Pulmonary hypertension is a life-threatening medical condition, and a growing body of evidence shows that the expression of connective tissue growth factor (CTGF) is significantly associated with its pathogenesis, making it an attractive therapeutic target. Our earlier work revealed that plasmid-based CTGF-specific short hairpin RNA (shRNA) could attenuate pulmonary artery smooth muscle cell (PASMC) proliferation and pulmonary vascular remodeling in rats exposed to cigarette smoke. In this study, we explored the therapeutic role of this shRNA plasmid in the treatment of monocrotaline-induced pulmonary vascular remodeling in rats, and demonstrated that the upregulation of CTGF in PASMCs following a single injection of monocrotaline could be attenuated by administration of the shRNA. Accordingly, this shRNA was found to repress monocrotaline-induced pulmonary vascular remodeling, as evidenced by its ability to reduce the percentage of muscularized vessels and the wall thickness of pulmonary vessels. We concluded that plasmid-based shRNA against CTGF attenuated pulmonary vascular remodeling in monocrotaline-treated rats. CTGF might be a potential target for the treatment of pulmonary vascular remodeling and pulmonary hypertension.
Oxidative stress and disturbances of mitochondria function in the brain have been recognized to play a crucial role in the pathophysiological mechanism of Alzheimer’s Disease (AD). However, little is known about these changes at an early age of AD, which could be crucial for therapeutic strategy for the disease. In this study, we used biochemical, and quantitative polymerase chain reaction for determination of expression of genes encoding enzymes related to the antioxidative defence including Sirtuins (Sirts) and DNA-bound poly (ADP-ribose) polymerases (PARPs). Moreover, expression of genes related to mitochondrial dynamic, biogenesis and function in the brain cortex of 3- and 6-month-old FVB mice with London mutation (V7171) was analysed and compared with mice without transgene. Results indicated significant decreases in mRNA expression encoding SOD2, Sirt1 and PARP1 in the 3-month-old AD Tg mice and an increase in expression of PARP-1 in the 6-month-old AD Tg. Although levels of mRNA encoding subunits of mitochondrial respiratory complexes (I-III) were negligible altered, there was upregulation of gene encoding subunit of complex IV and proteins related to mitochondria biogenesis and dynamic, such as the Neuronal Respiratory Factors (NRF1) and NRF2, Opa1, Fis1, and Drp1 in the AD mice. Our data indicate downregulation of genes related to antioxidation and activation of genes encoding mitochondrial biogenesis and fission / fusion at early age of the AD mice. The ability to identify changes in gene expression for Sirt1, SOD2, Fis1 and Drp1 at an early age suggest potential therapeutic targets for retarding the pathological progression in AD.
We document the first report of Dissoconium proteae from China. This fungus was found on the cuticle of apple fruit collected from orchards in Shaanxi Province. Its morphology is compared with other Dissoconium species and a phylogenetic analysis based on ITS sequence
is presented.
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