Guohao Dai
Dr. Dai is currently an Associate Professor in the Department of Biomedical Engineering at Rensselaer Polytechnic Institute. Dr. Dai graduated from Beijing University, China with B.S. in Mechanics and M.S. in Biomechanics. He received his Ph.D. in Biomedical Engineering from MIT’s HST Program (Harvard-MIT Division of Health Science and Technology). He then completed Post-doctoral training at Harvard Medical School (Center for Excellence in Vascular Biology), and subsequently joined the faculty at Rensselaer Polytechnic Institute. Current researches in his lab focus on the 3-D bioprinting technology, stem cells technology and vascular bioengineering, and are funded by major grants from NSF, NIH and American Heart Association. Dr. Dai received the Scientist Development Award from American Heart Association, Faculty Early Career Award from National Science Foundation, Rising Star Award from Biomedical Engineering Society, and Institute’s Faculty Career Award (RPI).
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Papers by Guohao Dai
OBJECTIVE: To establish the critical role of PPAP2B in endothelial responses to hemodynamics.
METHODS AND RESULTS: Reduced PPAP2B was detected in vivo in mouse and swine aortic arch endothelia exposed to chronic disturbed flow, and in mouse carotid artery endothelia subjected to surgically-induced acute disturbed flow. In humans, PPAP2B was reduced in the downstream part of carotid plaques where low shear stress prevails. In culture, reduced PPAP2B was measured in human aortic endothelial cells (HAEC) under athero-susceptible waveform mimicking flow in human carotid sinus. Flow-sensitive microRNA-92a and transcription factor KLF2 were identified as upstream inhibitor and activator of endothelial PPAP2B, respectively. PPAP2B suppression abrogated athero-protection of unidirectional flow; Inhibition of lysophosphatidic acid receptor 1 (LPAR1) restored the flow-dependent, anti-inflammatory phenotype in PPAP2B-deficient cells. PPAP2B inhibition resulted in myosin-light-chain phosphorylation and intercellular gaps, which were abolished by LPAR1/2 inhibition. Expression-quantitative-trait-locus-mapping demonstrated PPAP2B CAD risk allele is not linked to PPAP2B expression in various human tissues but significantly associated with reduced PPAP2B in HAEC.
CONCLUSIONS: Athero-relevant flows dynamically modulate endothelial PPAP2B expression through miR-92a and KLF2. Mechano-sensitive PPAP2B plays a critical role in promoting anti-inflammatory phenotype and maintaining vascular integrity of endothelial monolayer under athero-protective flow.
RESULTS: The printed hMSCs were evenly distributed in the polymerized PEG-GelMA scaffold during layer-by-layer assembly. The procedure showed a good biocompatibility with >80% of the cells surviving the printing process and the resulting constructs provided strong mechanical support to the embedded cells. The printed mesenchymal stem cells showed an excellent osteogenic and chondrogenic differentiation capacity. Both osteogenic and chondrogenic differentiation as determined by specific gene and protein expression analysis (RUNX2, SP7, DLX5, ALPL, Col1A1, IBSP, BGLAP, SPP1, Col10A1, MMP13, SOX9, Col2A1, ACAN) was improved by PEG-GelMA in comparison to PEG alone. These observations were consistent with the histological evaluation.
CONCLUSIONS: Inkjet bioprinted-hMSCs in simultaneously photocrosslinked PEG-GelMA hydrogel scaffolds demonstrated an improvement of mechanical properties and osteogenic and chondrogenic differentiation, suggesting its promising potential for usage in bone and cartilage tissue engineering.
OBJECTIVE: To establish the critical role of PPAP2B in endothelial responses to hemodynamics.
METHODS AND RESULTS: Reduced PPAP2B was detected in vivo in mouse and swine aortic arch endothelia exposed to chronic disturbed flow, and in mouse carotid artery endothelia subjected to surgically-induced acute disturbed flow. In humans, PPAP2B was reduced in the downstream part of carotid plaques where low shear stress prevails. In culture, reduced PPAP2B was measured in human aortic endothelial cells (HAEC) under athero-susceptible waveform mimicking flow in human carotid sinus. Flow-sensitive microRNA-92a and transcription factor KLF2 were identified as upstream inhibitor and activator of endothelial PPAP2B, respectively. PPAP2B suppression abrogated athero-protection of unidirectional flow; Inhibition of lysophosphatidic acid receptor 1 (LPAR1) restored the flow-dependent, anti-inflammatory phenotype in PPAP2B-deficient cells. PPAP2B inhibition resulted in myosin-light-chain phosphorylation and intercellular gaps, which were abolished by LPAR1/2 inhibition. Expression-quantitative-trait-locus-mapping demonstrated PPAP2B CAD risk allele is not linked to PPAP2B expression in various human tissues but significantly associated with reduced PPAP2B in HAEC.
CONCLUSIONS: Athero-relevant flows dynamically modulate endothelial PPAP2B expression through miR-92a and KLF2. Mechano-sensitive PPAP2B plays a critical role in promoting anti-inflammatory phenotype and maintaining vascular integrity of endothelial monolayer under athero-protective flow.
RESULTS: The printed hMSCs were evenly distributed in the polymerized PEG-GelMA scaffold during layer-by-layer assembly. The procedure showed a good biocompatibility with >80% of the cells surviving the printing process and the resulting constructs provided strong mechanical support to the embedded cells. The printed mesenchymal stem cells showed an excellent osteogenic and chondrogenic differentiation capacity. Both osteogenic and chondrogenic differentiation as determined by specific gene and protein expression analysis (RUNX2, SP7, DLX5, ALPL, Col1A1, IBSP, BGLAP, SPP1, Col10A1, MMP13, SOX9, Col2A1, ACAN) was improved by PEG-GelMA in comparison to PEG alone. These observations were consistent with the histological evaluation.
CONCLUSIONS: Inkjet bioprinted-hMSCs in simultaneously photocrosslinked PEG-GelMA hydrogel scaffolds demonstrated an improvement of mechanical properties and osteogenic and chondrogenic differentiation, suggesting its promising potential for usage in bone and cartilage tissue engineering.