Overexpression of chromodomain helicase DNA binding protein 5 (CHD5) inhibits cell proliferation and induces cell cycle arrest and apoptosis in chronic myeloid leukemia.

Background: Chromodomain helicase DNA binding protein 5 (CHD5) was reported to be a tumor suppressor and our previous work showed CHD5 was epigenetically inactivated in human chronic myeloid leukemia (CML). This study aimed to investigate the effect of its overexpression on CML tumorigenesis.

Methods: Quantitative reverse-transcriptase PCR and Western blotting analysis were used to detect the expression of CHD5 in human CML cell lines.

Chromodomain Helicase DNA-Binding Protein 5 Inhibits Renal Cell Carcinoma Tumorigenesis by Activation of the p53 and RB Pathways.

Chromodomain helicase DNA-binding protein 5 (CHD5) plays a crucial tumor suppressor role in multiple types of tumors. For this study, we investigated its clinical significance and the molecular mechanism(s) underlying tumorigenesis in renal cell carcinoma (RCC). Initially, CHD5 expression was assessed in primary tumor tissue and in tissue array.

Grape seed proanthocyanidin extract protects lymphocytes against histone-induced apoptosis.

Apoptosis of lymphocytes is associated with immunosuppression and poor prognosis in sepsis. Our previous report showed that histones, nuclear proteins released from damaged or dying cells in sepsis, can mediate lymphocyte apoptosis via mitochondria damage. Grape seed proanthocyanidin extract (GSPE), a natural substance with protective properties against oxidative stress, plays a vital role in cell and mitochondria protection.

MiR-344b-1-3p targets TLR2 and negatively regulates TLR2 signaling pathway.

Objectives: COPD is an abnormal inflammatory response characterized by decreased expression of TLR2 in patients, which is suggested to induce invasive pulmonary aspergillosis (IPA). MicroRNAs (miRNAs) have been shown to play important roles in the pathogenesis of human respiratory system disorders. Therefore, the aim of this study was to identify the miRNAs involved in the regulation of TLR2 signaling in COPD.

Effect of SQW on the bladder function of mice lacking TRPV1.

Background: Suo Quan Wan (SQW) is an effective traditional Chinese prescription on treated lower urinary tract symptoms (LUTS), and has been proved have modulation effect on the expression of transient receptor potential vanilloid 1 (TRPV1) in accordance with the recovery of bladder function of overactive bladder rat. This study further investigated the mechanism of SQW modulated TRPV1 signaling and bladder function using TRPV1 knockout (KO) mice.

Methods: Study was conducted using wild type and TRPV1 KO mice.

Effect of the Chinese traditional prescription Suo Quan Wan on TRPV1 expression in the bladder of rats with bladder outlet obstruction.

Background: Suo Quan Wan (SQW) is a Chinese traditional prescription that has been used in clinical treatment of lower urinary tract symptoms for centuries. However, scientific basis of SQW efficacy and mechanism is still needed. This study investigated the effect of SQW on bladder function and transient receptor potential vanilloid 1 (TRPV1) expression in the bladder of rats with bladder outlet obstruction (BOO).

CHD5 a tumour suppressor is epigenetically silenced in hepatocellular carcinoma.

Background: Chromodomain helicase DNA binding protein 5 (CHD5) has recently been identified as a potent tumour suppressor by acting as a master regulator of a tumour-suppressive network. Its inactivation resulted from aberrant methylation in the promoter occurs in several types of human malignancy and is associated with malignant tumour behaviour. In human hepatocellular carcinoma (HCC), CHD5 gene expression, methylation status and tumour-suppressive function have not been elucidated.

Silencing of CHD5 gene by promoter methylation in leukemia.

Chromodomain helicase DNA binding protein 5 (CHD5) was previously proposed to function as a potent tumor suppressor by acting as a master regulator of a tumor-suppressive network. CHD5 is down-regulated in several cancers, including leukemia and is responsible for tumor generation and progression. However, the mechanism of CHD5 down-regulation in leukemia is largely unknown.

Transdermal siRNA-TGFβ1-337 patch for hypertrophic scar treatment.

Hypertrophic scarring (HSc) is a fibroproliferative disorder of the dermis characterized by erythematous, swollen, and pruritic lesions of healing skin. An increased understanding of the role of TGFβ1 in the development of HSc provides the potential for treating HSc by down-regulating TGFβ1 expression. siRNAs that effectively interfered with TGFβ1 expression were screened.

CHD5, a tumor suppressor that is epigenetically silenced in lung cancer.

Chromodomain helicase DNA binding protein 5 (CHD5) is a potent tumor suppressor that serves as a master regulator of a tumor-suppressive network. Examination of the role played by CHD5 in a wide range of human cancers is warranted. In this study, we focused on the epigenetic modification and tumor-suppressive role of CHD5 in lung cancer.

[Protective effects of nicotine on inflammatory cytokines in myocardial ischemia/reperfusion injury in rats].

Objective: To investigate the effect of nicotine on inflammatory cytokines in myocardial ischemia/reperfusion (I/R) injury in rat.

Methods: Fifty male Sprague-Dawley (SD) rats were divided into five groups by random numbers table (each n=10): sham operation group (S group), I/R group, nicotine 400 μg/kg group (H group), nicotine 40 μg/kg group (L group) and α-bungarotoxin (α-BGT,1 μg/kg) group. The anterior descending branch of left coronary artery was occluded for 30 minutes followed by 90 minutes reperfusion to reproduce myocardial I/R injury rat model, while in S group the anterior descending branch of left coronary artery was only exposed without occlusion procedure.

Generation of an external guide sequence library for a reverse genetic screen in Caenorhabditis elegans.

Background: A method for inhibiting the expression of particular genes using external guide sequences (EGSs) has been developed in bacteria, mammalian cells and maize cells.

Results: To examine whether EGS technology can be used to down-regulate gene expression in Caenorhabditis elegans (C. elegans), we generated EGS-Ngfp-lacZ and EGS-Mtgfp that are targeted against Ngfp-lacZ and Mtgfp mRNA, respectively.