Long-term effects of sprint interval training on expression of cardiac genes involved in energy efficiency

Purpose

The real mechanisms of intensive exercise training-induced energy efficiency have not yet been well examined. Therefore, the aim of the present study was to investigate the effects of sprint interval training (SIT) on gene expression of uncoupling proteins (UCPs) and endothelial nitric oxide synthase (eNOS).

Methods

For this purpose, 16 Albino Wistar rats (250–300 g) were randomly divided into equal groups of control and sprint training. The animals run on treadmill for 10 weeks, 5 days per week at intensity corresponding to 90–95% maximal oxygen consumption. The gene expression of UCP2, UCP3 and eNOS was analyzed by RT-PCR method in hearts. The data were analyzed by independent samples T test at P?<?0.05 level.

Results

Sprint interval training significantly decreased mRNA expression of UCP2 (t₁₄?=?4.818, P?=?0.001) and UCP3 (t₁₄?=?4.620, P?=?0.001) in cardiac muscle of rats. In contrast, mRNA expression of eNOS in cardiac muscle significantly increased following sprint interval training (t₁₄?=?7.967, P?=?0.001).

Conclusion

This study elucidates that SIT through reduction in gene expression of uncoupling proteins can improve energy efficiency. But, more studies are needed to confirm this hypothesis.

     

Used protocols for isolation and propagation of ovarian stem cells,different cells with different traits

Although existence of ovarian stem cells (OSCs) in mammalian postnatal ovary is still under controversy, however, it has been almost accepted that OSCs are contributing actively to folliculogenesis and neo-oogenesis. Recently, various methods with different efficacies have been employed for OSCs isolation from ovarian tissue, which these methods could be chosen depends on aim of isolation and accessible equipments and materials in lab. Although isolated OSCs from different methods have various traits and characterizations, which might become from their different nature and origin, however these stem cells are promising source for woman infertility treatment or source of energy for women with a history of repeat IVF failure in near future. This review has brought together and summarized currently used protocols for isolation and propagation of OSCs in vitro.     

Therapeutic potential of bevacizumab (Avastin) in herpetic stromal keratitis (HSK)

In the stromal keratitis caused by herpes simplex virus (HSV), the formation of new vessels is the essential step for the pathogenesis of keratitis. Inhibition of angiogenesis diminishes the formation of corneal lesion induced by HSV. Procedures which suppress angiogenesis are proposed as a valuable therapeutic approach to control HSK. The mechanism by which HSV ocular infection results in corneal angiogenesis is not understood. Recent reports identified anti-vascular endothelial growth factor (VEGF) as a molecule that is highly expressed in the HSV infected eye and clearly involved in angiogenesis. The advent of VEGF treatments marks a major advancement in the treatment of angiogenic eye disease. Off-label use of bevacizumab (Avastin), a recombinant humanized monoclonal antibody directed against VEGF, in some neovascular disorders of the eye has been associated with promising short term results. Based on these evidences herein we hypothesize topical application of bevacizumab could inhibit corneal neovascularization and also scarring in HSK. We propose this drug as a novel adjunct to current anti-inflammatory strategies in HSK.     

Effects of JC virus infection on anti-apoptotic protein survivin in progressive multifocal leukoencephalopathy

Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease of the central nervous system resulting from the productive infection of oligodendrocytes by the opportunistic polyomavirus JC virus (JCV). Apoptosis is a host defense mechanism to dispose of damaged cells; however, certain viruses have the ability to deregulate apoptotic pathways to complete their life cycles. One such pathway involves survivin, a member of the inhibitor of apoptosis family, which is abundantly expressed during development in proliferating tissues but should be absent in normal, terminally differentiated cells. Immunohistochemistry performed in 20 cases of PML revealed the presence of survivin in JCV-infected oligodendrocytes and bizarre astrocytes within demyelinated plaques. Survivin up-regulation was also found in oligodendroglial and astrocytic cultures infected with JCV. Cell cycle analysis and DNA laddering demonstrated a significantly lower number of cells undergoing apoptosis on JCV infection compared with noninfected cultures; small interfering RNA inhibition of survivin resulted in a dramatic increase in apoptotic cells in JCV-infected cultures. This is the first report describing the activation of survivin by JCV infection in vitro and in PML clinical cases. These observations provide new insights into the anti-apoptotic mechanisms used by JCV to complete its lytic cycle and may suggest new therapeutic targets for PML.