Changes in Distance Between the Flexor Pollicis Longus Tendon and Volar Locking Plate: An Ultrasonographic Study.

PURPOSE: Flexor pollicis longus rupture is a major complication after volar locking plate fixation of distal radius fractures. Although the distance between the flexor pollicis longus tendon and the plate (plate-tendon distance) measured by ultrasonography is used to predict tendon rupture risk, the timing of the ultrasonography can affect the measurements. Therefore, this study aimed to analyze the chronological change of the plate-tendon distance between the tendon and plate. METHODS: A total of 166 wrists underwent the plate-tendon distance measurement twice or more times within 15 months after surgery. Longitudinal ultrasonography scans with the wrist in a neutral position and the thumb flexed were used to measure the plate-tendon distance. The plate-tendon distances at 0-5 months, 5-10 months, and 10-15 months after surgery were compared. A multiple linear regression analysis was performed to evaluate the influence of the interval between surgery and examination, Soong grade, and plate type on the plate-tendon distance. RESULTS: The plate-tendon distance decreased as the interval between surgery and examination increased. The plate-tendon distance was an average of 2.0 ± 1.1 mm, 1.4 ± 0.9 mm, and 1.2 ± 0.9 mm at 0-5 months, 5-10 months, and 10-15 months after surgery, respectively. Significant differences were observed between 0-5 months and 5-10 months and between 5-10 months and 10-15 months after surgery. A multiple linear regression showed that significant predictors of the plate-tendon distance were the intervals between surgery and examination and Soong grade. CONCLUSIONS: The plate-tendon distance decreased as the time since surgery increased. When ultrasonography is used for the assessment of tendon rupture risk, it should be considered that the plate-tendon distance decreases as the interval between the surgery and examination increases. TYPE OF STUDY/LEVEL OF EVIDENCE: Prognosis IV.

CARM1 regulates proliferation of PC12 cells by methylating HuD.

HuD is an RNA-binding protein that has been shown to induce neuronal differentiation by stabilizing labile mRNAs carrying AU-rich instability elements. Here, we show a novel mechanism of arginine methylation of HuD by coactivator-associated arginine methyltransferase 1 (CARM1) that affected mRNA turnover of p21cip1/waf1 mRNA in PC12 cells. CARM1 specifically methylated HuD in vitro and in vivo and colocalized with HuD in the cytoplasm. Inhibition of HuD methylation by CARM1 knockdown elongated the p21cip1/waf1 mRNA half-life and resulted in a slow growth rate and robust neuritogenesis in response to nerve growth factor (NGF). Methylation-resistant HuD bound more p21cip1/waf1 mRNA than did the wild type, and its overexpression upregulated p21cip1/waf1 protein expression. These results suggested that CARM1-methylated HuD maintains PC12 cells in the proliferative state by committing p21cip1/waf1 mRNA to its decay system. Since the methylated population of HuD was reduced in NGF-treated PC12 cells, downregulation of HuD methylation is a possible pathway through which NGF induces differentiation of PC12 cells.

p21Cip1/WAF1 regulates radial axon growth and enhances motor functional recovery in the injured peripheral nervous system.

Recent studies have provided evidence that p21Cip1/WAF1 has not only cell cycle-associated activities but also other biological activities like neurite elongation. To investigate the role of p21Cip1/WAF1 in the in vivo axonal regeneration in the peripheral nervous system, we developed a p21Cip1/WAF1 knockout (KO) mice sciatic nerve injury model. We performed quantitative assessments of the functional, histological, and electrophysiological recoveries after sciatic nerve injury in p21Cip1/WAF1 KO mice and compared the results with those of the wild-type mice. p21Cip1/WAF1 KO mice showed a significant delay of the motor functional recovery between 21 and 42 days after sciatic nerve injury. The values of motor conduction velocity in p21Cip1/WAF1 KO mice were significantly lower than those in the wild-type mice on postoperative day 28. The mean percent neural tissue and the mean nerve axon width of p21Cip1/WAF1 KO mice were significantly less than those of the wild-type mice, which was caused by hyperphosphorylation of neurofilaments. Therefore, p21Cip1/WAF1 was considered to be involved in radial axon growth and to be essential for the motor functional recovery following peripheral nervous system injury.

Local protein synthesis by BDNF is potentiated in hippocampal neurons exposed to ephrins.

Local protein synthesis in neuronal dendrites is one of the mechanisms that may mediate a rapid and synapse-specific mobilization of proteins from the resident mRNAs. A great deal of effort has been made in analyzing the dynamic state of protein synthesis in the living cells chiefly by quantifying protein level. However, the protein level cannot mirror the spatiotemporal alteration of translation because it can be affected, not only by protein synthesis, but also by other factors, like degradation. Therefore, it is problematic to visualize the dynamic state of translation by the present methods. To solve the problem, we applied fluorescence resonance energy transfer (FRET) technique to in situ detection of the assembly and disassembly cycle among a pair of translation initiation factors [eukaryotic initiation factors (eIFs)], thereby showing that BDNF and ephrin could potentiate local protein synthesis in the dendrites of hippocampal neurons.