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Abstract 5417: Inducible 20S β Subunit LMP-2 is Down-Regulated in db/db Mouse Hearts with Diabetic Cardiomyopathy
Lingyun Zu, Djahida Bedja, Lewis C Becker and Zheqing P Cai

Circulation. 2008;118:S_546
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Abstract 1005: Rac1 Deletion Impairs Ischemic Preconditioning In Mouse Hearts
Zheqing P Cai, Zhenyun Shen and Lewis C Becker

Circulation. 2007;116:II_200
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Abstract 1258: Proteasome β Subunit LMP-2 Is Required For Ischemic Preconditioning In Mouse Hearts
Zheqing P Cai, Zhenyun Shen and Lewis C Becker

Circulation. 2007;116:II_256
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Abstract 413: PTEN Knockdown Induces Cardioprotection In Mouse Hearts.
Zheqing P Cai, Zhenyun Shen and Lewis C Becker

Circulation. 2007;116:II_67
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Endoplasmic Reticulum Stress Participates in Aortic Valve Calcification in Hypercholesterolemic AnimalsSignificance
Zhejun Cai, Fei Li, Wei Gong, Wanjun Liu, Quanlu Duan, Chen Chen, Li Ni, Yong Xia, Katherine Cianflone, Nianguo Dong and Dao Wen Wang

Arteriosclerosis, Thrombosis, and Vascular Biology. 2013;33:2345-2354, originally published September 11, 2013
https://doi.org/10.1161/ATVBAHA.112.300226

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Endoplasmic Reticulum Stress Participates in Aortic Valve Calcification in Hypercholesterolemic AnimalsSignificance
Zhejun Cai, Fei Li, Wei Gong, Wanjun Liu, Quanlu Duan, Chen Chen, Li Ni, Yong Xia, Katherine Cianflone, Nianguo Dong, Dao Wen Wang

Arteriosclerosis, Thrombosis, and Vascular Biology October 2013, 33 (10) 2345-2354; DOI: https://doi.org/10.1161/ATVBAHA.112.300226

Figure 1.
Induction of endoplasmic reticulum (ER) stress in aortic valve (AV) leaflets of patients with calcified AV s...
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Induction of endoplasmic reticulum (ER) stress in aortic valve (AV) leaflets of patients with calcified AV stenosis (CAVS). Immunoblotting for osteoblast differentiation markers Runx2 and osteocalcin, and ER stress markers in AV leaflet samples from patients with CAVS as well as normal leaflets. Runx2 and osteocalcin expressions were strongly induced, and the expressions of phosphorylated-protein kinase-like ER kinase (p-PERK), phosphorylated-inositol-requiring transmembrane kinase and endonuclease-1α (p-IRE1α), and C/EBP homologous protein (CHOP) were markedly increased in calcified AV compared with normal AV (**P<0.01 vs normal).
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Endoplasmic Reticulum Stress Participates in Aortic Valve Calcification in Hypercholesterolemic AnimalsSignificance
Zhejun Cai, Fei Li, Wei Gong, Wanjun Liu, Quanlu Duan, Chen Chen, Li Ni, Yong Xia, Katherine Cianflone, Nianguo Dong, Dao Wen Wang

Arteriosclerosis, Thrombosis, and Vascular Biology October 2013, 33 (10) 2345-2354; DOI: https://doi.org/10.1161/ATVBAHA.112.300226

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Table 1.
Hemodynamic Parameters of Animals After Different InterventionsShow More

Hemodynamic Parameters of Animals After Different InterventionsShow Less
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Endoplasmic Reticulum Stress Participates in Aortic Valve Calcification in Hypercholesterolemic AnimalsSignificance
Zhejun Cai, Fei Li, Wei Gong, Wanjun Liu, Quanlu Duan, Chen Chen, Li Ni, Yong Xia, Katherine Cianflone, Nianguo Dong, Dao Wen Wang

Arteriosclerosis, Thrombosis, and Vascular Biology October 2013, 33 (10) 2345-2354; DOI: https://doi.org/10.1161/ATVBAHA.112.300226

Figure 2.
Aortic valve (AV) calcification of animals with different intervention. A, Alizarin red sta...
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Aortic valve (AV) calcification of animals with different intervention. A, Alizarin red staining for calcified nodules in AV leaflets of animals with indicated intervention. Scale bars, 200 μm in rabbits or 100 μm in ApoE^−/− mice. B and C, High-cholesterol (HC)+vitamin D₂ (vitD₂) diet led to significant AV calcification in rabbits, and HC diet caused marked calcification in AV leaflets of ApoE^−/− mice as well. Tauroursodeoxycholic acid (TUDCA) treatment markedly reduced these effects (in rabbits: control, n=6; HC+vitD₂, n=7; HC+vitD₂+TUDCA, n=7; in ApoE^−/− mice: control, n=15; HC, n=15; HC +TUDCA, n=15; **P<0.01 vs control; ##P<0.01 vs HC+vitD₂ in rabbits or HC in ApoE^−/− mice).
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Endoplasmic Reticulum Stress Participates in Aortic Valve Calcification in Hypercholesterolemic AnimalsSignificance
Zhejun Cai, Fei Li, Wei Gong, Wanjun Liu, Quanlu Duan, Chen Chen, Li Ni, Yong Xia, Katherine Cianflone, Nianguo Dong, Dao Wen Wang

Arteriosclerosis, Thrombosis, and Vascular Biology October 2013, 33 (10) 2345-2354; DOI: https://doi.org/10.1161/ATVBAHA.112.300226

Figure 3.
Aortic valve (AV) endoplasmic reticulum (ER) stress induction in animals with different intervention. Repres...
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Aortic valve (AV) endoplasmic reticulum (ER) stress induction in animals with different intervention. Representative staining of ER stress markers, KDEL and C/EBP homologous protein (CHOP), in AV leaflets of rabbits (A) and ApoE^−/− mice (B) with indicated intervention. Scale bars, 200 μm in rabbits or 100 μm in ApoE^−/− mice. High-cholesterol (HC)+vitamin D₂ (vitD₂) or HC diet led to significant KDEL and CHOP induction in AV leaflets of indicated animals. Tauroursodeoxycholic acid (TUDCA) treatment markedly relieved these effects (in rabbits: control, n=6; HC+vitD₂, n=7; HC+vitD₂+TUDCA, n=7; in ApoE^−/− mice: control, n=15; HC, n=15; HC +TUDCA, n=15; **P<0.01 vs control; ##P<0.01 vs HC+vitD₂ in rabbits or HC in ApoE^−/− mice).
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Endoplasmic Reticulum Stress Participates in Aortic Valve Calcification in Hypercholesterolemic AnimalsSignificance
Zhejun Cai, Fei Li, Wei Gong, Wanjun Liu, Quanlu Duan, Chen Chen, Li Ni, Yong Xia, Katherine Cianflone, Nianguo Dong, Dao Wen Wang

Arteriosclerosis, Thrombosis, and Vascular Biology October 2013, 33 (10) 2345-2354; DOI: https://doi.org/10.1161/ATVBAHA.112.300226

Figure 4.
TUDCA administration reduces osteoblastic differentiation and macrophage infiltration in aortic valve (AV) l...
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TUDCA administration reduces osteoblastic differentiation and macrophage infiltration in aortic valve (AV) leaflets induced by high-cholesterol (HC) diet in ApoE^−/− mice. A, Osteoblastic differentiation markers, osterix, Runx2, and osteocalcin, and macrophage marker F4/80 staining in AV leaflets of indicated groups. Scale bars, 100 μm. HC diet significantly induced AV osterix (B), Runx2 (C), and osteocalcin (D) staining, and increased AV macrophage infiltration (E) in ApoE^−/− mice. Tauroursodeoxycholic acid (TUDCA) effectively suppressed these effects (control, n=15; HC, n=15; HC +TUDCA, n=15; **P<0.01 vs control; ##P<0.01 vs HC).
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