Analysis of HSPA1B (+1267A>G) Genetic Polymorphism in Patients with Vibration Disease in Combination with Metabolic Syndrome.

In 167 men with vibration syndrome (VS), allele and genotype frequencies of HSPA1B (+1267A>G) genetic polymorphism (rs1061581) were studied depending on the type of vibration exposure and on the presence or absence of metabolic syndrome (MetS). The examined subjects were divided into two groups: VS patients (n=80) and VS+MetS patients (n=87). The differences in the lipid profiles between groups were revealed against the background of the lack of distinctions in the age of patients for A/G and G/G genotypes carriers. An increase in A/A (p=0.03) and a decrease in A/G (p=0.04) genotype frequencies in VS patients caused by hand-transmitted vibration in comparison with those in whom the disease was caused by a combination of hand-transmitted and whole-body vibration were found. The shifts in the frequencies of the above genotypes (p=0.01) were similar in patients with both types of vibration exposure in the VS+MetS group in comparison with VS group; the carriage of genotypes with the G allele in VS group exceeded that in VS+MetS group (p=0.01).

Interleukin 6 decreases nociceptor expression of the potassium channel KV1.4 in a rat model of hand-arm vibration syndrome.

Chronic muscle pain is a prominent symptom of the hand-arm vibration syndrome (HAVS), an occupational disease induced by exposure to vibrating power tools, but the underlying mechanism remains unknown. We evaluated the hypothesis that vibration induces an interleukin 6 (IL-6)-mediated downregulation of the potassium voltage-gated channel subfamily A member 4 (KV1.4) in nociceptors leading to muscle pain. Adult male rats were submitted to a protocol of mechanical vibration of the right hind limb. Twenty-four hours after vibration, muscle hyperalgesia was observed, concomitant to increased levels of IL-6 in the gastrocnemius muscle and decreased expression of KV1.4 in the dorsal root ganglia. Local injection of neutralizing antibodies against IL-6 attenuated the muscle hyperalgesia induced by vibration, whereas antisense knockdown of this channel in the dorsal root ganglia mimicked the muscle hyperalgesia observed in the model of HAVS. Finally, knockdown of the IL-6 receptor signaling subunit glycoprotein 130 (gp130) attenuated both vibration-induced muscle hyperalgesia and downregulation of KV1.4. These results support the hypothesis that IL-6 plays a central role in the induction of muscle pain in HAVS. This likely occurs through intracellular signaling downstream to the IL-6 receptor subunit gp130, which decreases the expression of KV1.4 in nociceptors.

Systemic Effects of Segmental Vibration in an Animal Model of Hand-Arm Vibration Syndrome.

OBJECTIVE: Epidemiology suggests that occupational exposure to hand-transmitted (segmental) vibration has local and systemic effects. This study used an animal model of segmental vibration to characterize the systemic effects of vibration. METHODS: Male Sprague Dawley rats were exposed to tail vibration for 10 days. Genes indicative of inflammation, oxidative stress, and cell cycle, along were measured in the heart, kidney, prostate, and liver. RESULTS: Vibration increased oxidative stress and pro-inflammatory gene expression, and decreased anti-oxidant enzymes in heart tissue. In the prostate and liver, vibration resulted in changes in the expression of pro-inflammatory factors and genes involved in cell cycle regulation. CONCLUSIONS: These changes are consistent with epidemiological studies suggesting that segmental vibration has systemic effects. These effects may be mediated by changes in autonomic nervous system function, and/or inflammation and oxidative stress.

Transcriptional Pathways Altered in Response to Vibration in a Model of Hand-Arm Vibration Syndrome.

OBJECTIVE: The aim of this study was to use an established model of vibration-induced injury to assess frequency-dependent changes in transcript expression in skin, artery, and nerve tissues. METHODS: Transcript expression in tissues from control and vibration-exposed rats (4 h/day for 10 days at 62.5, 125, or 250 Hz; 49 m/s, rms) was measured. Transcripts affected by vibration were used in bioinformatics analyses to identify molecular- and disease-related pathways associated with exposure to vibration. RESULTS: Analyses revealed that cancer-related pathways showed frequency-dependent changes in activation or inhibition. Most notably, the breast-related cancer-1 pathway was affected. Other pathways associated with breast cancer type 1 susceptibility protein related signaling, or associated with cancer and cell cycle/cell survivability were also affected. CONCLUSION: Occupational exposure to vibration may result in DNA damage and alterations in cell signaling pathways that have significant effects on cellular division.

[Forecasting formation and course of vibration disease on basis of genetic metabolic markers study].

Analyzing distribution of genotype polymorphism occurrence of Pro l98Leu gene of GPX1 (glutathion peroxidase) and Ala 16 Val gene of MnSOD (superoxide dismutase), the authors presented major mechanisms and leading pathogenetic factors of vibration disease formation and course in post-contact period. The article covers also results of metabolic processes evaluation in patients with varying resistence to occupational vibration, for forecasting its course after discontinued contact with the factor.

A pilot study of gene expression analysis in workers with hand-arm vibration syndrome.

The purpose of this pilot study was to examine differences in gene expressions by cDNA microarray analysis of hand-arm vibration syndrome (HAVS) patients. Vein blood samples were collected and total RNA was extracted. All blood samples were obtained in the morning in one visit after a standard light breakfast. We performed microarray analysis with the labeled cDNA prepared by reverse transcription from RNA samples, using the Human CHIP version 1 (DNA Chip Research Inc, Yokohama, Japan). There are 2,976 genes on the chip, and these genes were selected from a cDNA library prepared with human peripheral white blood cells (WBC). Different gene levels between the HAVS patients and controls, and between groups of HAVS with different levels of symptoms, were indicated by the randomized variance model. The most up-regulated genes were analyzed for their possible functions and association with the occurrence of HAVS. From the results of this pilot study, although the results were obtained a limited number of subjects, it would appear that cDNA microarray analysis of HAVS patients has potential as a new objective method of HAVS diagnosis. Further research is needed to examine the gene expression with increased numbers of patients at different stages of HAVS.