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. 2016 Feb 1;37(4):425–443. doi: 10.1038/aps.2015.145

Table 1. Studies of endoplasmic reticulum stress in cardiovascular physiology function.

Reference Protein level Experiment cell Effect Mild ERS Severe ERS ERS inducer
Riek et al 62 β1, β2 integrin Monocyte Enhance adhesion; enhance proliferation Yes No Thapsigargin
Nakamura et al 63 Bip/T-cadherin Human retinal microvascular endothelial cells (HRMEC) Enhance proliferation; enhance migration Yes No Tunicamycin Thapsigargin
Bip/T-cadherin Human retinal microvascular endothelial cells (HRMEC) Suppress proliferation; suppress migration No Yes Tunicamycin Thapsigargin
Bip/T-cadherin OIR model mice Enhance neovascularization Yes No Tunicamycin Thapsigargin
Yang et al 67 GRP78, CHOP, caspase 12 Human umbilical vein endothelial cells (HUVECs) Induce cells apoptosis No Yes Intermittent/persistent hypoxia
Yi et al 70 XBP1, GRP94, ATF6 Vascular smooth muscle cells (VSMC); SD rats aortic endothelialcell cells Suppress abnormal proliferation and migration No Yes Tunicamycin