Role of osteopontin in early phase of renal crystal formation: immunohistochemical and microstructural comparisons with osteopontin knock-out mice.

Osteopontin (OPN) is an important matrix protein of renal calcium stone. However, the function of OPN in the early phase of renal crystal formation is not well defined. In this study, we examined OPN expression in the early phase of renal crystal formation with ultra-microstructural observations and immuno-TEM (transmission electron microscopy) in control and OPN knock-out (OPN-KO) mice.

Morphological conversion of calcium oxalate crystals into stones is regulated by osteopontin in mouse kidney.

An important process in kidney stone formation is the conversion of retentive crystals in renal tubules to concrete stones. Osteopontin (OPN) is the major component of the kidney calcium-containing stone matrix. In this study, we estimated OPN function in early morphological changes of calcium oxalate crystals using OPN knockout mice: 100 mg/kg glyoxylate was intra-abdominally injected into wildtype mice (WT) and OPN knockout mice (KO) for a week, and 24-h urine oxalate excretion showed no significant difference between WT and KO.

Successful formation of calcium oxalate crystal deposition in mouse kidney by intraabdominal glyoxylate injection.

The establishment of an experimental animal model would be useful to study the mechanism of kidney stone formation. A calcium kidney stone model in rats induced by ethylene glycol has been used for research; however, to investigate the genetic basis affecting kidney stone formation, which will contribute to preventive medicine, the establishment of a kidney stone model in mice is essential. This study indicates the optimum conditions for inducing calcium oxalate stones in normal mouse kidney.

Function and regulation of osteopontin in response to mechanical stress.

Unlabelled: Extensive histological study revealed the impairment of bone remodeling caused by mechanical stress in OPN knockout mice in a tooth movement system. Analysis of OPN promoter transgenic mice showed the mechanical stress response element(s) in the 5.5-kb upstream region.

Identification of promoter regions involved in cell- and developmental stage-specific osteopontin expression in bone, kidney, placenta, and mammary gland: an analysis of transgenic mice.

Unlabelled: Cell-specific expression of GFP under the control of different lengths of the osteopontin promoter in transgenic mice identified the positive and negative regulatory regions for respective cell types. The results provide new insights for physiological and pathological expression of the osteopontin gene.

Introduction: Osteopontin (OPN) is a major non-collagenous bone matrix protein that is involved in normal and pathological calcification and is expressed in a tissue-specific manner.

Difference of osteopontin gene regulation between bone and kidney.

Osteopontin is a sialoprotein that is expressed in various cells. It plays a variety of important roles in cell adhesion, migration, signaling, calcification, and immunity. Its diverse functions indicate that the regulation of osteopontin may also vary extensively among tissues.

Enhanced expression of Runx2/PEBP2alphaA/CBFA1/AML3 during fracture healing.

The cause of the dramatic increase in expression of the osteopontin gene during fracture healing was studied in a mouse experimental model. Semiquantitative reverse transcription-polymerase chain reaction, Northern blotting, and in situ hybridization analysis showed that the enhanced expression took place prior to callus formation. The change in the expression pattern of collagenous and noncollagenous bone matrix proteins in addition to Ets-1 and Runx2, major transcription factors of osteopontin, were examined and compared to that of osteopontin.

A pivotal role for CC chemokine receptor 5 in T-cell migration to tumor sites induced by interleukin 12 treatment in tumor-bearing mice.

Interleukin (IL) 12 treatment in the CSA1M and OV-HM, but not in Meth A tumor models,induces tumor regression that is associated with T-cell migration to tumor sites.Here, we investigated the role of the CC chemokine receptor (CCR)5 in T-cell migration induced after IL-12 treatment. In the two IL-12-responsive tumor models (CSA1M and OV-HM), IL-12 treatment up-regulated the mRNA expression of CCR5 in splenic T cells as well as ligands for CCR5, such as macrophage inflammatory protein (MIP) 1alpha and MIP-1beta in tumor masses.