Biology subjects

Lian, P.

Publications and source records attributed to Lian, P..

3 recordsLinked to original sources

bioRxiv2025

Radiation exposure induced blood-brain barrier injury via mitochondria-mediated sterile inflammation

Radiation-induced brain injury (RIBI) is caused by exposure to high doses of ionizing radiation and characterized by severe cognitive dysfunction and brain necrosis. The widespread application of radiotherapy and rapid development of deep space exploration have substantially increased the risk of RIBI. However, the pathogenesis of RIBI is not fully understood, and no effective intervention is available. This work described a blood-brain barrier (BBB) microphysiological system (MPS), that allowed to explore the responses of BBB and distinct brain cells to radiation exposure. This BBB MPS can recapitulate the interface structure and function of BBB in brain microenvironment, including brain endothelial cells, astrocytes, pericytes and microglia co-cultured under flow condition. Following acute exposure to radiation of X-ray or {gamma}-ray, characteristic RIBI-associated pathological responses were observed, including BBB compromise, DNA breaks, inhibited cell proliferation, cell hypertrophy and pro-inflammatory cytokine release. Among the distinctive types of cells, brain endothelial cells showed the highest radiosensitivity as compared to other cells in the MPS. Intriguingly, X-ray and {gamma}-ray radiation consistently induced prominent sterile inflammation responses, especially type I interferon response, in the BBB MPS. These responses were mediated by radiation-induced mitochondrial DNA release and subsequent activation of cGAS-STING signaling pathway. Furthermore, we found abrocitinib (JAK1 inhibitor) and idebenone (mitochondrial protectant) can attenuate radiation-induced inflammation and ameliorate BBB injury. These findings revealed the involvement of mitochondria-mediated inflammation in RIBI pathogenesis, identifying mitochondria as a potential target for new radioprotective measures.

neuroscience↗

bioRxiv2024

Exercise training at different intensities induces heat stress, disrupts barrier function and alters microbiota in the gut of mice

Exercise is generally beneficial for health but strenuous exercise can have detrimental effects on the gastrointestinal tract. The combination of ischemia and heat shock during exercise is a crucial contributor to intestinal epithelial damage. Growing evidence points towards an important regulatory role of gut microbes in intestinal homeostasis. Here, we characterize and compare the effects of moderate and vigorous exercise training on intestinal epithelial damage, stress response, inflammatory response, and gut microbiota alterations in mice and investigate the mechanisms underlying exercise-induced intestinal injury. Exercise training for six weeks caused heat stress in the intestine, resulting in the disruption of the intestinal epithelial barrier and local inflammation. This was characterized by increased colonic HSP-70 and HSF-1 protein expression, increased epithelial permeability, decreased colonic expression of tight junction proteins ZO-1 and occludin and intestinal morphological changes. Daily moderate exercise training caused hereby more severe injury than vigorous training on alternating days. Furthermore, exercise training altered the gut microbiota profile. The abundance of Lactobacillaceae was reduced, potentially contributing to the deteriorated intestinal status, while the abundance of short-chain fatty acid-producing Lachnospiraceae was increased, especially following vigorous training. This increase in short-chain fatty acid-producing bacteria following vigorous training possibly counteracted the impairment of the intestinal barrier function. In summary, exercise disrupts the intestinal barrier function, with vigorous exercise training with intermittent rest days being less damaging than daily moderate exercise training.

physiology↗

bioRxiv2019

Effects of a novel thermophilic cellulose-degrading agent on the quality of compost and change in microbial community of garden waste

Knowledge about the microbial communities in composting has advanced, but definitive knowledge concerning the application of actinomycetal communities in garden waste composting is still lacking. In this study, we compared the effects of amending compost with mixed agent M1 (five high-degradability strains) and other agents on the physicochemical indices and microbial community succession. The results showed that Pile A (only applying M1), exhibited a pH closer to neutral, the complete degradation of organic matter, and the highest remaining levels of nitrogen, phosphorus, and potassium. The seed germination rate, root length, and seed germination index values were significantly higher in piles amended with M1 and/or commercially available agents than in piles without exogenous microbial agents. Analyzing the microbial communities, these treatments were dominated by Proteobacteria, Firmicutes, Actinobacteria, and Bacteroidetes during composting. The amount of Streptomyces was negatively correlated with the carbon/nitrogen ratio and positively correlated with total phosphorus and total potassium. Adding M1 increased microbial diversity, and the dominant microbial communities at the end of composting were similar to those found in the commercial microbial inoculum. Overall, agent M1 can shorten the composting process and increase the extent of degradation. This research provides additional insights into the potential function of Actinomycetes in compost ecology.

microbiology↗