@article {70354,
	title = {Luminal surface proteome of the brain vasculature uncovers blood-brain barrier regulators.},
	journal = {Science},
	volume = {392},
	year = {2026},
	month = {2026 Apr 09},
	pages = {eaea2100},
	abstract = {<p>At the blood-tissue interface, vasculature luminal surface is critical for molecular transport, signaling transduction, and cell extravasation. Here, we present a method for proteomic profiling of the vasculature luminal surface in vivo, broadly applicable to any vertebrate. Quantitative mass spectrometry revealed the luminal surface proteome of the mouse brain vasculature and its temporal evolution from development to aging. In vivo genetic perturbation found that the arginine transporter SLC7A1 and the nitric oxide synthase NOS3 are needed for blood-brain barrier integrity in neonatal but not adult mice, whereas the hyaluronan degradation enzyme HYAL2 safeguards the barrier throughout the lifespan. By characterizing the proteomic dynamics of the vasculature luminal surface, the study links the metabolism of nitric oxide and hyaluronan to blood-brain barrier integrity.</p>
},
	keywords = {Aging, Animals, Blood-Brain Barrier, Brain, Cell Adhesion Molecules, Hyaluronic Acid, Mice, Nitric Oxide, Nitric Oxide Synthase Type III, Proteome, Proteomics},
	issn = {1095-9203},
	doi = {10.1126/science.aea2100},
	url = {https://doi.org/10.1126/science.aea2100},
	author = {Zhu, Zijian and Jiang, Zuzhi and Wang, Yupu and Nguyen, Khanh and Zhang, Yuxiang and Lian, Cameron Genxuan and Mani, D R and Zheng, Jun and Ding, Lang and Gao, Shihong Max and Xia, Ruyue Alps and Kuszpit, Anne and Lindo, Sarah and Lopez, Crystall and Lindsey, Catherine and Groff, Brooke and Chen, Xinhong and Wu, Jiahui and Xia, Weiliang and Li, Wei and Liu, Xiaorong and Gradinaru, Viviana and Carr, Steven A and Udeshi, Namrata D and Li, Jiefu}
}
@article {70184,
	title = {Chemical modulation of gut bacterial metabolism induces colanic acid and extends the lifespan of nematode and mammalian hosts.},
	journal = {PLoS Biol},
	volume = {23},
	year = {2025},
	month = {2025 Nov 11},
	pages = {e3002749},
	abstract = {<p>Microbiota-derived metabolites have emerged as key regulators of longevity. The metabolic activity of the gut microbiota, influenced by dietary components and ingested chemical compounds, profoundly impacts host fitness. While the benefits of dietary prebiotics are well-known, chemically targeting the gut microbiota to enhance host fitness remains largely unexplored. Here, we report a novel chemical approach to induce a pro-longevity bacterial metabolite in the host gut. We discovered that wild-type Escherichia coli strains overproduce colanic acids (CAs) when exposed to a low dose of cephaloridine, leading to an increased life span in the host organism Caenorhabditis elegans. In the mouse gut, oral administration of low-dose cephaloridine induced transcription of the capsular polysaccharide synthesis (cps) operon responsible for CA biosynthesis in commensal E. coli at 37 {\textdegree}C, and attenuated age-related metabolic changes. We also found that low-dose cephaloridine overcomes the temperature-dependent inhibition of CA biosynthesis and promotes its induction through a mechanism mediated by the membrane-bound histidine kinase ZraS, independently of cephaloridine{\textquoteright}s known antibiotic properties. Our work lays a foundation for microbiota-based therapeutics through chemical modulation of bacterial metabolism and highlights the promising potential of leveraging bacteria-targeting drugs in promoting host longevity.</p>
},
	keywords = {Animals, Caenorhabditis elegans, Escherichia coli, Gastrointestinal Microbiome, Longevity, Mice, Polysaccharides},
	issn = {1545-7885},
	doi = {10.1371/journal.pbio.3002749},
	url = {https://doi.org/10.1371/journal.pbio.3002749},
	author = {Hu, Guo and Savini, Marzia and Cooke, Matthew Brandon and Wei, Xin and Deng, Dinghuan and Gao, Shihong M and Xia, Ruyue Alps and Guan, Youchen and Wen, Alice X and Yu, Xin and Wang, Jin and Jiang, Chao and Herman, Christophe and Li, Jiefu and Wang, Meng C}
}
