Publications by authors named "Jiani Bei"
Article Synopsis
- The study focuses on how exosomes from Alzheimer's disease (AD) patients contribute to problems with the blood-brain barrier (BBB), particularly affecting the integrity of adherens junction proteins in brain microvascular endothelial cells (BMECs).
- Researchers isolated exosomes from the blood of AD patients and normal controls to investigate their effects, finding that AD exosomes reduced levels of VE-cadherin (a key protein for cell junctions) and weakened BBB integrity.
- Results showed that the damaging effects of AD exosomes on VE-cadherin were linked to their RNA content, and AD brains exhibited lower VE-cadherin levels compared to healthy controls, emphasizing the role of exosomal RNA
We previously reported that microRNA (miR)23a and miR30b are selectively sorted into exosomes derived from rickettsia-infected endothelial cells (R-ECExos). Yet, the mechanism remains unknown. Cases of spotted fever rickettsioses have been increasing, and infections with these bacteria cause life-threatening diseases by targeting brain and lung tissues.
View Article and Find Full Text PDFBackground: Blood-brain barrier (BBB) breakdown is a component of the progression and pathology of Alzheimer's disease (AD). BBB dysfunction is primarily caused by reduced or disorganized tight junction or adherens junction proteins of brain microvascular endothelial cell (BMEC). While there is growing evidence of tight junction disruption in BMECs in AD, the functional role of adherens junctions during BBB dysfunction in AD remains unknown.
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- Researchers found that specific microRNAs (miR23a and miR30b) are packed into exosomes from rickettsia-infected endothelial cells, but they're still uncovering how this happens.
- The study highlights that these exosomes disrupt important cell junctions in microvascular endothelial cells, leading to barrier dysfunction in lung cells, which can be harmful.
- Analysis revealed that these microRNAs are selectively enriched in the exosomes, indicating a potential link between their levels and the harmful effects caused by rickettsia infections.
Spotted fever group rickettsioses caused by () are devastating human infections, which mainly target microvascular endothelial cells (ECs) and can induce lethal EC barrier dysfunction in the brain and lungs. Our previous evidence reveals that exosomes (Exos) derived from rickettsialinfected ECs, namely -ECExos, can induce disruption of the tight junctional (TJ) protein ZO-1 and barrier dysfunction of human normal recipient brain microvascular endothelial cells (BMECs). However, the underlying mechanism remains elusive.
View Article and Find Full Text PDFIn this article, a review of a series of applications of atomic force microscopy (AFM) and fluidic Atomic Force Microscopy (fluidic AFM, hereafter fluidFM) in single-cell studies is presented. AFM applications involving single-cell and extracellular vesicle (EV) studies, colloidal force spectroscopy, and single-cell adhesion measurements are discussed. FluidFM is an offshoot of AFM that combines a microfluidic cantilever with AFM and has enabled the research community to conduct biological, pathological, and pharmacological studies on cells at the single-cell level in a liquid environment.
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- - The study investigates how intracellular cAMP receptor exchange proteins influence the ability of rickettsial bacteria to adhere to and invade vascular endothelial cells, aiming to clarify the mechanisms involved in this process.
- - Researchers utilized a unique in vivo system combined with fluidic force microscopy to analyze bacterial adhesion, finding that the absence of a specific gene significantly reduces rickettsial binding to endothelial cells.
- - Results indicated that rickettsial protein OmpB has variable binding strength depending on the host, and phosphorylation at a specific site (Y23) plays a crucial role in modulating this adhesion, suggesting that the cAMP signaling pathway is key in rickettsial infection.
Article Synopsis
- Coagulopathy, which involves problems with blood clotting, is linked to inflammation and infections like COVID-19 caused by SARS-CoV-2, indicating a complex relationship between these conditions.
- A protein called von Willebrand factor (vWF) is released during inflammation, and its secretion is regulated by EPAC1, an intracellular receptor that generally helps suppress inflammation.
- Studies using EPAC1-deficient mice showed that without EPAC1, there was increased vWF release during inflammation, suggesting that targeting EPAC1 could be a new approach to managing blood clotting issues associated with inflammatory conditions.
Article Synopsis
- Spotted fever group rickettsioses (SFRs) are severe infections primarily affecting vascular endothelial cells, leading to harmful edema in the brain and lungs.
- This study investigated the role of exosomes (Exos) derived from infected endothelial cells and mouse plasma in the dysfunction of brain microvascular endothelial cells (BMECs).
- Findings revealed that rickettsial infection increased the release of specific exosomes which negatively impacted BMEC barrier function, highlighting the importance of exosomal RNA cargo in this process.
Talin and vinculin, both actin-cytoskeleton-related proteins, have been documented to participate in establishing bacterial infections, respectively, as the adapter protein to mediate cytoskeleton-driven dynamics of the plasma membrane. However, little is known regarding the potential role of the talin-vinculin complex during spotted fever group rickettsial and Ebola virus infections, two dreadful infectious diseases in humans. Many functional properties of proteins are determined by their participation in protein-protein complexes, in a temporal and/or spatial manner.
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