Journal: Scientific Reports

Article Title: Loss of CEACAM1, a Tumor-Associated Factor, Attenuates Post-infarction Cardiac Remodeling by Inhibiting Apoptosis

doi: 10.1038/srep21972

Figure Lengend Snippet: ( A ), Raw data of serum CEACAM1 in patients with AMI (n = 26) and healthy controls (n = 24). ( B ), Logarithmically-transformed serum CEACAM1 data for patients with AMI.

Article Snippet: Vectors carrying small interfering RNA targeting CEACAM1 (si-CEACAM1) or the negative control (si-NC) were generated by an external company (Genechem, Shanghai, China).

Techniques: Transformation Assay

Journal: Scientific Reports

Article Title: Loss of CEACAM1, a Tumor-Associated Factor, Attenuates Post-infarction Cardiac Remodeling by Inhibiting Apoptosis

doi: 10.1038/srep21972

Figure Lengend Snippet: ( A ), Time course of CEACAM1 mRNA level in sham, non-infarct area and infarct area. * P < 0.05 vs. sham 6h. Expression of CEACAM1 mRNA ( B ) and protein ( C ) in the left ventricle of wild-type (WT) mice with MI for 3 days (n = 4 in each group). * P < 0.01 vs. sham. ( D ), Immunohistochemical staining shows elevated myocardial CEACAM1 expression in mice with MI than in mice with sham operation (non-infarct area). ( E ), Immunoblotting of CEACAM1 expression in neonatal rat cardiomyocytes exposed to hypoxia for 24 hours (n = 5 in each group). * P < 0.01 vs. normoxia. ( F ), The CEACAM1 mRNA level in neonatal rat cardiomyocytes exposed to hypoxia (for 3h), angiotensin II (AngII, 1 umol/L), endothelin 1(0.1 umol/L) and H 2 O 2 (0.15 umol/L) for 24 hours. * P < 0.05 vs. normoxia.

Article Snippet: Vectors carrying small interfering RNA targeting CEACAM1 (si-CEACAM1) or the negative control (si-NC) were generated by an external company (Genechem, Shanghai, China).

Techniques: Expressing, Immunohistochemical staining, Staining, Western Blot

Journal: Scientific Reports

Article Title: Loss of CEACAM1, a Tumor-Associated Factor, Attenuates Post-infarction Cardiac Remodeling by Inhibiting Apoptosis

doi: 10.1038/srep21972

Figure Lengend Snippet: ( A ), Wild-type (WT) and CEACAM1 knockout (KO) mice were subjected to sham operation or MI. Then survival was monitored for 8 weeks. ( B ) Masson trichromatic staining of WT and KO mouse hearts at 8 weeks after MI (blue indicates collagen). ( C ) Quantification of the length of fibrosis in the infarct area (relative to the total LV circumference) and the fibrotic area in the border zone and the remote area. * P < 0.05 vs. the corresponding WT group, n = 6 in each group. ( D ) Representative echocardiographic images from the four groups. ( E ) Quantification of left ventricular end-systolic and end-diastolic diameter (LVESd, LVEDd), and left ventricular fractional shortening (LVFS). * P < 0.01 vs. corresponding sham group, # P < 0.05 vs. WT MI. (n = 4 in sham groups; n = 9 in MI groups).

Article Snippet: Vectors carrying small interfering RNA targeting CEACAM1 (si-CEACAM1) or the negative control (si-NC) were generated by an external company (Genechem, Shanghai, China).

Techniques: Knock-Out, Staining

Journal: Scientific Reports

Article Title: Loss of CEACAM1, a Tumor-Associated Factor, Attenuates Post-infarction Cardiac Remodeling by Inhibiting Apoptosis

doi: 10.1038/srep21972

Figure Lengend Snippet: ( A ). TUNEL staining of cardiomyocytes exposed to normoxia or hypoxia in the presence/absence of recombinant human CEACAM1(rhCEACAM1). Scale bar, 50 μm. ( B ), Quantitation of TUNEL-positive cells in the four groups shown in A. * P < 0.01 vs. normoxia, and # P < 0.01 vs. hypoxia, n = 6 in each group. ( C ), Representative pictures of TUNEL-stained cultured cardiomyocytes exposed to normoxia or hypoxia in the presence/absence of lentivirus carrying si-RNA for CEACAM1. Scale bar, 20 μm.( D ), Quantitation of TUNEL-positive cells in the 6 groups shown in C. * P < 0.01 vs. normoxia, # P < 0.05 vs. hypoxia +negative control-siRNA (si-NC), n = 10 in each group.

Article Snippet: Vectors carrying small interfering RNA targeting CEACAM1 (si-CEACAM1) or the negative control (si-NC) were generated by an external company (Genechem, Shanghai, China).

Techniques: TUNEL Assay, Staining, Recombinant, Quantitation Assay, Cell Culture, Negative Control

Journal: Scientific Reports

Article Title: Loss of CEACAM1, a Tumor-Associated Factor, Attenuates Post-infarction Cardiac Remodeling by Inhibiting Apoptosis

doi: 10.1038/srep21972

Figure Lengend Snippet: Cleaved caspase-3, mitochondrial Bax (Mito Bax), and cytosolic cytochrome C (Cyto C) were analyzed by Western blotting under either normoxic or hypoxic conditions. CoxIV and β-actin served as internal controls. ( A ) Representative western blots of the target and loading control proteins from cardiomyocytes with/without recombinant human CEACAM1 (rhCEACAM1). ( B ) Quantitative analysis of the protein expression shown in A. * P < 0.05 vs. normoxia, # P < 0.05 vs. hypoxia, n = 5 in each group. ( C ) Western blotting of cleaved caspase-3, mitochondrial Bax, and cytosolic cytochrome C in cardiomyocytes treated with negative control siRNA (si-NC) or siRNA for CEACAM1 (si-CEACAM1). * P < 0.01 vs. normoxia, # P < 0.05 vs. hypoxia+ si-NC, n = 5 in each group. ( E ) Quantitative analysis of GRP78 and CHOP mRNA levels from cardiomyocytes with/without recombinant human CEACAM1 (rhCEACAM1). * P < 0.05 vs. normoxia, # P < 0.05 vs. hypoxia, n = 5 in each group. ( F ) The GRP78 and CHOP mRNA levels in cardiomyocytes treated with si-NC or si-CEACAM1. * P < 0.01 vs. normoxia, # P < 0.05 vs. hypoxia+ si-NC, n = 5 in each group.

Article Snippet: Vectors carrying small interfering RNA targeting CEACAM1 (si-CEACAM1) or the negative control (si-NC) were generated by an external company (Genechem, Shanghai, China).

Techniques: Western Blot, Control, Recombinant, Expressing, Negative Control

Journal: Scientific Reports

Article Title: Loss of CEACAM1, a Tumor-Associated Factor, Attenuates Post-infarction Cardiac Remodeling by Inhibiting Apoptosis

doi: 10.1038/srep21972

Figure Lengend Snippet: Both in vitro and in vivo , CEACAM1 induces mitochondrial translocation of Bax and mitochondria dysfunction with consequent activation of the cytochrome C-caspase-3 apoptotic signaling pathway, which promotes hypoxia-induced apoptosis and of post-infarction cardiac remodeling. In addition, CEACAM1 promotes hypoxia-induced cardiomyocyte apoptosis through GRP78 and CHOP pathway.

Article Snippet: Vectors carrying small interfering RNA targeting CEACAM1 (si-CEACAM1) or the negative control (si-NC) were generated by an external company (Genechem, Shanghai, China).

Techniques: In Vitro, In Vivo, Translocation Assay, Activation Assay