Long noncoding RNA NEAT1/microRNA-125a axis predicts increased major adverse cardiac and cerebrovascular event risk independently in patients with unprotected left main coronary artery disease underwent coronary artery bypass grafting.

BACKGROUND: The study aimed to investigate the long noncoding RNA nuclear-enriched abundant transcript 1 (lnc-NEAT1) and microRNA-125a (miR-125a) expressions, and further explore the role of lnc-NEAT1/miR-125a axis in predicting major adverse cardiac and cerebrovascular event (MACCE) risk in patients with unprotected left main coronary artery disease (ULMCAD) underwent coronary artery bypass grafting (CABG). METHODS: A total of 280 patients with ULMCAD underwent CABG were consecutively enrolled in our prospective study, and their plasma samples were collected before CABG for the detection of lnc-NEAT1 and miR-125a expressions by reverse transcription quantitative polymerase chain reaction. Lnc-NEAT1/miR-125a axis was calculated via dividing lnc-NEAT1 by miR-125a. After CABG, regular follow-up was continued until MACCE occurrence or 36 months. RESULTS: Lnc-NEAT1 expression, miR-125a expression, and lnc-NEAT1/miR-125a axis were 0.998 (IQR: 0.440-1.720, range: 0.116-5.771), 0.997 (IQR: 0.461-1.650, range: 0.055-3.621), and 1.018 (IQR: 0.384-2.782, range: 0.041-52.832), respectively. And lnc-NEAT1 was negatively associated with miR-125a. The 1-, 2-, and 3-year MACCE occurrence was 19 (6.8%), 29 (10.4%), and 38 (13.6%), respectively. Lnc-NEAT1/miR-125a axis (χ2  = 11.207, P = .001) and lnc-NEAT1 expression (χ2  = 5.345, P = .021) positively associated with accumulating MACCE occurrence, while miR-125a expression (χ2  = 5.869, P = .015) negatively correlated with accumulating MACCE occurrence. Notably, lnc-NEAT1/miR-125a axis presented numerically better predictive value compared with lnc-NEAT1 or miR-125a alone for MACCE risk. Furthermore, lnc-NEAT1/miR-125a axis high, elderly age, increased BMI, diabetes, previous stroke, LVEF, and higher disease extent (all P < .05) were independent predictive factors for increased accumulating MACCE occurrence. CONCLUSION: Lnc-NEAT1/miR-125a axis, as a combined index, presents potential value to be a prognostic biomarker for MACCE risk in ULMCAD management.

miR167d-ARFs Module Regulates Flower Opening and Stigma Size in Rice.

Flower opening and stigma exertion are two critical traits for cross-pollination during seed production of hybrid rice (Oryza sativa L.). In this study, we demonstrate that the miR167d-ARFs module regulates stigma size and flower opening that is associated with the elongation of stamen filaments and the cell arrangement of lodicules. The overexpression of miR167d (OX167d) resulted in failed elongation of stamen filaments, increased stigma size, and morphological alteration of lodicule, resulting in cleistogamy. Blocking miR167d by target mimicry also led to a morphological alteration of the individual floral organs, including a reduction in stigma size and alteration of lodicule cell morphology, but did not show the cleistogamous phenotype. In addition, the four target genes of miR167d, namely ARF6, ARF12, ARF17, and ARF25, have overlapping functions in flower opening and stigma size. The loss-of-function of a single ARF gene did not influence the flower opening and stigma size, but arf12 single mutant showed a reduced plant height and aborted apical spikelets. However, mutation in ARF12 together with mutation in either ARF6, ARF17, or ARF25 led to the same defective phenotypes that were observed in OX167d, including the failed elongation of stamen filaments, increased stigma size, and morphological alteration of lodicule. These findings indicate that the appropriate expression of miR167d is crucial and the miR167d-ARFs module plays important roles in the regulation of flower opening and stigma size in rice.

Peroxisome proliferator-activated receptor-gamma activation attenuates diabetic cardiomyopathy via regulation of the TGF-ß/ERK pathway and epithelial-to-mesenchymal transition.

Diabetic cardiomyopathy (DCM) is a kind of disease caused by metabolic disorders and microangiopathy. The main pathophysiological changes of DCM include fibrosis, myocardial cell apoptosis and autonomic neuropathy. Therefore, treatment aimed at these processes may benefit patients with DCM. We designed an experiment with the peroxisome proliferator-activated receptor-gamma (PPARγ) agonist GW 1929 to detect whether the activation of PPARγ could alleviate the degree of DCM. To further detect the mechanism of PPARγ in DCM, we used the PPARγ antagonist GW 9662 and ERK antagonist PD 098059 both in vitro and in vivo and found that PPARγ functioned by inhibiting ERK. We also performed Western blot, PCR, ELISA, immunohistochemistry, TUNEL assay, Sirius red staining and gelatin zymography to investigate inflammation, apoptosis, MMP activity and epithelial-to-mesenchymal transition (EMT). The results showed that the activation of PPARγ inhibited these reactions and inhibiting ERK also simulated this phenomenon. In conclusion, these results demonstrated that PPARγ activation in the diabetic myocardium of mice reduces myocardial fibrosis via regulation of the TGF-ß/ERK pathway and EMT.