The Experts below are selected from a list of 321261 Experts worldwide ranked by ideXlab platform
John A Elefteriades - One of the best experts on this subject based on the ideXlab platform.
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fate of distal aorta after frozen elephant trunk and total arch replacement for type a aortic dissection in marfan syndrome
The Journal of Thoracic and Cardiovascular Surgery, 2019Co-Authors: Yu Chen, Lingeng Lu, Jun Zheng, Wei Zhang, John A ElefteriadesAbstract:Abstract Objective The use of the frozen elephant trunk technique for type A aortic dissection in Marfan syndrome is limited by the lack of imaging evidence for long-term aortic remodeling. We seek to evaluate the changes of the distal aorta and late outcomes after frozen elephant trunk and total arch replacement for type A aortic dissection in patients with Marfan syndrome. Methods Between 2003 and 2015, we performed frozen elephant trunk + total arch replacement for 172 patients with Marfan syndrome suffering from type A aortic dissection (94 acute; 78 chronic). Mean age was 34.6 ± 9.3 years, and 121 were male (70.3%). Early mortality was 8.1% (14/172), and follow-up was complete in 98.7% (156/158) at a mean of 6.2 ± 3.3 years. Aortic dilatation was defined as a maximal diameter of greater than 50 mm or an average growth rate of greater than 5 mm/year at any segment detected by computed tomographic angiography. Temporal changes in the false and true Lumens and maximal aortic size were analyzed with linear mixed modeling. Results After surgery, false Lumen obliteration occurred in 86%, 39%, 26%, and 21% at the frozen elephant trunk, unstented descending aorta, diaphragm, and renal artery, respectively. The true Lumen expanded significantly over time at all segments (P .05). Maximal aortic size was stable at the frozen elephant trunk and renal artery (P > .05), but grew at the descending aorta (P = .001) and diaphragm (P Conclusions The frozen elephant trunk technique can expand the true Lumen across the aorta, decrease or stabilize the false Lumen, and stabilize the distal aorta in patients with Marfan syndrome with type A aortic dissection, thereby inducing favorable remodeling in the distal aorta. This study adds long-term clinical and radiologic evidence supporting the use of the frozen elephant trunk technique for type A dissection in Marfan syndrome.
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fate of distal aorta after frozen elephant trunk and total arch replacement for type a aortic dissection in marfan syndrome
The Journal of Thoracic and Cardiovascular Surgery, 2019Co-Authors: Yu Chen, Jun Zheng, Wei Zhang, Aihua Zhi, Yongmin Liu, Junming Zhu, John A ElefteriadesAbstract:Abstract Objective The use of the frozen elephant trunk technique for type A aortic dissection in Marfan syndrome is limited by the lack of imaging evidence for long-term aortic remodeling. We seek to evaluate the changes of the distal aorta and late outcomes after frozen elephant trunk and total arch replacement for type A aortic dissection in patients with Marfan syndrome. Methods Between 2003 and 2015, we performed frozen elephant trunk + total arch replacement for 172 patients with Marfan syndrome suffering from type A aortic dissection (94 acute; 78 chronic). Mean age was 34.6 ± 9.3 years, and 121 were male (70.3%). Early mortality was 8.1% (14/172), and follow-up was complete in 98.7% (156/158) at a mean of 6.2 ± 3.3 years. Aortic dilatation was defined as a maximal diameter of greater than 50 mm or an average growth rate of greater than 5 mm/year at any segment detected by computed tomographic angiography. Temporal changes in the false and true Lumens and maximal aortic size were analyzed with linear mixed modeling. Results After surgery, false Lumen obliteration occurred in 86%, 39%, 26%, and 21% at the frozen elephant trunk, unstented descending aorta, diaphragm, and renal artery, respectively. The true Lumen expanded significantly over time at all segments (P .05). Maximal aortic size was stable at the frozen elephant trunk and renal artery (P > .05), but grew at the descending aorta (P = .001) and diaphragm (P Conclusions The frozen elephant trunk technique can expand the true Lumen across the aorta, decrease or stabilize the false Lumen, and stabilize the distal aorta in patients with Marfan syndrome with type A aortic dissection, thereby inducing favorable remodeling in the distal aorta. This study adds long-term clinical and radiologic evidence supporting the use of the frozen elephant trunk technique for type A dissection in Marfan syndrome.
Jun Zheng - One of the best experts on this subject based on the ideXlab platform.
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fate of distal aorta after frozen elephant trunk and total arch replacement for type a aortic dissection in marfan syndrome
The Journal of Thoracic and Cardiovascular Surgery, 2019Co-Authors: Yu Chen, Lingeng Lu, Jun Zheng, Wei Zhang, John A ElefteriadesAbstract:Abstract Objective The use of the frozen elephant trunk technique for type A aortic dissection in Marfan syndrome is limited by the lack of imaging evidence for long-term aortic remodeling. We seek to evaluate the changes of the distal aorta and late outcomes after frozen elephant trunk and total arch replacement for type A aortic dissection in patients with Marfan syndrome. Methods Between 2003 and 2015, we performed frozen elephant trunk + total arch replacement for 172 patients with Marfan syndrome suffering from type A aortic dissection (94 acute; 78 chronic). Mean age was 34.6 ± 9.3 years, and 121 were male (70.3%). Early mortality was 8.1% (14/172), and follow-up was complete in 98.7% (156/158) at a mean of 6.2 ± 3.3 years. Aortic dilatation was defined as a maximal diameter of greater than 50 mm or an average growth rate of greater than 5 mm/year at any segment detected by computed tomographic angiography. Temporal changes in the false and true Lumens and maximal aortic size were analyzed with linear mixed modeling. Results After surgery, false Lumen obliteration occurred in 86%, 39%, 26%, and 21% at the frozen elephant trunk, unstented descending aorta, diaphragm, and renal artery, respectively. The true Lumen expanded significantly over time at all segments (P .05). Maximal aortic size was stable at the frozen elephant trunk and renal artery (P > .05), but grew at the descending aorta (P = .001) and diaphragm (P Conclusions The frozen elephant trunk technique can expand the true Lumen across the aorta, decrease or stabilize the false Lumen, and stabilize the distal aorta in patients with Marfan syndrome with type A aortic dissection, thereby inducing favorable remodeling in the distal aorta. This study adds long-term clinical and radiologic evidence supporting the use of the frozen elephant trunk technique for type A dissection in Marfan syndrome.
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fate of distal aorta after frozen elephant trunk and total arch replacement for type a aortic dissection in marfan syndrome
The Journal of Thoracic and Cardiovascular Surgery, 2019Co-Authors: Yu Chen, Jun Zheng, Wei Zhang, Aihua Zhi, Yongmin Liu, Junming Zhu, John A ElefteriadesAbstract:Abstract Objective The use of the frozen elephant trunk technique for type A aortic dissection in Marfan syndrome is limited by the lack of imaging evidence for long-term aortic remodeling. We seek to evaluate the changes of the distal aorta and late outcomes after frozen elephant trunk and total arch replacement for type A aortic dissection in patients with Marfan syndrome. Methods Between 2003 and 2015, we performed frozen elephant trunk + total arch replacement for 172 patients with Marfan syndrome suffering from type A aortic dissection (94 acute; 78 chronic). Mean age was 34.6 ± 9.3 years, and 121 were male (70.3%). Early mortality was 8.1% (14/172), and follow-up was complete in 98.7% (156/158) at a mean of 6.2 ± 3.3 years. Aortic dilatation was defined as a maximal diameter of greater than 50 mm or an average growth rate of greater than 5 mm/year at any segment detected by computed tomographic angiography. Temporal changes in the false and true Lumens and maximal aortic size were analyzed with linear mixed modeling. Results After surgery, false Lumen obliteration occurred in 86%, 39%, 26%, and 21% at the frozen elephant trunk, unstented descending aorta, diaphragm, and renal artery, respectively. The true Lumen expanded significantly over time at all segments (P .05). Maximal aortic size was stable at the frozen elephant trunk and renal artery (P > .05), but grew at the descending aorta (P = .001) and diaphragm (P Conclusions The frozen elephant trunk technique can expand the true Lumen across the aorta, decrease or stabilize the false Lumen, and stabilize the distal aorta in patients with Marfan syndrome with type A aortic dissection, thereby inducing favorable remodeling in the distal aorta. This study adds long-term clinical and radiologic evidence supporting the use of the frozen elephant trunk technique for type A dissection in Marfan syndrome.
George E. Davis - One of the best experts on this subject based on the ideXlab platform.
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Cellular and molecular mechanisms of vascular Lumen formation.
Developmental cell, 2009Co-Authors: M. Luisa Iruela-arispe, George E. DavisAbstract:The formation of vascular Lumens by endothelial cells is a critical step in the angiogenic process that occurs during invasion and growth of the incipient vascular sprout. Once a Lumen is established, capillaries are rapidly exposed to the physical forces associated with the flow of blood which, together with genetic information, regulate the ultimate size of inner vessel diameter. Here we review the recent literature on vascular Lumen formation and compare it to Lumen formation in other epithelial systems. We also discuss the regulation of Lumen diameter after vascular morphogenesis has been completed.
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an integrin and rho gtpase dependent pinocytic vacuole mechanism controls capillary Lumen formation in collagen and fibrin matrices
Microcirculation, 2003Co-Authors: George E. Davis, Kayla J BaylessAbstract:A major question that remains unanswered concerning endothelial cell (EC) morphogenesis is how Lumens are formed in three-dimensional extracellular matrices (ECMs). Studies from many laboratories have revealed a critical role for an ECM-integrin-cytoskeletal signaling axis during EC morphogenesis. We have discovered a mechanism involving intracellular vacuole formation and coalescence that is required for Lumen formation in several in vitro models of morphogenesis. In addition, a series of studies have observed vacuoles in vivo during angiogenic events. These vacuoles form through an integrin-dependent pinocytic mechanism in either collagen or fibrin matrices. In addition, we have shown that the Cdc42 and Rac1 guanosine triphosphatases (GTPases), which control actin and microtubule cytoskeletal networks, are required for vacuole and Lumen formation. These GTPases are also known to regulate integrin signaling and are activated after integrin-matrix interactions. Furthermore, the expression of green fluorescent protein-Rac1 or -Cdc42 chimeric proteins in ECs results in the targeting of these fusion proteins to intracellular vacuole membranes during Lumen formation. Thus, a matrix-integrin-cytoskeletal signaling axis involving both the Cdc42 and Rac1 GTPases regulates the process of EC Lumen formation in three-dimensional collagen or fibrin matrices.
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an α2β1 integrin dependent pinocytic mechanism involving intracellular vacuole formation and coalescence regulates capillary Lumen and tube formation in three dimensional collagen matrix
Experimental Cell Research, 1996Co-Authors: George E. Davis, Charles W CamarilloAbstract:Abstract Human endothelial cells, when suspended within three-dimensional collagen matrices, develop intracellular vacuoles that coalesce to form capillary Lumens and tubes. Vacuole and Lumen formation are completely dependent on the collagen-binding integrin α2β1, while other endothelial cell integrins had no apparent influence. Vacuole formation occurs by a pinocytic process with internalization of plasma membrane and molecules from the extracellular space, such as fluorescent tracers. By immunofluorescence, vacuole membranes were found to contain associated cell surface proteins, proteins involved in endosomal trafficking (i.e., caveolin and annexin II), and F-actin. Furthermore, some vacuole compartments contained von Willebrand factor. Integrin-regulated vacuole formation and coalescence are major mechanisms controlling capillary Lumen and tube formation within a three-dimensional extracellular matrix.
Yu Chen - One of the best experts on this subject based on the ideXlab platform.
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fate of distal aorta after frozen elephant trunk and total arch replacement for type a aortic dissection in marfan syndrome
The Journal of Thoracic and Cardiovascular Surgery, 2019Co-Authors: Yu Chen, Lingeng Lu, Jun Zheng, Wei Zhang, John A ElefteriadesAbstract:Abstract Objective The use of the frozen elephant trunk technique for type A aortic dissection in Marfan syndrome is limited by the lack of imaging evidence for long-term aortic remodeling. We seek to evaluate the changes of the distal aorta and late outcomes after frozen elephant trunk and total arch replacement for type A aortic dissection in patients with Marfan syndrome. Methods Between 2003 and 2015, we performed frozen elephant trunk + total arch replacement for 172 patients with Marfan syndrome suffering from type A aortic dissection (94 acute; 78 chronic). Mean age was 34.6 ± 9.3 years, and 121 were male (70.3%). Early mortality was 8.1% (14/172), and follow-up was complete in 98.7% (156/158) at a mean of 6.2 ± 3.3 years. Aortic dilatation was defined as a maximal diameter of greater than 50 mm or an average growth rate of greater than 5 mm/year at any segment detected by computed tomographic angiography. Temporal changes in the false and true Lumens and maximal aortic size were analyzed with linear mixed modeling. Results After surgery, false Lumen obliteration occurred in 86%, 39%, 26%, and 21% at the frozen elephant trunk, unstented descending aorta, diaphragm, and renal artery, respectively. The true Lumen expanded significantly over time at all segments (P .05). Maximal aortic size was stable at the frozen elephant trunk and renal artery (P > .05), but grew at the descending aorta (P = .001) and diaphragm (P Conclusions The frozen elephant trunk technique can expand the true Lumen across the aorta, decrease or stabilize the false Lumen, and stabilize the distal aorta in patients with Marfan syndrome with type A aortic dissection, thereby inducing favorable remodeling in the distal aorta. This study adds long-term clinical and radiologic evidence supporting the use of the frozen elephant trunk technique for type A dissection in Marfan syndrome.
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fate of distal aorta after frozen elephant trunk and total arch replacement for type a aortic dissection in marfan syndrome
The Journal of Thoracic and Cardiovascular Surgery, 2019Co-Authors: Yu Chen, Jun Zheng, Wei Zhang, Aihua Zhi, Yongmin Liu, Junming Zhu, John A ElefteriadesAbstract:Abstract Objective The use of the frozen elephant trunk technique for type A aortic dissection in Marfan syndrome is limited by the lack of imaging evidence for long-term aortic remodeling. We seek to evaluate the changes of the distal aorta and late outcomes after frozen elephant trunk and total arch replacement for type A aortic dissection in patients with Marfan syndrome. Methods Between 2003 and 2015, we performed frozen elephant trunk + total arch replacement for 172 patients with Marfan syndrome suffering from type A aortic dissection (94 acute; 78 chronic). Mean age was 34.6 ± 9.3 years, and 121 were male (70.3%). Early mortality was 8.1% (14/172), and follow-up was complete in 98.7% (156/158) at a mean of 6.2 ± 3.3 years. Aortic dilatation was defined as a maximal diameter of greater than 50 mm or an average growth rate of greater than 5 mm/year at any segment detected by computed tomographic angiography. Temporal changes in the false and true Lumens and maximal aortic size were analyzed with linear mixed modeling. Results After surgery, false Lumen obliteration occurred in 86%, 39%, 26%, and 21% at the frozen elephant trunk, unstented descending aorta, diaphragm, and renal artery, respectively. The true Lumen expanded significantly over time at all segments (P .05). Maximal aortic size was stable at the frozen elephant trunk and renal artery (P > .05), but grew at the descending aorta (P = .001) and diaphragm (P Conclusions The frozen elephant trunk technique can expand the true Lumen across the aorta, decrease or stabilize the false Lumen, and stabilize the distal aorta in patients with Marfan syndrome with type A aortic dissection, thereby inducing favorable remodeling in the distal aorta. This study adds long-term clinical and radiologic evidence supporting the use of the frozen elephant trunk technique for type A dissection in Marfan syndrome.
John E Shively - One of the best experts on this subject based on the ideXlab platform.
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mirna 342 regulates ceacam1 induced Lumen formation in a three dimensional model of mammary gland morphogenesis
Journal of Biological Chemistry, 2016Co-Authors: Chunyue Weng, Tung Nguyen, John E ShivelyAbstract:Lumen formation of breast epithelium is rapidly lost during tumorigenesis along with expression of cell adhesion molecule CEACAM1. CEACAM1 induces Lumena in a three-dimensional culture of MCF7/CEACAM1 cells that otherwise fail to form Lumena. We hypothesized miRNAs may be involved because >400 genes were up- or down-regulated in MCF7/CEACAM1 cells and miRNAs may modify global expression patterns. Comparative analysis of miRNA expression in MCF7 versus MCF7/CEACAM1 cells revealed two miRNAs significantly down-regulated (hsa-miR-30a-3p by 6.73-fold and hsa-miR-342-5p by 5.68-fold). Location of miR-342 within an intron of the EVL gene, hypermethylated and involved in tumorigenesis, suggested that miR-342 overexpression may block Lumen formation. In fact, overexpression of miR-342 in MCF7/CEACAM1 cells significantly blocked Lumen formation (p < 0.001). ID4, a dominant-negative inhibitor of basic helix-loop-helix transcription factors, up-regulated in MCF7/CEACAM1 cells, down-regulated in breast cancer, and containing a miR-342 binding site, was tested as a potential target of miR-342. The ratio of ID4 to miR-342 increased from 1:2 in MCF7 cells to 30:1 in MCF7/CEACAM1 cells and a miR-342 inhibitor was able to induce 3'-UTR ID4 reporter activity in MCF7 cells. Because 5-methylcytosine methyltransferase DNMT1 is also a potential target of miR-342, we inhibited miR-342 in MCF7 cells and found DNMT1 was up-regulated with no change in EVL expression, suggesting that miR-342 regulates DNMT1 expression but DNMT1 does not affect the EVL expression in these cells. We conclude that the regulation of Lumen formation by miR-342 involves at least two of its known targets, namely ID4 and DNMT1.
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role of calpain 9 and pkc δ in the apoptotic mechanism of Lumen formation in ceacam1 transfected breast epithelial cells
Experimental Cell Research, 2010Co-Authors: Charngjui Chen, Tung Nguyen, John E ShivelyAbstract:CEACAM1-4S (carcinoembryonic antigen-related cell adhesion molecule 1) is a type I membrane protein with a short (12 amino acid) cytoplasmic tail. Wild type CEACAM1-4S transfected MCF7 cells form glands with Lumena when grown in 3D culture, while null mutations of two putative phosphorylation sites (T457A and S459A) in the cytoplasmic domain fail to undergo Lumen formation. When gene chip analysis was performed on mRNA isolated from both wild type and T457A,S459A mutated CEACAM1-4S transfected MCF7 cells grown in 3D culture, calpain-9 (CAPN9) was identified out of over 400 genes with a >2 log 2 difference as a potential inducer of Lumen formation. Inhibition of CAPN9 expression in MCF7/CEACAM1-4S cells by RNAi or by calpeptin or PD150606 inhibited Lumen formation. Transfection of CAPN9 into wild type MCF7 cells restores Lumen formation demonstrating that calpain-9 may plays a critical role in Lumen formation. Additionally, we demonstrate that the apoptosis related kinase, PKC-δ is activated by proteolytic cleavage during Lumen formation exclusively in wild type CEACAM1-4S transfected MCF7 cells grown in 3D culture, and that Lumen formation is inhibited by either RNAi to PKC-δ or by the PKC-δ inhibitor rottlerin.
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mutational analysis of the cytoplasmic domain of ceacam1 4l in humanized mammary glands reveals key residues involved in Lumen formation stimulation by thr 457 and inhibition by ser 461
Experimental Cell Research, 2009Co-Authors: Chunxia Li, Charngjui Chen, John E ShivelyAbstract:Abstract CEACAM1 (carcinoembryonic antigen-related cell adhesion molecule 1), a type I transmembrane glycoprotein involved in cell–cell adhesion, undergoes extensive alternative splicing, resulting in isoforms with 1–4 Ig-like extracellular domains (ECDs) with either long or short cytoplasmic tails. We have previously shown that CEACAM1-4L (4 ECDs with a long cytoplasmic domain) formed glands with Lumena in humanized mammary mouse fat pads in NOD/SCID mice. In order to identify the key residues of CEACAM1-4L that play essential roles in Lumen formation, we introduced phosphorylation mimic (e.g., Thr-457 or Ser-461 to Asp) or null mutations (Thr-457 or Ser-461 to Ala) into the cytoplasmic domain of CEACAM1-4L and tested them in both the in vivo mouse model and in vitro Matrigel model of mammary morphogenesis. MCF7 cells stably expressing CEACAM1-4L with the single mutation T457D or the double mutant T457D+S461D, but not the null mutants induced central Lumen formation in 3D Matrigel and in humanized mammary fat pads. However, the single phosphorylation mimic mutation S461D, but not the null mutation blocked Lumen formation in both models, suggesting that S461 has inhibitory function in glandular Lumen formation. Compared to our results for the -4S isoform (Chen et al., J. Biol. Chem, 282: 5749–5760, 2008), the T457A null mutation blocks Lumen formation for the -4L but not for the -4S isoform. This difference is likely due to the fact that phosphorylation of S459 (absent in the -4L isoform) positively compensates for loss of T457 in the -4S isoform, while S461 (absent in the -4S isoform) negatively regulates Lumen formation in the -4L isoform. Thus, phosphorylation of these key residues may exert a fine control over the role of the -4L isoform (compared to the -4S isoform) in Lumen formation.
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ceacam1 4s a cell cell adhesion molecule mediates apoptosis and reverts mammary carcinoma cells to a normal morphogenic phenotype in a 3d culture
Proceedings of the National Academy of Sciences of the United States of America, 2003Co-Authors: Julia Kirshner, Charngjui Chen, Jie Huang, John E ShivelyAbstract:In a 3D model of breast morphogenesis, CEACAM1 (carcinoembryonic antigen-related cell adhesion molecule 1) plays an essential role in Lumen formation in a subline of the nonmalignant human breast cell line (MCF10A). We show that mammary carcinoma cells (MCF7), which do not express CEACAM1 or form Lumena when grown in Matrigel, are restored to a normal morphogenic program when transfected with CEACAM1-4S, the short cytoplasmic isoform of CEACAM1 that predominates in breast epithelia. During the time course of Lumen formation, CEACAM1-4S was found initially between the cells, and in mature acini, it was found exclusively in an apical location, identical to its expression pattern in normal breast. Lumena were formed by apoptosis as opposed to necrosis of the central cells within the alveolar structures, and apoptotic cells within the Lumena expressed CEACAM1-4S. Dying cells exhibited classical hallmarks of apoptosis, including nuclear condensation, membrane blebbing, caspase activation, and DNA laddering. Apoptosis was mediated by Bax translocation to the mitochondria and release of cytochrome c into the cytoplasm, and was partially inhibited by culturing cells with caspase inhibitors. The dynamic changes in CEACAM1 expression during morphogenesis, together with studies implicating extracellular matrix and integrin signaling, suggest that a morphogenic program integrates cell–cell and cell–extracellular matrix signaling to produce the Lumena in mammary glands. This report reveals a function of CEACAM1-4S relevant to cellular physiology that distinguishes it from its related long cytoplasmic domain isoform.
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ceacam1 4s a cell cell adhesion molecule mediates apoptosis and reverts mammary carcinoma cells to a normal morphogenic phenotype in a 3d culture
Proceedings of the National Academy of Sciences of the United States of America, 2003Co-Authors: Julia Kirshner, Charngjui Chen, Jie Huang, Pingfang Liu, John E ShivelyAbstract:In a 3D model of breast morphogenesis, CEACAM1 (carcinoembryonic antigen-related cell adhesion molecule 1) plays an essential role in Lumen formation in a subline of the nonmalignant human breast cell line (MCF10A). We show that mammary carcinoma cells (MCF7), which do not express CEACAM1 or form Lumena when grown in Matrigel, are restored to a normal morphogenic program when transfected with CEACAM1-4S, the short cytoplasmic isoform of CEACAM1 that predominates in breast epithelia. During the time course of Lumen formation, CEACAM1-4S was found initially between the cells, and in mature acini, it was found exclusively in an apical location, identical to its expression pattern in normal breast. Lumena were formed by apoptosis as opposed to necrosis of the central cells within the alveolar structures, and apoptotic cells within the Lumena expressed CEACAM1-4S. Dying cells exhibited classical hallmarks of apoptosis, including nuclear condensation, membrane blebbing, caspase activation, and DNA laddering. Apoptosis was mediated by Bax translocation to the mitochondria and release of cytochrome c into the cytoplasm, and was partially inhibited by culturing cells with caspase inhibitors. The dynamic changes in CEACAM1 expression during morphogenesis, together with studies implicating extracellular matrix and integrin signaling, suggest that a morphogenic program integrates cell–cell and cell–extracellular matrix signaling to produce the Lumena in mammary glands. This report reveals a function of CEACAM1-4S relevant to cellular physiology that distinguishes it from its related long cytoplasmic domain isoform.
