Zona Glomerulosa-Derived Klotho Modulates Aldosterone Synthase Expression in Young Female Mice.

Klotho plays a critical role in the regulation of ion and fluid homeostasis. A previous study reported that haplo-insufficiency of Klotho in mice results in increased aldosterone synthase (CYP11B2) expression, elevated plasma aldosterone, and high blood pressure. This phenotype was presumed to be the result of diminished Klotho expression in zona glomerulosa (zG) cells of the adrenal cortex; however, systemic effects on adrenal aldosterone production could not be ruled out.

Specific disruption of calcineurin-signaling in the distal convoluted tubule impacts the transcriptome and proteome, and causes hypomagnesemia and metabolic acidosis.

Adverse effects of calcineurin inhibitors (CNI), such as hypertension, hyperkalemia, acidosis, hypomagnesemia and hypercalciuria, have been linked to dysfunction of the distal convoluted tubule (DCT). To test this, we generated a mouse model with an inducible DCT-specific deletion of the calcineurin regulatory subunit B alpha (CnB1-KO). Three weeks after CnB1 deletion, these mice exhibited hypomagnesemia and acidosis, but no hypertension, hyperkalemia or hypercalciuria.

A five amino acids deletion in NKCC2 of C57BL/6 mice affects analysis of NKCC2 phosphorylation but does not impact kidney function.

Aim: The phosphorylation level of the furosemide-sensitive Na -K -2Cl cotransporter (NKCC2) in the thick ascending limb (TAL) is used as a surrogate marker for NKCC2 activation and TAL function. However, in mice, analyses of NKCC2 phosphorylation with antibodies against phosphorylated threonines 96 and 101 (anti-pT96/pT101) give inconsistent results. We aimed (a) to elucidate these inconsistencies and (b) to develop a phosphoform-specific antibody that ensures reliable detection of NKCC2 phosphorylation in mice.

Hyperglycemia-Induced Aberrant Cell Proliferation; A Metabolic Challenge Mediated by Protein O-GlcNAc Modification.

Chronic hyperglycemia has been associated with an increased prevalence of pathological conditions including cardiovascular disease, cancer, or various disorders of the immune system. In some cases, these associations may be traced back to a common underlying cause, but more often, hyperglycemia and the disturbance in metabolic balance directly facilitate pathological changes in the regular cellular functions. One such cellular function crucial for every living organism is cell cycle regulation/mitotic activity.

-Linked -Acetylglucosamine Transiently Elevates in HeLa Cells during Mitosis.

-linked -acetylglucosamine (-GlcNAc) is a dynamic post-translational modification of serine and threonine residues on nuclear and cytoplasmic proteins. -GlcNAc modification influences many cellular mechanisms, including carbohydrate metabolism, signal transduction and protein degradation. Multiple studies also showed that cell cycle might be modulated by -GlcNAc.

Protein O-GlcNAc Modification Increases in White Blood Cells After a Single Bout of Physical Exercise.

Background: Protein O-linked -acetylglucosamine (O-GlcNAc) is a dynamic posttranslational modification influencing the function of many intracellular proteins. Recently it was revealed that O-GlcNAc regulation is modified under various stress states, including ischemia and oxidative stress. Aside from a few contradictory studies based on animal models, the effect of exercise on O-GlcNAc is unexplored.

The Role of Stress-Induced O-GlcNAc Protein Modification in the Regulation of Membrane Transport.

O-linked N-acetylglucosamine (O-GlcNAc) is a posttranslational modification that is increasingly recognized as a signal transduction mechanism. Unlike other glycans, O-GlcNAc is a highly dynamic and reversible process that involves the addition and removal of a single N-acetylglucosamine molecule to Ser/Thr residues of proteins. UDP-GlcNAc-the direct substrate for O-GlcNAc modification-is controlled by the rate of cellular metabolism, and thus O-GlcNAc is dependent on substrate availability.

Timed, sequential administration of paclitaxel improves its cytotoxic effectiveness in a cell culture model.

Paclitaxel (taxol) is a chemotherapeutic agent frequently used in combination with other anti-neoplastic drugs. It is most effective during the M phase of the cell-cycle and tends to cause synchronization in malignant cells lines. In this study, we investigated whether timed, sequential treatment based on the cell-cycle characteristics could be exploited to enhance the cytotoxic effect of paclitaxel.

Marginal Zone Macrophage Receptor MARCO Is Trapped in Conduits Formed by Follicular Dendritic Cells in the Spleen.

The marginal zone (MZ) region of the spleen plays an important role in leukocyte traffic and the removal of blood-borne pathogens by resident macrophages. Macrophage receptor with a collagenous structure (MARCO), expressed by MZ macrophages, recognizes several microbial ligands and is also involved in the retention of MZ B cells. Here, we report that MARCO is also associated with follicular dendritic cells (FDCs) in the spleen.

Histological diagnosis determines complications of percutaneous renal biopsy: a single-center experience in 353 patients.

Background: We studied the connection between complication occurrence related to renal biopsies and histological diagnoses of the biopsy specimen. We also analyzed the distribution of diagnoses in our population.

Methods: We retrospectively studied 353 patients undergoing renal biopsy at the same center.

Fibroblastic reticular cells of the peripheral lymphoid organs: unique features of a ubiquitous cell type.

The highly ordered structure in peripheral lymphoid tissues is maintained by continuous interactions between their hemopoietic and stromal components. The main reticular cell type, fibroblastic reticular cells (FRCs) emerged as a considerably heterogeneous group of the stroma. These cells have diverse roles beyond architectural scaffolding.