Mechanism and Treatment Strategy of Osteoporosis after Transplantation.

Osteoporosis (OP) has emerged as a frequent and devastating complication of organ solid transplantation process. Bone loss after organ transplant is related to adverse effects of immunosuppressants on bone remodeling and bone quality. Many factors contribute to the pathogenesis of OP in transplanted patients. Many mechanisms of OP have been deeply approached. Drugs for OP can be generally divided into "bone resorption inhibitors" and "bone formation accelerators," the former hindering bone resorption by osteoclasts and the latter increasing bone formation by osteoblasts. Currently, bisphosphonates, which are bone resorption inhibitors drugs, are more commonly used clinically than others. Using the signaling pathway or implantation bone marrow stem cell provides a novel direction for the treatment of OP, especially OP after transplantation. This review addresses the mechanism of OP and its correlation with organ transplantation, lists prevention and management of bone loss in the transplant recipient, and discusses the recipients of different age and gender.

Multifaceted role of prohibitin in cell survival and apoptosis.

Human eukaryotic prohibitin (prohibitin-1 and prohibitin-2) is a membrane protein with different cellular localizations. It is involved in multiple cellular functions, including energy metabolism, proliferation, apoptosis, and senescence. The subcellular localization of prohibitin may determine its functions. Membrane prohibitin regulate the cellular signaling of membrane transport, nuclear prohibitin control transcription activation and the cell cycle, and mitochondrial prohibitin complex stabilize the mitochondrial genome and modulate mitochondrial dynamics, mitochondrial morphology, mitochondrial biogenesis, and the mitochondrial intrinsic apoptotic pathway. Moreover, prohibitin can translocates into the nucleus or the mitochondria under apoptotic signals and the subcellular shuttling of prohibitin is necessary for apoptosis process. Apoptosis is the process of programmed cell death that is important for the maintenance of normal physiological functions. Consequently, any alteration in the content, post-transcriptional modification (i.e. phosphorylation) or the nuclear or mitochondrial translocation of prohibitin may influence cell fate. Understanding the mechanisms of the expression and regulation of prohibitin may be useful for future research. This review provides an overview of the multifaceted and essential roles played by prohibitin in the regulation of cell survival and apoptosis.

[Mechanism of ATP release from cultured marginal cells of stria vascularis in neonatal rat].

OBJECTIVE: To further confirm release of adenosine triphosphate (ATP) from cultured marginal cells in vitro of stria vascularis in neonatal rat, and to explore the mechanism of ATP release from marginal cells. METHODS: Isolation and in vitro culture of marginal cells of neonatal rats' cochlea. ATP released by marginal cells in extracellular fluid were detected using bioluminescence assay when add regain separately as follow: bafilomycin A(1), didecyl adipate (DDA), extracellular K(+), thapsigargin, extracellular Ca(2+), U73122, and aristolochic acid. RESULTS: The concentrations of ATP in the extracellular fluid significantly and gradually decreased along with increasing concentrations of bafilomycin A(1). The concentrations of ATP in the extracellular fluid were in linear increased with DDA was added to marginal cell suspensions. ATP concentrations increased as the concentration of extracellular K(+) was increased, and reached the peak with a K(+) concentration of 9.15 mmol/L. At higher K(+) concentrations, ATP concentrations decreased. With the addition of increasing concentrations of thapsigargin to test marginal cells, ATP concentrations were significantly decreased. When extracellular Ca(2+) was completely chelated, marginal cells continued to release ATP. Moreover, as extracellular Ca(2+)increased, the release of ATP decreased. However, the amount of ATP releas remained to a baseline when extracellular concentration of Ca(2+) reached 1.25 mmol/L or above. When concentrations of U73122 remained within the range of 0.25 to 1.25 µmol/L, as U73122 increased, the release of ATP decreased. When concentrations of aristolochic acid ranging from 12.5 to 100.0 µmol/L were added to the marginal cells suspension, the release of ATP was significantly decreased. However, with concentrations of aristolochic acid less than 100.0 µmol/L, the release of ATP tended to be not significantly different from the amount of ATP released by control group. CONCLUSIONS: ATP could be release from marginal cells cultured in vitro of vascular stria in neonatal rats. ATP release from marginal cells has relevant with calcium pump, K(+) channel state and signaling pathway related enzymes.