Magic™ Anti-NT-proBNP (aa 64-67) Monoclonal Antibody, clone IN256

Objective: To detect expression of ClC chloride channel mRNA in tooth germ and odontoblasts, and explore the affect Of chloride channel function on cell proliferation and cell cycle. Design: We extracted total RNA of tooth germ from newborn. C57BL mice and mouse odontoblast-like cells (MDPC-23), then detected mRNA expression of chloride channel genes Clcn1-7 with RT-PCR. We used chloride channel blocker 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) to interfere with chloride channel function of MDPC-23 cells. Cell proliferation rate and cell cycle were detected with MTT assay and flow cytometry, respectively. Student's t-test was used to determine statistical significance between control and treatment groups. Results: The mRNA of Clcn1-7 chloride channel genes was expressed in tooth germ of newborn mice. Clcn3, Clcn5 and Clcn7 mRNAs; were expressed in MDPC-23 cells. NPPB slowed down the proliferation rate of MDPC-23 cells from day 2 to day 4 (P < 0.01), and also changed the proportion of cell cycle phase. Comparing to the control, the proportion of G2/M phase cells reduced from 3.93 +/- 2.62% to 0.54 +/- 0.25% (P < 0.05). The ratio of G1/G2 increased from 1.86 +/- 0.01 to 1.95 +/- 0.02 (P < 0.05). Conclusions: There is abundant chloride channel gene expression in tooth germ. Some of these chloride channels may regulate tooth development through effects on cell proliferation and cell cycle signal pathway. (C) 2008 Elsevier Ltd. All rights reserved.

Background: Sestrins (Sesns) are originally identified as critical antioxidant proteins and involved in complex regulation of cell viability in response to diverse stress conditions. However, the exact expression and function of Sesns in heart failure (HF) remains unclear. Methods and results: Sesns expression was detected in heart samples from end-stage HF patients and unmatched donors by real-time polymerase chain reaction (RT-PCR), Western Blotting and Immunofluorescence. Mice myocardial ischemia/reperfusion (I/R) and myocardial infarction (MI) models and doxorubicin induced rat HF model were established to confirm the heart expression of Sesns. Sesn2 was significantly increased, whereas, no alteration for Sesn1 or Sesn3 in failing hearts when comparing with control hearts. Unexpectedly, the mRNA expression of Sesn2 in ischemic cardiomyopathy was higher than that in dilated cardiomyopathy. Immunofluorescence staining revealed all Sesns were expressed in non-cardiomyocytes in human heart. Furthermore, Sesn2 was co-expressed with vimentin, a marker for fibroblasts. Correlation analysis demonstrated Sesn2 levels were significantly correlated with expression levels of natriuretic peptide B (NPPB) and connective tissue growth factor (CTGF), markers for severity of HF and cardiac fibrosis. Meanwhile, the increased Sesn2 was validated in mice I/R and MI models, and also in doxorubicin induced rat HF model. Conclusions: Sesn2, which is expressed in cardiac fibroblasts, could be a potential biomarker to reflect the severity of HF and might play an important role during cardiac remodeling.