Table 2:
Material | Cell Type(s) | Blood flow conditions | Experiment | Ref. |
---|---|---|---|---|
PDMS | Mouse olfactory harvested arterial segments | Perfusion inlet was subjected to 45 mmHg and the outlet at atmospheric pressure. | Artery segments were reversibly loaded onto device; verified cellular arrangement of artery in chip by staining SMC nuclei, actin, and voltage gated calcium channels; vessel constriction was reduced by 50% after incubating with calcium-blocker nifedipine | Yasotharan et al.[68] |
PDMS coated with VWF/fibrinogen | HUVECs | Parallel microchannels with one-side stenosis of 20, 30, 40, 60, or 80 percent lumen reduction; human blood was perfused at 1,000 s−1 input wall shear rates | Stenotic chambers demonstrated enhanced platelet aggregation in 60 – 80% occlusion over a range of input wall shear rates; flow increases EC VWF secretion in stenotic outlet, causing platelet aggregation and post-stenotic thrombus formation | Westein et al.[74] |
Gelatin-Agarose IPN | HUVECs, HDMVECs, HLMVECs | Physiologically relevant stiffness ~ 20 kPa (stiffness of healthy arteries between 1 and 35 kPa); Flow velocity in smallest channels set to ~2.8 mm s−1 (corresponding to a wall shear stress ~8.8 dynes cm−2) | Stiffer IPNs (~50 kPa) resulted in increased permeability compared to soft devices (~5 kPa); Extracellular haem (haemolytic by-product) induces delayed and reversible EC permeability (dose-dependent manner) | Qui et al.[164] |
PDMS and collagen | hBMSCs, hFs, HUVECs, HASMCs | No profusion mentioned | Inflammatory factors (LPS, thrombin, and TNFα) compromises EC barrier function; Simultaneous inhibition of Rac1and activation of RhoA induced loss of HASMC exposure to HUVECs and reduced barrier function; CRISPRmediated knockout of N-cadherin in HASMCs led to loss of barrier function and over expression in HUVECs N-cadherin (validated in mouse model) | Alimperti et al. [165] |
PDMS coated with collagen | HUVECs | Perfused human citrated whole blood at a flow rate of 0.29 mL min−1, yielding a shear rate of ~1,000 s−1 | SLA printed miniaturized vascular structures that closely mimic stenotic and healthy blood vessel architecture; 15 minutes of blood perfusion revealed induced thrombosis down stream and at the stenotic regions whereas healthy geometries showed no platelet adhesion | Costa et al.[161] |
PDMS | Resistance arteries isolated from wile | Harvested arteries were fixed at periphery and subjected to external pressure of 45 mmHg | Developed a microfluidic platform to assess resistance artery structure and function; fully automated acquisition of up to ten does-response sequences of | Gṻnther et al.[166] |
type CD1 mice or CD1 mice expressing Tie2-GFP transgene in ECs | above atmosphere (aligned artery); Disk of sapphire uniformly distributed heat generated by thermoelectric heater; Flow in channels between 0 – 4 mL h−1 | intact mouse mesenteric artery segments; Exposure of phenylephrine or acetylcholine yield dose-response relationship identical to human response | ||
PDMS | HUVECs, HMVEC | Citrated human blood was perfused to obtain a wall shear rate of 750 sec−1 (~10 dynes cm−2 stress); for plateletendothelial dynamics, higher wall shear rate was used (750 sec−1; ~30 dynes cm−2 stress) | Performed quantitative analysis of organ-level contributions to inflammation-induced thrombosis; LPS endotoxin directly stimulates intravascular thrombosis by activated alveolar epithelium; analyzed inhibition of EC activation and thrombosis due to PAR=1 antagonist | Jain et al.[167] |
Fibronectin crosslinked gelatin | iPSC, NRVMs | Bulk elastic modulus of ca 50 – 100 kPa; lower concentrations obtained modulus between 1 and 15 kPa | Micropatterned gelatin hydrogels using laser-etching to obtain surface grooves and pillar structures with a resolution of 15 μm; verified structural organization, contractile function, and long-term viability compared to manually patterned gelatin substrates | Janna et al.[168] |
PDMS | HAECs and HASMCs | Vacuum side channels induce cyclic strain of 5 – 8% to mimic stretching and relaxation of the channels; flow in EC chamber produced a wall shear stress of 1 – 1.5 PA | Culture of SMCs and EC with a porous membrane separating the two chambers lead to prolonged viability of cells that exhibited physiological morphology and organization through cell-cell contact; | Engeland et al.[169] |
Abbreviations: IPN, inter-penetrating network; HUVECs, human umbilical vein endothelial cells; HDMVECs, human dermal microvascular endothelial cells; HDMVECs, human lung microvascular endothelial cells; PDMS, poly(dimethylsiloxane); hBMSCs, human bone marrow stromal cells; hFs, human lung fibroblasts; HASMCs, human aortic smooth muscle cells; LPS, lipopolysaccharides; HMVEC, human lung microvascular endothelial cells; PAR-1, protease activated receptor-1; iPSC, induced pluripotent stem cells derived cardiomyocytes; NRVMs, neonatal rat ventricular myocytes.