECM junctions in association with differentiation of keratinocytes. As diseased cells, epidersolysis bullosa simplex was studied. In cultured keranocytes. keratin interradiate filaments were found io be aggregated ant to form a ball-like structure. This was the first report (1989) in the world, suggesting that this disease has an intrinsic abnoramlity in keratin filaments. The effects of pesphigus antibody on oral mucasal keratinocytes were studied and different effects from on epidernal keratinocytes were found.
|
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
[Publications] Kitajima, Y., Sheu, H-M., Owaribe, K., Nishizawa, Y. Yaoita, H.: "Involvement of protein kinase C in the control of cell-cell and cell-matrix junctions in relation to differentiation of ketatinocytes" The Proceedings of The Japan-US Seminar on the Biology of Eidermis.Editors, Okawara, A., and McGuire, J., Elsevier, Amsterdam. (1992)
Description
「研究成果報告書概要(欧文)」より
-
-
[Publications] Hayashi, H., Owada, M. K., Sonobe, S., Domae, K., Yamanouchi, T., Kakunaga, T., Kitajima, Y. and Yaoita, H.: "Monoclonal antibodies specific to a Ca^<2+>-bound form of lipocortin I distinguish its Ca^<2+>-dependent phospholipidbinding ability from its ability to inhibit phospholipase A_2." Biochemical Journal.269. 709-715 (1990)
Description
「研究成果報告書概要(欧文)」より
-
-
