Knockdown of PLOD2 inhibits pulmonary artery smooth muscle cell glycolysis under chronic intermittent hypoxia via PI3K/AKT signal.

Objective: This study aimed to investigate the role and potential mechanism of procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (PLOD2) in chronic intermittent hypoxia (CIH)-induced mice and pulmonary arterial smooth muscle cells (PASMCs).

Methods: CIH mouse model was pre-injected with AAV-shPLOD2 by tail vein, and the pathological changes of lung was evaluated using hematoxylin-eosin (H&E) and α-SMA immunostaining. Enriched KEGG pathway analyses of PLOD2 targeted genes were performed using GSE11341 and GSE131425 datasets.

Chromogranin A deficiency in transgenic mice leads to aberrant chromaffin granule biogenesis.

The biogenesis of dense-core secretory granules (DCGs), organelles responsible for the storage and secretion of neurotransmitters and neuropeptides in chromaffin cells, is poorly understood. Chromogranin A (CgA), which binds catecholamines for storage in the lumen of chromaffin granules, has been shown to be involved in DCG biogenesis in neuroendocrine PC12 cells. Here, we report that downregulation of CgA expression in vivo by expressing antisense RNA against CgA in transgenic mice led to a significant reduction in DCG formation in adrenal chromaffin cells.

[The genetics of human monogenic obesity].

Obesity is a clinical syndrome caused by genetic and environmental factors and has a relatively high heretability. Seven genes, of whose mutations each can independently result in severe human obesity, have been cloned. Six of them are involved in the appetite controlling by the central nervous system, and one is related to the regulation of adipocyte differentiation.