In silico genomic and proteomic analyses of three heat shock proteins (HSP70, HSP90-a, and HSP90-b) in even-toed ungulates

BACKGROUND Heat shock proteins (HSPs) play important roles in the responses to different environmental stresses. In this study, the genomic and proteomic characteristics of three HSPs (HSP70, HSP90-a and HSP90-b) in five even-toed ungulates (sheep, goats, water buffalo, Zebu cattle and cattle) were analyzed using Multiple sequence alignment, SWISS modeling and phylogenetics analysis tools. RESULTS The bioinformatic analysis revealed that the HSP70 gene in cattle, Zebu cattle, and goat is located on chromosome 23, and is intronless, while in water buffalo and sheep it is located on chromosomes 2 and 20, respectively, and contains two exons linked by one intron. The HSP90-a gene is located on chromosome 21 in cattle, Zebu cattle, and goat, while in water buffalo and sheep it is located on chromosomes 20 and 18, respectively. The HSP90-b gene is located on the same chromosome as the HSP70 gene and contains 12 exons interspersed by 11 introns in all studied animals. In silico Expasy translate tool analysis revealed that HSP70, HSP90-a and HSP90-b encode 641, 733, and 724 amino acids, respectively. The data revealed that goat HSP70 protein has seven variable amino acid residues, while in both sheep and cattle only one such amino acid was detected. CONCLUSIONS This study will be supportive in providing new insights into HSPs for adaptive machinery in these studied animals and selection of target genes for molecular adaptation of livestock

Histological investigation of experimentally induced diabetes effects on the distribution of transforming growth factor (TGF beta), nuclear factor kappa b (Nf-KB), heat schock 90 beta (Hsp beta) and E-cadherin proteins in testicular tissue / Investigación histológica de los efectos de la diabetes inducida experimentalmente en la distribución del factor de crecimiento transformante (TGFß), nuclear factor kappa b (Nf-KB), y proteinas heat schock 90ß (Hsp90ß) y E-cadherina en tejido testicular

SUMMARY: Diabetes is a metabolic disorder characterized by high blood sugar levels and it causes complications in many systems, including the reproductive system. As a result of diabetic conditions, one of the mechanisms that can cause repression of reproductive activity is testicular oxidant stress. The identification of diabetes on the cell signaling molecules axis is still under discussion. The aim of this study was to determine the effect of Transforming Growth Factor (TGFβ), Nuclear Factor kappa B (NF-kB), Heat-schock 90β (HSP90β) signal pathways and E-cadherin cell adhesion molecule on infertility in diabetic rat testicular tissue. In our study, includes histological, molecular and biochemical analysis of testicular tissue removed at the end of the 2 weeks experiment period. A total of 14 adult male rats were divided as control and diabetes. No intervention was given to 7 male rats in the control group. For the diabetic group, 7 male rats were injected by intraperitoneal with a single dose of 55 mg/kg streptozotocin (STZ). TGFβ, NF-kB, HSP90β and E-cadherin proteins were immunohistochemically studied to investigate possible tissue damage, inflammatory process, cell stabilization and integrity due to diabetes. In order to determine oxidant stress, lipid peroxidation product malondialdehyde (MDA), glutathione (GSH) and glutathione peroxidase (GPx) analyzes were performed. Fibrosis, inflammatory changes and loss of spermatogenetic series are prominent findings in the diabetic group. On analysis of all the samples with immunostaining, in the diabetic group, TGFβ and NF-kB immunoexpression significantly increased, while Hsp90β and E-cadherin immunoexpression significantly decreased compared with control groups. Experimental diabetes was found to cause fibrosis, inflammation, disrupting cell adhesion and stabilization in testicular tissue. These results suggest that cellular therapy studies are needed for possible damage.

RESUMEN: La diabetes es una enfermedad metabólica caracterizada por niveles altos de azúcar en sangre y causa complicaciones en muchos sistemas, incluido el sistema reproductivo. Como resultado de las condiciones diabéticas, uno de los mecanismos que puede causar alteraciones en la actividad reproductiva es el estrés oxidativo testicular. La identificación de la diabetes en el eje de las moléculas de señalización celular aún está en discusión. El objetivo de este estudio fue determinar el efecto del factor de crecimiento transformante (TGFβ), el factor nuclear kappa B (NF-kB), las vías de señalización de Heat-Schock 90b (HSP90β) y la molécula de adhesión celular de E-cadherina sobre la infertilidad en testículo de rata diabética. Al término de dos semanas se realizaron análisis histológico, molecular y bioquímico del tejido testicular extraído. Las 7 ratas macho del grupo control no fueron intervenidas. Para el grupo de diabéticos, 7 ratas macho fueron inyectadas por vía intraperitoneal con una dosis única de 55 mg / kg de estreptozotocina (STZ). Se estudiaron inmunohistoquímicamente las proteínas TGFβ, NF-kB, HSP90β y E-cadherina para investigar el posible daño tisular, el proceso inflamatorio, la estabilización celular y la integridad debido a la diabetes. Para determinar el estrés oxidativo, se realizaron análisis del producto de peroxidación lipídica malondialdehído (MDA), glutatión (GSH) y glutatión peroxidasa (GPx). La fibrosis, los cambios inflamatorios y la pérdida de series espermatogenéticas son hallazgos destacados en el grupo de ratas diabéticas. En el análisis de todas las muestras con inmunotinción, en el grupo diabético, la inmunoexpresión de TGFβ y NF-kB aumentó significativamente, mientras que la inmunoexpresión de Hsp90β y e-cadherina disminuyó significativamente en comparación con los grupos control. Se encontró que la diabetes experimental causa fibrosis, inflamación, alteración de la adhesión celular y estabilización en el tejido testicular. Estos resultados sugieren que son necesarios estudios de terapia celular para verificar posibles daños.

Association of HSP90B1 gene polymorphisms with systemic lupus erythemat-osus patients / 中国免疫学杂志

Objective:To explore the association of HSP90B1 gene polymorphisms with susceptibility of systemic lupus erythematosus(SLE) in Chinese Han population.Methods: We recruited 360 SLE patients from hospital as case group and selected 360 age- and sex-matched individuals without autoimmune diseases as control group.Multiplex SNaPshot was used for genotyp-ing.Benjamin-Hamburg(BH) method based on false discovery rate(FDR) standard was used for multiple testing correction.Results:The rs1165681 polymorphism(Crude OR=0.621,95% CI=0.450-0.856,P=0.004;Adjusted OR=0.619,95% CI=0.449-0.855,P=0.004) was significantly associated with SLE risk reduction in dominant model,and the rs10778306 polymorphism(crude OR=0.568, 95% CI=0.328-0.984,P=0.044;Adjusted OR=0.570,95% CI=0.329-0.988,P=0.045) and the rs2722188 polymorphism(Crude OR=0.227,95% CI=0.076-0.681,P=0.008;Adjusted OR=0.227,95% CI=0.076-0.682,P=0.008) were significantly associated with SLE risk reduction in recessive model.After adjustment using BH method,genotype distribution of rs1165681 was statistical difference in two groups(PBH= 0.044).Significant associations were found between four haplotypes of HSP90B1 gene CCATTAGGCAT (OR=0.323,95% CI=0.154-0.680,P=0.002),CCCTTAGGCAC(OR=1.324,95% CI=1.014-1.729,P=0.039),TCCCTAGTCGC (OR=0.465,95% CI=0.221-0.979,P=0.039)and TTCTCGGGCAT(OR=0.443,95% CI=0.224-0.875,P=0.016)and SLE risk.After adjustment using BH method,the frequency of CCATTAGGCAT distribution difference was statistically significant in two groups(PBH= 0.028),but there were no statistical difference in other haplotypes frequency distributions (P>0.05).Conclusion:HSP90B1gene polymorphisms may be associated with the susceptibility of SLE in Chinese Han population.