Smooth Muscle α-Actin Downregulation in Cultured Chick Aortic Smooth Muscle and Neural Crest Cells Is Associated with Altered Cell Shape

Mishima, Noboru; Matsukawa, Takashi; Kirby, Margaret L.

doi:10.1006/excr.1996.0129

Cited by 2 publications

(3 citation statements)

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“…expressed in both smooth muscle cells and neural crest cells. 37 No differences in expression of ␣-smooth muscle actin were observed between the antisense-and missensetreated cells (data not shown).…”

Section: Attenuated Expression Of Chira In Cardiac Neural Crestmentioning

confidence: 98%

HIRA, a DiGeorge Syndrome Candidate Gene, Is Required for Cardiac Outflow Tract Septation

Farrell¹,

Stadt²,

Wallis³

et al. 1999

Circulation Research

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Abstract-DiGeorge syndrome (DGS) is a congenital disease characterized by defects in organs and tissues that depend on contributions by cell populations derived from neural crest for proper development. A number of candidate genes that lie within the q11 region of chromosome 22 commonly deleted in DGS patients have been identified. Orthologues of the DGS candidate gene HIRA are expressed in the neural crest and in neural crest-derived tissues in both chick and mouse embryos. By exposing a portion of the premigratory chick neural crest to phosphorothioate end-protected antisense oligonucleotides, ex ovo, followed by orthotopic backtransplantation to the untreated embryos, we have shown that the functional attenuation of cHIRA in the chick cardiac neural crest results in a significantly increased incidence of persistent truncus arteriosus, a phenotypic change characteristic of DGS, but does not affect the repatterning aortic arch arteries, the ventricular function, or the alignment of the outflow tract. (Circ Res. 1999;84:127-135.)

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Section: Attenuated Expression Of Chira In Cardiac Neural Crestmentioning

confidence: 98%

HIRA, a DiGeorge Syndrome Candidate Gene, Is Required for Cardiac Outflow Tract Septation

Farrell¹,

Stadt²,

Wallis³

et al. 1999

Circulation Research

Self Cite

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“…Moreover, the morphology, the proliferative potential as well as the induction of a-sm actin in these cells with time in culture, suggested that neointima formation, which includes cell translocation along with gradual a-sm actin induction, primarily arises from type I1 cells rather than from intrinsically myodifferentiated vascular myocytes (127). Another approach to inhibit a-sm actin has been to infect aortic smooth muscle and neural crest cells with an antisense a-sm actin ribozymecontaining CXL retrovirus (128). The antisense nucleotide sequence used in this study covers nucleotides 16-48 after the initiation codon, and therefore is not directly comparable to the ODNs used in our study.…”

Section: The Functional Significance Of Cx-sm Actinmentioning

confidence: 99%

“…The antisense nucleotide sequence used in this study covers nucleotides 16-48 after the initiation codon, and therefore is not directly comparable to the ODNs used in our study. The mecha-nism of antisense ribozyme inhibition could not be addressed because neural crest cell cultures comprised few cells only, and aortic smooth muscle cells were not easily infected (128). In both chick neural crest cells and human breast fibroblasts, however, profound changes in cell shape are elicited by antisense suppression of a-sm actin induction (1 19, 128).…”

Section: The Functional Significance Of Cx-sm Actinmentioning

confidence: 99%

Stromal Reaction to Invasive Cancer: The Cellular Origin of the Myofibroblast and Implications for Tumor Development

Rønnov‐Jessen

1996

Breast Journal

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Many epithelial malignancies are associated with an extensive conversion of the surrounding normal stroma reminiscent of the transient activation seen during wound healing, albeit in a more chronic form. The most outstanding feature of the altered stroma is the accumulation of peritumoral myofibroblasts. Here, I have focused on the cellular origin of myofibroblasts in human breast cancer, the tumor cell-derived activity responsible for their occurrence, and the possible function of their most pronounced cytoskeletal change. In the field of myofibroblast research, the use of newly developed cell-culture based technologies have been instrumental. Stromal cells in short-term cultures have been thoroughly characterized using markers defined by their staining patterns in the tissue of origin. Efforts t o purify nonactivated fibroblasts prior to cultivation and the introduction of chemically defined culture conditions have allowed the elements of conversion to be studied at the molecular level. Furthermore, the development of a so called tumor environment assay, in which tumor cell-stromal cell interactions result in functional replicas of typical tumor histology, has proven a powerful tool in the search for the contribution of the individual stromal cell types to the complex scenario of peritumoral myofibroblasts. The cell-cell interactions seen in the tumor environment assay have been validated by in vivo coinoculation of tumor cells and myofibroblasts in nude mice. The most recent data point t o the function of fibroblast cytoskeletal conversion in immobilizing the cells in close apposition to tumor cells. The comprehensive participation of norAddress correspondence and reprint requests to: Lone R~jnnov-Jessen, ma1 fibroblasts in malignancies promise for future new therapeutic strategies directed against tumor cell-fibroblast interaction.Key Words: fibroblast activation, a-sm actin, breast neoplasia ransition of preinvasive carcinoma to the invasive T phenotype coincides with radical changes in tissue organization with respect to cellular composition and extracellular matrix deposition. The most frequently encountered breast carcinoma, the infiltrating ductal carcinoma, is characterized by a particularly striking stromal response (desmoplasia) (1-4). The stromal reaction has at different times been reported either to promote or to inhibit tumor formation (2, 5) (for review see reference 6). However, although much attention has been focused on the variable contribution of stromal cells to tumor development (7-14), the complexity of the stroma still leaves much behind to discover. One of the hypotheses that has escaped the chaotic stromal scenario suggests that the observed differences might reflect a balance between the interactive processes at the invasive front versus the central part of the tumor (6). Clearly, the invasive front is different from the central sclerotic area in terms of cells and extracellular matrix. The invasive front is characterized by numerous stromal cells (myofibroblasts), tenascin, hyaluroni...

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Smooth Muscle α-Actin Downregulation in Cultured Chick Aortic Smooth Muscle and Neural Crest Cells Is Associated with Altered Cell Shape

Cited by 2 publications

References 0 publications

HIRA, a DiGeorge Syndrome Candidate Gene, Is Required for Cardiac Outflow Tract Septation

HIRA, a DiGeorge Syndrome Candidate Gene, Is Required for Cardiac Outflow Tract Septation

Stromal Reaction to Invasive Cancer: The Cellular Origin of the Myofibroblast and Implications for Tumor Development

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