Source:http://linkedlifedata.com/resource/pubmed/id/17311296
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2007-6-4
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| pubmed:abstractText |
Different rigidities of adhesive collagen substrate affect cellular functions with unclear mechanisms. Here, we cultured a renal epithelial cell line (LLC-PK1) and a tumor cell line (HeLa) on substrates of different rigidities and compared the cell type-specific responses. The culture dish was coated with a very thin layer of collagen gel (control group) or overlaid with collagen gel (soft substrate). LLC-PK1 cells contracted as they grew on collagen gel and the apoptotic bodies obviously appeared with time. The protein levels of procaspase-12 and its downstream target procaspase-3 were decreased when LLC-PK1 cells cultured on collagen gel. Mu-calpain was activated on collagen gel. Collage gel also induced the cleavage of alpha-spectrin which resulted in the disorganization of actin cytoskeleton. In contrast, there was no significant change in cytochrome c revelation, mitochondrial membrane potential, and the protein levels of procaspase-8 and procaspase-9. Moreover, soft substrate caused elevated cytosolic Ca(2+), Ca(2+) overload in ER and upregulation of capacitative calcium entry. Ca(2+) chelator or channel blocker partially rescued the collagen-gel induced apoptosis by inhibiting mu-calpain activation. In contrast, for HeLa cells cultured either on collagen gel or on gel-coated dish, there was no significant change in positive Annexin V staining, no activation of procaspase-12 and no cleavage of mu-calpain. Thus, soft substrate induces apoptosis in LLC-PK1 cells by the disturbance of Ca(2+) homeostasis.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calpain,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 12,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Collagen Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Gels,
http://linkedlifedata.com/resource/pubmed/chemical/Spectrin,
http://linkedlifedata.com/resource/pubmed/chemical/mu-calpain
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| pubmed:status |
MEDLINE
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| pubmed:month |
Aug
|
| pubmed:issn |
0021-9541
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
212
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
401-10
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| pubmed:meshHeading |
pubmed-meshheading:17311296-Actins,
pubmed-meshheading:17311296-Animals,
pubmed-meshheading:17311296-Apoptosis,
pubmed-meshheading:17311296-Calcium,
pubmed-meshheading:17311296-Calpain,
pubmed-meshheading:17311296-Caspase 12,
pubmed-meshheading:17311296-Caspase 3,
pubmed-meshheading:17311296-Collagen Type I,
pubmed-meshheading:17311296-Cytoskeleton,
pubmed-meshheading:17311296-Endoplasmic Reticulum,
pubmed-meshheading:17311296-Enzyme Activation,
pubmed-meshheading:17311296-Epithelial Cells,
pubmed-meshheading:17311296-Female,
pubmed-meshheading:17311296-Gels,
pubmed-meshheading:17311296-HeLa Cells,
pubmed-meshheading:17311296-Homeostasis,
pubmed-meshheading:17311296-Humans,
pubmed-meshheading:17311296-Kidney,
pubmed-meshheading:17311296-LLC-PK1 Cells,
pubmed-meshheading:17311296-Spectrin,
pubmed-meshheading:17311296-Swine,
pubmed-meshheading:17311296-Time Factors,
pubmed-meshheading:17311296-Uterine Cervical Neoplasms
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| pubmed:year |
2007
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| pubmed:articleTitle |
Soft substrate induces apoptosis by the disturbance of Ca2+ homeostasis in renal epithelial LLC-PK1 cells.
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| pubmed:affiliation |
Institute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.
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| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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