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Genetics and pathophysiology of mammalian sulfate biology

Journal of Genetics and Genomics 2017年第1期44卷 7-20页

作者： rachel langford Elizabeth Hurrion Paul A. Dawson Mater Research Institute University of Queensland Woolloongabba 4102 Queensland Australia Mater Mothers' Hospital South Brisbane 4101 Queensland Australia

Nutrient sulfate is essential for numerous physiological functions in mammalian growth and development. Accordingly, disruptions to any of the molecular processes that maintain the required biological ratio of sulfonated and unconjugated substrates are likely to have detrimental consequences for mammalian physiology. Molecular processes of sulfate biology can be broadly grouped into four categories： firstly, intracellular sulfate levels are maintained by intermediary metabolism and sulfate transporters that mediate the transfer of sulfate across the plasma membrane; secondly, sulfate is converted to 3＇-phosphoadenosine 5＇-phosphosulfate （PAPS）, which is the universal sulfonate donor for all sulfonation reactions; thirdly, sulfotransferases mediate the intracellular sulfonation of endogenous and exogenous substrates; fourthly, sulfate is removed from substrates via sulfatases. From the literature, we curated 91 human genes that encode all known sulfate transporters, enzymes in pathways of sulfate generation, PAPS synthetases and transporters, sulfotransferases and sulfatases, with a focus on genes that are linked to human and animal pathophysiology. The predominant clinical features linked to these genes include neurological dysfunction, skeletal dysplasias, reduced fecundity and reproduction, and cardiovascular pathologies. Collectively, this review provides reference information for genetic investigations of perturbed mammalian sulfate biology.

关键词： Sulfate Pathogenetics Transport Sulfotransferase Sulfatase PAPS

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Advanced bioactive glue tethering Lubricin/PRG4 to promote integrated healing of avascular meniscus tears

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Bioactive Materials 2023年第10期28卷 61-73页

作者： Solaiman Tarafder Jaskirti Ghataure David langford rachel Brooke Ryunhyung Kim Samantha Lewis Eyen Julian Bensadoun Jeffrey T.Felix James L.Cook Chang H.Lee Regenerative Engineering Laboratory Columbia University Medical Center630 W.168 St.-VC12-212New YorkNY10032USA Thompson Laboratory for Regenerative Orthopaedics Missouri Orthopedic InstituteUniversity of Missouri1100 Virginia AvenueColumbi1MO65212USA

Meniscus injuries are extremely common with approximately one million patients undergoing surgical treatment annually in the U.S. alone, but no regenerative therapy exist. Previously, we showed that controlled applications of connective tissue growth factor (CTGF) and transforming growth factor beta 3 (TGFβ3) via fibrin-based bio-glue facilitate meniscus healing by inducing recruitment and stepwise differentiation of synovial mesenchymal stem/progenitor cells. Here, we first explored the potential of genipin, a natural crosslinker, to enhance fibrin-based glue’s mechanical and degradation properties. In parallel, we identified the harmful effects of lubricin on meniscus healing and investigated the mechanism of lubricin deposition on the injured meniscus surface. We found that the pre-deposition of hyaluronic acid (HA) on the torn meniscus surface mediates lubricin deposition. Then we implemented chemical modifications with heparin conjugation and CD44 on our bioactive glue to achieve strong initial bonding and integration of lubricin pre-coated meniscal tissues. Our data suggested that heparin conjugation significantly enhances lubricin-coated meniscal tissues. Similarly, CD44, exhibiting a strong binding affinity to lubricin and hyaluronic acid (HA), further improved the integrated healing of HA/lubricin pre-coated meniscus injuries. These findings may represent an important foundation for developing a translational bio-active glue guiding the regenerative healing of meniscus injuries.

关键词： Knee meniscus Bioactive glue Stem cell recruitment Lubricin

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