A critical review on plant annexin: Structure, function, and mechanism.

Plant annexins are evolutionary conserved protein family widely exist in almost all plant species, characterized by a shorter N-terminal region and four conservative annexin repeats. Plant annexins have Ca2+ channel-regulating activity and peroxidase as well as ATPase/GTPase activities, which give annexins functional specificity. They are widely involved in regulating diverse aspects of biochemical and cellular processes, plant growth and development, and responses to biotic and abiotic environmental stresses. Though many studies have reviewed the function of annexins, great progress have been made in the study of plant annexins recently. In this review, we outline the current understanding of basic properties of plant annexins and summarize the emerging advances in understanding the functional roles of annexins in plants and highlight the regulation mechanisms of annexin protein in response to stress especially to salt and cold stress. The interesting questions related to plant annexin that remain to be further elucidated are also discussed.

DMPE-PEG scaffold binding with TGF-ß1 receptor enhances cardiomyogenic differentiation of adipose-derived stem cells.

BACKGROUND: Heart failure has become a global health problem with increasing incidences worldwide. Traditional pharmacological treatments can delay but cannot reverse the underlying disease processes. The clinical application of myocardial tissue engineering represents a promising strategy because it features cell-based replacement therapies that replace partially or fully damaged cardiac tissues with in vitro-generated tissue equivalents. However, the effectiveness of this therapy is limited by poor viability and differentiation of the grafted cells. This limitation could be overcome by rapidly increasing the numbers of functional cardiomyocytes. In this study, we aimed to obtain functional myocardial tissue engineering seed cells with high proliferation and differentiation rates by combining 1,2-dimyristoyl-sn-glycero-3-phosphoethan-olamine-polyethylene glycol (DMPE-PEG) and recombinant transforming growth factor-ß1 receptor I (rTGF-ß1 RI), followed by binding to human adipose-derived stromal cells (hADSCs). METHODS: To induce higher expression level of TGF-ß1 RI, DMPE-PEG was inoculated with rTGF-ß1 RI to modify the surface of hADSCs. The differentiation ability and morphological characteristics of the modified hADSCs were examined in vitro and in vivo. RESULTS: The caridiomyocartic differentiation ability of TGF-ß1 RI-modified hADSCs was significantly enhanced, as indicated by elevated expression levels of the cardiac markers cardiac troponin T (cTnT) and α-smooth muscle actin (SMA) via increased phosphorylation of the Smad signaling pathway-related proteins. CONCLUSION: Our findings provide new insights into stem cell transplantation therapy in myocardial tissue engineering.

Association between connexin 40 and potassium voltage-gated channel subfamily A member 5 expression in the atrial myocytes of patients with atrial fibrillation.

Structural and electrical remodeling within the atrium mediate the pathogenesis of atrial fibrillation (AF). Two key genes that sever a role in this remodeling are connexin 40 (Cx40) and potassium voltage-gated channel subfamily A member 5 (KCNA5), respectively. Electrical remodeling is considered to induce structural remodeling during AF. In the present study, the left atrial appendage section and atrial myocytes of patients with AF were evaluated. It was observed that Cx40 and KCNA5 mRNA (P<0.05) and protein (P<0.01) expression was significantly downregulated in AF compared with rheumatic heart disease. In addition, a positive correlation between the mRNA expression Cx40 and KCNA5 was observed in the atrial myocytes of patients with AF (P<0.05; r=0.42). The association between Cx40 and KCNA5 expression was subsequently investigated in primary cultured atrial myocytes using siRNA transfection. In atrial myocytes, downregulation of Cx40 inhibited the expression of KCNA5. Similarly, silencing of KCNA5 suppressed the expression of Cx40. These results indicate that synergistic regulation may occur between Cx40 and KCNA5 expression. Furthermore, the combined effects of electrical and structural remodeling in the atrial myocytes of patients with AF may contribute to the pathogenesis of AF.