Abstract：
:Transforming growth factor beta (TGF-beta) and connective tissue growth factor (CTGF) have been described to induce the production of extracellular matrix (ECM) proteins and have been reported to be increased in different fibrotic disorders. Skeletal muscle fibrosis is a common feature of Duchenne muscular dystrophy (DMD). The mdx mouse diaphragm is a good model for DMD since it reproduces the muscle degenerative and fibrotic changes. Fibronectin (FN) and proteoglycans (PG) are some of the ECM proteins upregulated in dystrophic conditions. In view of understanding the fibrotic process involved in DMD we have isolated fibroblasts from dystrophic mdx diaphragms. Here we report that regardless of the absence of degenerative myofibers, adult mdx diaphragm fibroblasts show increased levels of FN and condroitin/dermatan sulfate PGs synthesis. Fibroblasts isolated from non fibrotic tissue, such as 1 week old mice diaphragms or skin, do not present elevated FN levels. Furthermore, mdx fibroblast conditioned media is able to stimulate FN synthesis in control fibroblasts. Autocrine TGF-beta signaling was unaltered in mdx cells. When control fibroblasts are exposed to TGF-beta and CTGF, FN increases as expected. Paradoxically, in mdx cells it decreases in a concentration dependent manner and this decrease is not due to a downregulation of FN synthesis. According to this data we hypothesize that a pathological environment is able to reprogram fibroblasts into an activated phenotype which can be maintained through generations.
journal_name
J Cell Commun Signaljournal_title
Journal of cell communication and signalingauthors
Mezzano V,Cabrera D,Vial C,Brandan Edoi
10.1007/s12079-008-0018-2subject
Has Abstractpub_date
2007-12-01 00:00:00pages
205-17issue
3-4eissn
1873-9601issn
1873-961Xjournal_volume
1pub_type
杂志文章abstract：:PEGylation is a biochemical modification process of bioactive molecules with polyethylene glycol (PEG), which lends several desirable properties to proteins/peptides, antibodies, and vesicles considered to be used for therapy or genetic modification of cells. However, PEGylation of proteins is a complex process and ca...
journal_title：Journal of cell communication and signaling
pub_type： 杂志文章,评审
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abstract：:We recently reported that transgenic mice with cardiac-restricted overexpression of CCN2/CTGF have substantially increased tolerance towards ischemia/reperfusion injury. The purpose of this study was to investigate to what extent fully differentiated cardiac myocytes are direct targets of CCN2, and to resolve the sign...
journal_title：Journal of cell communication and signaling
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journal_title：Journal of cell communication and signaling
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更新日期：2018-03-01 00:00:00
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journal_title：Journal of cell communication and signaling
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doi：10.1007/s12079-011-0156-9
更新日期：2012-03-01 00:00:00
abstract：:The Fifth International Workshop on the CCN Family of Genes was held in Toronto October 18-22, 2008. This bi-annual workshop provides a unique opportunity for the presentation and discussion of cutting edge research in the CCN field. The CCN family members have emerged as extracellular matrix associated proteins which...
journal_title：Journal of cell communication and signaling
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doi：10.1007/s12079-009-0036-8
更新日期：2008-12-01 00:00:00
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journal_title：Journal of cell communication and signaling
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-015-0281-y
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journal_title：Journal of cell communication and signaling
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-017-0421-7
更新日期：2018-03-01 00:00:00
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-015-0316-4
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-014-0251-9
更新日期：2014-12-01 00:00:00
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章,评审
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-017-0428-0
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-008-0021-7
更新日期：2007-12-01 00:00:00
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-012-0189-8
更新日期：2013-06-01 00:00:00
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-012-0185-z
更新日期：2013-06-01 00:00:00
abstract：:Inflammation is a crucial component in the pathogenesis of many vascular diseases, such as atherosclerosis and diabetes. Inflammasomes are intracellular signalling complexes whose activation promotes inflammation. Nucleotide-binding domain and Leucine-rich repeat Receptor containing a Pyrin domain 3 (NLRP3) is a patte...
journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-017-0396-4
更新日期：2017-09-01 00:00:00
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-013-0210-x
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
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更新日期：2018-12-01 00:00:00
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-015-0306-6
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-015-0261-2
更新日期：2015-06-01 00:00:00
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-011-0121-7
更新日期：2011-06-01 00:00:00
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-013-0207-5
更新日期：2013-12-01 00:00:00
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-012-0176-0
更新日期：2012-12-01 00:00:00
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-008-0034-2
更新日期：2008-12-01 00:00:00
abstract：:Mice lacking the pro-adhesive matricellular protein connective tissue growth factor (CTGF/CCN2) display an embryonic lethal phenotype due to defects in bone and cartilage. However, the specific role of CCN2 in skin development is unknown. Here, we generated mice deleted for CCN2 in the entire body (using a cre/lox sys...
journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-011-0129-z
更新日期：2011-08-01 00:00:00
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-007-0009-8
更新日期：2007-09-01 00:00:00
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-010-0108-9
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journal_title：Journal of cell communication and signaling
pub_type： 杂志文章
doi：10.1007/s12079-014-0220-3
更新日期：2014-06-01 00:00:00
