Characterization of Dendrobium catenatum CBL-CIPK signaling networks and their response to abiotic stress.

Dendrobium catenatum is a traditional Chinese medicine listing as rare and endangered due to environmental impacts. But little is known about its stress resistance mechanism. The CBL-CIPK signaling pathway played vital roles in various stress responses. In this study, we identified 9 calcineurin B-like (CBL) genes and 28 CBL-interacting protein kinase (CIPK) genes from D. catenatum. Phylogenetic analysis showed that DcCBL and DcCIPK families could be divided into four and six subgroups, respectively. Members in each subgroup had similar gene structures. Cis-acting element analyses showed that these genes were involved in stress responses and hormone signaling. Spatial expression profiles showed that they were tissue-specific, and expressed lower in vegetative organs than reproductive organs. Gene expression analyses revealed that these genes were involved in drought, heat, cold, and salt responses and depended on abscisic acid (ABA) and salicylic acid (SA) signaling pathways. Furthermore, we cloned 19 DcCIPK genes and 9 DcCBL genes and detected ten interacting CBL-CIPK combinations using yeast two-hybrid system. Finally, we constructed 20 CBL-CIPK signaling pathways based on their expression patterns and interaction relationships. These results established CBL-CIPK signaling pathway responding to abiotic stress and provided a molecular basis for improving D. catenatum stress resistance in the future.

Traditional Chinese Medication Qiliqiangxin attenuates cardiac remodeling after acute myocardial infarction in mice.

In a multicenter randomized double-blind study we demonstrated that Qiliqiangxin (QLQX), a traditional Chinese medicine, had a protective effect in heart failure patients. However, whether and via which mechanism QLQX attenuates cardiac remodeling after acute myocardial infarction (AMI) is still unclear. AMI was created by ligating the left anterior descending coronary artery in mice. Treating the mice in the initial 3 days after AMI with QLQX did not change infarct size. However, QLQX treatment ameliorated adverse cardiac remodeling 3 weeks after AMI including better preservation of cardiac function, decreased apoptosis and reduced fibrosis. Peroxisome proliferator-activated receptor-γ (PPARγ) was down-regulated in control animals after AMI and up-regulated by QLQX administration. Interestingly, expression of AKT, SAPK/JNK, and ERK was not altered by QLQX treatment. Inhibition of PPARγ reduced the beneficial effects of QLQX in AMI remodeling, whereas activation of PPARγ failed to provide additional improvement in the presence of QLQX, suggesting a key role for PPARγ in the effects of QLQX during cardiac remodeling after AMI. This study indicates that QLQX attenuates cardiac remodeling after AMI by increasing PPARγ levels. Taken together, QLQX warrants further investigation as as a therapeutic intervention to mitigate remodeling and heart failure after AMI.