Intermediate-conductance Ca2+-activated K+channel:research advances / 国际药学研究杂志

Intermediate-conductance Ca2+-activated K+channel ,also known as KCa3.1,IKCa and SK4,is widely distributed in fibroblasts,proliferating smooth muscle cells,endothelial cells,T lymphocytes,plasma cells,macrophages,and epithelial cells, and involved in the pathological and physiological processes such as vascular contraction,inflammation ,calcification,tissue fibrosis, immune response,malignant tumor,internal and external secretory glands. In recent years,it has been found that blocking the KCa3.1 pathway or knockouting the gene can significantly prevent the pathophysiological process of its involvement. The recent use of the specific blocker TRAM-34 in animals and humans shows its safety and tolerability,providing a new direction for the treatment of related diseases. In this article,the research progress in KCa3.1 related diseases in recent years is reviewed.

Activation of TGR5 reduces high glucose-induced cardiomyocyte hyper-trophy by inhibiting CaN/NFAT3 signaling / 中国病理生理杂志

AIM: To investigate the role of G-protein-coupled bile acid receptor 1 ( GPBR1; also known as TGR5) activation in high glucose-induced cardiomyocyte hypertrophy and calcineurin (CaN)/nuclear factor of activated T-cells 3 (NFAT3) signaling.METHODS:Primarily cultured mouse cardiomyocytes were used in the study .The cell surface areas of the cardiomyocytes were measured by an image analysis system .The cell protein content was detected by BCA meth-od.The expression of TGR5, CaN and NFAT3 at mRNA and protein levels was determined by RT-PCR and Western blot . RESULTS:The mouse cardiomyocytes were successfully cultured .High glucose significantly induced the increases in the cell surface area, the cell protein content and the expression of CaN and NFAT 3 (P<0.05) in the cardiomyocytes.TGR5 activation or a CaN antagonist cyclosporin A inhibited high glucose-induced cardiomyocyte hypertrophy and the expression of CaN and NFAT3 (P<0.05).These effects of TGR5 activation were abolished by TGR5 gene interference (P<0.05). CONCLUSION:TGR5 activation reduces high glucose-induced cardiomyocyte hypertrophy by inhibiting CaN /NFAT3 sig-naling.

An improved method for primary culture of neonatal mouse cardiomyocytes / 中国比较医学杂志

Objective To establish a stable and fast method for primary culture of mouse cardiomyocytes. Methods Dishes were coated with polylysine firstly.A two-step approach was used to isolate and digest mouse cardiomyocytes cells (0.25%trypsin in 4°C overnight and 0.5 mg/mL to 1.0 mg/mL collagenase +5 mg/mL albumin collagen digestion liquid in 37°C for short-time digestion), then the cardiomyocytes were purified through differential adhesion for 70 min and 5-bromodeoxyuridine ( BrdU) .The cell morphology was observed under an inverted microscope. The survival rate of cardiacmyocytes was detected by trypan-blue staining and their purity was identified by α-actinin immunofluorescence staining.Results The cardiomyocytes were in good shape and pulsed spontaneously.The survival rate of the cardiomyocytes reached 98%and the purity was 95%.Conclusions This method described in this study is an ideal method for primary culture of mouse cardiomyocytes with a high survival rate and high purity.