A Pectate Lyase Gene Plays a Critical Role in Xylem Vascular Development in Arabidopsis.

As a major component of the plant primary cell wall, structure changes in pectin may affect the formation of the secondary cell wall and lead to serious consequences on plant growth and development. Pectin-modifying enzymes including pectate lyase-like proteins (PLLs) participate in the remodeling of pectin during organogenesis, especially during fruit ripening. In this study, we used Arabidopsis as a model system to identify critical PLL genes that are of particular importance for vascular development. Four PLL genes, named AtPLL15, AtPLL16, AtPLL19, and AtPLL26, were identified for xylem-specific expression. A knock-out T-DNA mutant of AtPLL16 displayed an increased amount of pectin, soluble sugar, and acid-soluble lignin (ASL). Interestingly, the atpll16 mutant exhibited an irregular xylem phenotype, accompanied by disordered xylem ray cells and an absence of interfascicular phloem fibers. The xylem fiber cell walls in the atpll16 mutant were thicker than those of the wild type. On the contrary, AtPLL16 overexpression resulted in expansion of the phloem and a dramatic change in the xylem-to-phloem ratios. Altogether, our data suggest that AtPLL16 as a pectate lyase plays an important role during vascular development in Arabidopsis.

Tanshinone IIA protects against chronic obstructive pulmonary disease via exosome­shuttled miR­486­5p.

Chronic obstructive pulmonary disease (COPD) is one of the major causes of death worldwide today, and its related morbidity has been predicted to show an increase in subsequent years. Recent studies have shown that Danshen, a Chinese herbal medicine, is a potential drug in the treatment of inflammation­related lung diseases. COPD was induced in this study using cigarette smoke (CS) exposure plus intranasal inhalation of lipopolysaccharide to ascertain whether the main pharmacological component from Danshen, tanshinone IIA (TIIA), and its water soluble form, sodium tanshinone IIA sulfonate (STS), protect against the development of COPD. The weight, lung function, hematoxylin and eosin staining, and Masson Trichrome determinations revealed that TIIA inhalation attenuated lung dysfunction in COPD mice induced by cigarette smoke and lipopolysaccharide exposure. In addition, exosomes derived from TIIA­treated COPD mice exerted similar protective effects against COPD, suggesting that TIIA may protect against COPD through exosome­shuttled signals. miR­486­5p was found to be a key molecule in mediating the protective effects of exosomes derived from TIIA­treated COPD mice using miRNA sequencing and cellular screening. Treatment of COPD mice with an agomiR of miR­486­5p protected lung function in COPD mice, and treatment of COPD mice with an antagomir of miR­486­5p abolished the protective effects of TIIA. Moreover, luciferase activity reporter assay, RT­qPCR, and western blot analyses showed that miR­486­5p exerted protective effects against COPD via targeting phosphoinositide­3­kinase regulatory subunit 1 (PIK3R1). These results suggest that STS protects against COPD through upregulation of miR­486­5p, and that TIIA or miR­486­5p is a potential drug for the treatment of COPD.