| First Author | Guzey M | Year | 2004 |
| Journal | J Cell Biochem | Volume | 93 |
| Issue | 1 | Pages | 133-41 |
| PubMed ID | 15352170 | Mgi Jnum | J:92877 |
| Mgi Id | MGI:3054685 | Doi | 10.1002/jcb.20172 |
| Citation | Guzey M, et al. (2004) Increased apoptosis of periprostatic adipose tissue in VDR null mice. J Cell Biochem 93(1):133-41 |
| abstractText | The vitamin D receptor (VDR) is a member of the steroid/retinoid receptor superfamily of nuclear receptors that controls mineral ion homeostatis and has potential tumor-suppressive functions for various cancer types, specifically prostate cancer. A VDR ablated transgenic animal model (VDDRII, vitamin D-dependent rickets type II) has been developed and the animals typically have various diseases including, hypocalcemia, hyperparathyroidism, rickets, osteomalacia, and alopecia. This transgenic mouse system provides us with a model to decipher the influences of the VDR on prostatic growth and function. VDRs are abundant both in prostatic epithelial and stromal cells, and vitamin D signaling can be studied in this model. Although, there were no gross differences between the prostate tissue of the experimental and control groups, VDR null mice showed fat necrosis and individual cell apoptosis in the periprostatic adipose tissue. This indicates a possible role of VDR in the signaling pathways resulting the prostate. This may be particularly attractive for VDR targets for the inhibition of cancer progression using VD(3) and its analogs as potential chemo-preventive agents. Copyright 2004 Wiley-Liss, Inc. |
