cAMP/PKA诱导卵母细胞减数分裂停滞的机制

大多数物种的卵母细胞在减数分裂前都要经历长时间停滞,其中cAMP对卵母细胞减数分裂停滞具有重要作用,本研究关注c AMP对卵母细胞减数分裂的影响及其机制。本研究通过将卵母细胞与cAMP预孵育,再用胰岛素刺激研究胰岛素诱导的卵母细胞成熟的影响,接着本研究通过显微注射和Zeiss 100TV显微镜分析cAMP对PKA在卵母细胞中定位的影响,并且本研究用Western blotting的方法研究cAMP/PKA对mos蛋白的表达和MAPK蛋白磷酸化的影响。结果显示,本研究通过亲和层析得到了高纯度的PKA蛋白,且cAMP/PKA能够抑制卵母细胞的成熟,而PKA的热稳定抑制剂PKI能够解除PKA对卵母细胞减数分裂的抑制,cAMP/PKA也能够影响mos的积累以及MAPK的磷酸化。cAMP能够影响PKA在卵母细胞中的定位,cAMP/PKA能够通过影响mos积累抑制卵母细胞的减数分裂,这可能与cAMP能够抑制MAPK磷酸化有关。     

Dominance complementation of Hd1 and Ghd8 contributes to extremely late flowering in two rice hybrids

Molecular Breeding - Lack of seed dormancy, a major cause of pre-harvest sprouting in rice and other cereal crops, causes significant reductions in grain yield and quality. Weedy rice is often...     

Berberine ameliorates cellular senescence and extends the lifespan of mice via regulating p16 and cyclin protein expression

Although aging and senescence have been extensively studied in the past few decades, however, there is lack of clinical treatment available for anti‐aging. This study presents the effects of berberine (BBR) on the aging process resulting in a promising extension of lifespan in model organisms. BBR extended the replicative lifespan, improved the morphology, and boosted rejuvenation markers of replicative senescence in human fetal lung diploid fibroblasts (2BS and WI38). BBR also rescued senescent cells with late population doubling (PD). Furthermore, the senescence‐associated β‐galactosidase (SA‐β‐gal)‐positive cell rates of late PD cells grown in the BBR‐containing medium were ~72% lower than those of control cells, and its morphology resembled that of young cells. Mechanistically, BBR improved cell growth and proliferation by promoting entry of cell cycles from the G₀ or G₁ phase to S/G₂‐M phase. Most importantly, BBR extended the lifespan of chemotherapy‐treated mice and naturally aged mice by ~52% and ~16.49%, respectively. The residual lifespan of the naturally aged mice was extended by 80%, from 85.5 days to 154 days. The oral administration of BBR in mice resulted in significantly improved health span, fur density, and behavioral activity. Therefore, BBR may be an ideal candidate for the development of an anti‐aging medicine.     

Circular RNA ciRS‐7 promotes tube formation in microvascular endothelial cells through downregulation of miR‐26a‐5p

Atherosclerosis is one of the most common and crucial heart diseases involving the heart and brain. At present, atherosclerosis and its major complications comprise the leading causes of death worldwide. Our purpose was to identify the role of ciRS‐7 in atherosclerosis. Tubulogenesis of HMEC‐1 cell was evaluated utilizing tube formation assay. Cell Counting Kit‐8 assay and flow cytometry were utilized to test viability and apoptosis. Migration assay was utilized to determine the migration capacity of experimental cells. Western blot was applied to examine apoptosis and tube formation‐associated protein expression. In addition, the above experiments were repeated when silencing ciRS‐7, overexpressing ciRS‐7, and upregulating miR‐26a‐5p. HMEC‐1 cells formed tube‐like structures over time. Silencing ciRS‐7 suppressed viability, migration, and tube formation but promoted apoptosis. Oppositely, overexpressing ciRS‐7 reversed the effect in HMEC‐1 cells. miR‐26a‐5p expression was elevated by silencing ciRS‐7 and reduced by overexpressing ciRS‐7. Moreover, overexpressing ciRS‐7 facilitated viability, migration, and tube formation via upregulating miR‐26a‐5p. Conclusively, overexpressing ciRS‐7 mobilized phosphoinositide 3‐kinase/protein kinase B (PI3K/AKT) pathway and suppressed c‐Jun N‐terminal kinase (JNK)/p38 pathway. ciRS‐7 exerted influence on apoptosis, viability, migration, and tube formation through mediating PI3K/AKT and JNK/p38 pathways by miR‐26a‐5p downregulation in HMEC‐1 cells.