Inhibition of apoptosis in rat mesangial cells by tissue inhibitor of metalloproteinase-1.

@article{Lin2002InhibitionOA,
  title={Inhibition of apoptosis in rat mesangial cells by tissue inhibitor of metalloproteinase-1.},
  author={Hongli Lin and Xiangmei Chen and Jianzhong Wang and Zhiheng Yu},
  journal={Kidney international},
  year={2002},
  volume={62 1},
  pages={
          60-9
        }
}
BACKGROUND Tissue inhibitor of metalloproteinase-1 (TIMP-1) is an important inhibitor of extracellular matrix degradation. Recently, it was reported that TIMP-1 also could inhibit apoptosis in B type lymphocyte. This study was designed to examine the effects of TIMP-1 on mesangial cell apoptosis. METHODS The full-length cDNA of TIMP-1 was cloned and used to construct two recombinant vectors, TIMP-1S and TIMP-1AS, encoding sense TIMP-1 and antisense TIMP-1, respectively. The vectors were… 
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33 Citations
Background Citations
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Methods Citations
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Results Citations
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33 Citations

Citation Type

Citation Type

Tissue inhibitor of metalloproteinase-1 exacerbated renal interstitial fibrosis through enhancing inflammation.
  • G. Cai, Xue-guang Zhang, +9 authors Xiangmei Chen
  • Biology, Medicine
    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
  • 2008
TLDR
Overexpression of TIMP-1 could promote renal interstitial fibrosis through the inflammatory pathway, which might be partly induced by upregulating ICAM-1.
Tissue inhibitor of metalloproteinase-1 promotes NIH3T3 fibroblast proliferation by activating p-Akt and cell cycle progression
TLDR
Overexpression of intracellular TIMP-1 stimulated NIH3T3 fibroblast proliferation in a matrix metalloproteinase (MMP)-independent manner by activating the p-Akt pathway and related cell cycle progression.
Exogenous Tissue Inhibitor of Metalloproteinase‐1 Promotes Endothelial Cell Survival Through Activation of the Phosphatidylinositol 3‐Kinase/Akt Pathway
TLDR
The findings suggest that TIMP‐1, generated upon inflammation, acts as an antiapoptotic molecule that can prevent EC apoptosis through activation of the PI3‐kinase and phosphorylation of the Akt kinase.
Tissue Inhibitor of Metalloproteinase-1 Protects Human Breast Epithelial Cells Against Intrinsic Apoptotic Cell Death via the Focal Adhesion Kinase/Phosphatidylinositol 3-Kinase and MAPK Signaling Pathway*
TLDR
TIMP-1-activated cell survival signaling down-regulates caspase-mediated classical apoptotic pathways induced by a variety of stimuli including anoikis, staurosporine exposure, and growth factor withdrawal, which greatly enhances apoptotic cell death.
TIMP-1 promotes age-related renal fibrosis through upregulating ICAM-1 in human TIMP-1 transgenic mice.
TLDR
The results indicated that TIMP-1 could promote age-related renal fibrosis, which was partly attributed to enhancing inflammation through upregulation of ICAM-1.
ANG II increases TIMP-1 expression in rat aortic smooth muscle cells in vivo.
TLDR
It is demonstrated that ANG II increases TIMP-1 expression in rat aortic smooth muscle cells occurs in the absence of histological changes at the vascular wall, as well as in the short- and long-term chronic ANG II treatments.
Tissue Inhibitor of Metalloproteinase 1 Activates Normal Human Granulocytes, Protects Them from Apoptosis, and Blocks Their Transmigration during Inflammation
TLDR
The data suggest that TIMP-1 specifically blocks the transmigration of granulocytes into urine, which might contribute to the pathogenesis of renal scarring following acute pyelonephritis.
Antifibrotic effects of a tissue inhibitor of metalloproteinase‐1 antibody on established liver fibrosis in rats
TLDR
Administration of a TIMP‐1 antibody attenuated CCl4‐induced liver fibrosis and decreased HSC activation and MMP‐2 activity.
The role of tissue inhibitors of metalloproteinases in tumorigenesis and metastasis.
TLDR
A comprehensive assessment of their function during tumorigenesis reveals substantial effects on cell proliferation, apoptosis, angiogenesis, invasion, and metastasis as well as a potential role in genomic instability.
The Role of Tissue Inhibitors of Metalloproteinases in Tumorigenesis and Metastasis
TLDR
A comprehensive assessment of their function during tumorigenesis reveals substantial effects on cell proliferation, apoptosis, angiogenesis, invasion, and metastasis as well as a potential role in genomic instability.
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References

SHOWING 1-10 OF 62 REFERENCES
Tissue inhibitor of metalloproteinase-1 inhibits apoptosis of human breast epithelial cells.
TLDR
It is demonstrated that TIMP-1 inhibits cell death induced by hydrogen peroxide, Adriamycin, or X-ray irradiation, suggesting that the antiapoptotic activity of TIMp-1 does not depend on its ability to stabilize cell-matrix interactions.
Divergent effects of tissue inhibitor of metalloproteinase-1, -2, or -3 overexpression on rat vascular smooth muscle cell invasion, proliferation, and death in vitro. TIMP-3 promotes apoptosis.
TLDR
This study is the first to compare systematically the effect of overexpression of three TIMPs in any cell, and found similar effects on invasion mediated by inhibition of MMP activity, but widely divergent effects on proliferation and death through actions of TIMP-2 and -3 independent of M MP inhibition.
In vitro suppression of programmed cell death of B cells by tissue inhibitor of metalloproteinases-1.
TLDR
It is demonstrated that TIMP-1 suppresses apoptosis in B cells and suggests a novel activity for TIMp-1 in tissue homeostasis.
Tissue inhibitor of metalloproteinase (TIMP)-1 induces differentiation and an antiapoptotic phenotype in germinal center B cells.
TLDR
A role for TIMP-1 in BLs is suggested, and its value as a prognostic factor is supported, as well as upregulation of activation and survival markers.
Cell growth-promoting activity of tissue inhibitor of metalloproteinases-2 (TIMP-2).
TLDR
TIMP-2 seems to be another new TIMP cell-growth factor in serum, besides TIMP-1, and the fact that both reductively alkylated TIMPs had no MMP inhibitory activity, but significantly stimulated cell proliferation clearly indicates that the cell-proliferation.
Metalloproteinase inhibition and erythroid potentiation are independent activities of tissue inhibitor of metalloproteinases-1.
TLDR
It is shown that the antiproteolytic and growth factor activities of the TIMP-1 molecule are physically and functionally distinct.
TIMP‐2 over‐expression reduces invasion and angiogenesis and protects B16F10 melanoma cells from apoptosis
TLDR
The data confirm the role of TIMP‐2 in the down‐regulation of metastasis and angiogenesis but indicate a possible involvement in tumor cell survival.
Interleukin-1 beta induces interstitial collagenase gene expression and protein secretion in renal mesangial cells.
TLDR
The data suggest that IL-1 beta stimulates interstitial collagenase synthesis and activation and that a tyrosine kinase pathway is involved in the signal transduction mechanisms and is not dependent on endogenous prostaglandin biosynthesis.
In situ hybridization studies of matrix metalloproteinase-3, tissue inhibitor of metalloproteinase-1 and type IV collagen in diabetic nephropathy.
TLDR
Results indicate that IV-C, MMP-3 and TIMP-1 mRNAs are expressed in glomerular resident cells, tubular epithelial cells and infiltrating cells in renal tissue of DN, and suggest that their expression changes with the degree of mesangial expansion and interstitial injury.
Glomerular expression of tissue inhibitor of metalloproteinase (TIMP-1) in normal and diabetic rats.
TLDR
Western blot analysis of glomerular proteins showed that there was an early increase in TIMP-1 expression during the rapid phase of glomersular hypertrophy that follows the onset of hyperglycemia, and this increase was ameliorated by insulin treatment that normalized blood glucose levels.
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