Project/Area Number |
18591737
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Urology
|
Research Institution | Hokkaido University |
Principal Investigator |
MORIYA Kimihiko Hokkaido University, 大学院・医学研究院, Hospital. Inst. (20374233)
|
Co-Investigator(Kenkyū-buntansha) |
TANAKA Hiroshi Hokkaido University, Hokkaido Univ. Hospital, Lecturer (60344470)
MITSUI Takahiko Hokkaido University, Hokkaido Univ. Hospital., Inst. (90421966)
NONOMURA Katsuya Hokkaido University, Hokkaido Univ. Hospital., Professor (60113750)
|
Project Period (FY) |
2006 – 2007
|
Project Status |
Completed (Fiscal Year 2007)
|
Budget Amount *help |
¥3,670,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2006: ¥2,500,000 (Direct Cost: ¥2,500,000)
|
Keywords | Bone marrow derived cells / Urinary tissue remodeling |
Research Abstract |
Objectives: We investigated the time course of the stromal cell-derived factor 1a (SDF1α) expression and behavior of intravenously administered bone-marrow derived stromal (MDS) cells in the urinary bladder of partial bladder outlet obstruction (PBOO) rats. Material and Methods: Study 1: Recombinant SDF1α or saline was directly injected into bladder wall of female rats followed by intravenous administration of MDS cells isolated from GFP transgenic rats, and the bladder was examined with immunohistochemistry. Study 2: Following surgery of PBOO or Sham in female rats, the bladder was exposed on Dayl, 3, 7, 10 and 14, and expression of hypoxia inducible factor la (HIF1α) and SDF1α were examined with real-time PCR. Study 3: Female rats underwent PBOO or Sham surgery followed by intravenous administration of GFP rats' MDS cells, and the bladder was examined with immunohistochemistry on Day1 and 14. Results: In the bladder with injection of SDF1 a, not saline, MDS cells were accumulated in the injection site of the bladder (Study 1). SDF1α and HIF1α increased and peaked on Day1 after PBOO compared to Sham (Study 2). More MDS cells were accumulated in the bladder of PBOO on Day1 as well as Day14, and some cells differentiated into smooth muscle phenotypes on Day 14 (Study 3). Conclusions: SDF1α induced with ischemia/hypoxia due to PBOO is implicated in homing of MDS cells to the bladder. Intravenous administration of MDS cells could have a potential to be an attractive cell therapy for the bladder dysfunction in bladder outlet obstruction.
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