μ-Calpain is involved in the regulation of TNF-α-induced matrix metalloproteinase-3 release in a rheumatoid synovial cell line

2006 ◽  
Vol 343 (3) ◽  
pp. 937-942 ◽  
Author(s):  
Masaji Morita ◽  
Yoshiko Banno ◽  
Taikoh Dohjima ◽  
Satoshi Nozawa ◽  
Kazunari Fushimi ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Cell Line ◽  
Synovial Cell ◽  
Matrix Metalloproteinase 3 ◽  
Tnf Α

scholarly journals Tissue Inhibitor of Metalloproteinase-3 Ameliorates Diabetes-Induced Retinal Inflammation

2022 ◽  
Vol 12 ◽  
Author(s):  
Ahmed M. Abu El-Asrar ◽  
Ajmal Ahmad ◽  
Mohd Imtiaz Nawaz ◽  
Mohammad Mairaj Siddiquei ◽  
Alexandra De Zutter ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Matrix Metalloproteinase ◽  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Tissue Inhibitor ◽  
Matrix Metalloproteinase 3 ◽  
Tnf Α ◽  
Brb Breakdown

Purpose: Endogenous tissue inhibitor of matrix metalloproteinase-3 (TIMP-3) has powerful regulatory effects on inflammation and angiogenesis. In this study, we investigated the role of TIMP-3 in regulating inflammation in the diabetic retina.Methods: Vitreous samples from patients with proliferative diabetic retinopathy (PDR) and non-diabetic patients were subjected to Western blot analysis. Streptozotocin-treated rats were used as a preclinical diabetic retinopathy (DR) model. Blood-retinal barrier (BRB) breakdown was assessed with fluorescein isothiocyanate (FITC)-conjugated dextran. Rat retinas, human retinal microvascular endothelial cells (HRMECs) and human retinal Müller glial cells were studied by Western blot analysis and ELISA. Adherence of human monocytes to HRMECs was assessed and in vitro angiogenesis assays were performed.Results: Tissue inhibitor of matrix metalloproteinase-3 in vitreous samples was largely glycosylated. Intravitreal injection of TIMP-3 attenuated diabetes-induced BRB breakdown. This effect was associated with downregulation of diabetes-induced upregulation of the p65 subunit of NF-κB, intercellular adhesion molecule-1 (ICAM-1), and vascular endothelial growth factor (VEGF), whereas phospho-ERK1/2 levels were not altered. In Müller cell cultures, TIMP-3 significantly attenuated VEGF upregulation induced by high-glucose (HG), the hypoxia mimetic agent cobalt chloride (CoCl2) and TNF-α and attenuated MCP-1 upregulation induced by CoCl2 and TNF-α, but not by HG. TIMP-3 attenuated HG-induced upregulation of phospho-ERK1/2, caspase-3 and the mature form of ADAM17, but not the levels of the p65 subunit of NF-κB and the proform of ADAM17 in Müller cells. TIMP-3 significantly downregulated TNF-α-induced upregulation of ICAM-1 and VCAM-1 in HRMECs. Accordingly, TIMP-3 significantly decreased spontaneous and TNF-α- and VEGF-induced adherence of monocytes to HRMECs. Finally, TIMP-3 significantly attenuated VEGF-induced migration, chemotaxis and proliferation of HRMECs.Conclusion:In vitro and in vivo data point to anti-inflammatory and anti-angiogenic effects of TIMP-3 and support further studies for its applications in the treatment of DR.

scholarly journals A comparative proteomics study of a synovial cell line stimulated with TNF‐α

FEBS Open Bio ◽  
2016 ◽  
Vol 6 (5) ◽  
pp. 418-424 ◽  
Author(s):  
Seiji Shibasaki ◽  
Miki Karasaki ◽  
Shunsuke Aburaya ◽  
Hironobu Morisaka ◽  
Yumiko Takeda ◽  
...  
Keyword(s):  
Cell Line ◽  
Synovial Cell ◽  
Comparative Proteomics ◽  
Tnf Α ◽  
Proteomics Study

scholarly journals Matrix Metalloproteinase-3 in Odontoblastic Cells Derived from Ips Cells: Unique Proliferation Response as Odontoblastic Cells Derived from ES Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e83563 ◽  
Author(s):  
Taiki Hiyama ◽  
Nobuaki Ozeki ◽  
Makio Mogi ◽  
Hideyuki Yamaguchi ◽  
Rie Kawai ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Es Cells ◽  
Ips Cells ◽  
Matrix Metalloproteinase 3 ◽  
Proliferation Response

scholarly journals Follicle stimulating hormone and estradiol alter immune response in osteoarthritic mice in an opposite manner

2021 ◽  
Vol 35 ◽  
pp. 205873842110161
Author(s):  
Lyudmila Belenska-Todorova ◽  
Ralitsa Zhivkova ◽  
Maya Markova ◽  
Nina Ivanovska
Keyword(s):  
Follicle Stimulating Hormone ◽  
Endocrine System ◽  
Synovial Cell ◽  
Nuclear Factor Κb ◽  
Cartilage Degradation ◽  
Osteoclast Formation ◽  
Blue Staining ◽  
Serum Osteocalcin ◽  
Tnf Α ◽  
Stimulating Hormone

Although a number of studies have shown that the occurrence and progression of osteoarthritis (OA) is related to endocrine system dysfunction, there is limited evidence about what roles sex hormones play. The aim of the present study was to examine the capacity of 17β-estradiol (ED) and follicle stimulating hormone (FSH) to alter the differentiation of bone marrow (BM) cells in arthritic mice. The experiments were conducted in collagenase-induced osteoarthritis in mice. Cartilage degradation was observed by safranin and toluidine blue staining. Flow cytometry was used to define different BM and synovial cell populations. The influence of FSH and ED on osteoclastogenesis was studied in BM cultures and on the osteoblastogenesis in primary calvarial cultures. The levels of IL-8, TNF-α, FSH, and osteocalcin were estimated by ELISA. FSH increased cartilage degradation and serum osteocalcin levels, while ED abolished it and lowered serum osteocalcin. FSH elevated the percentage of monocytoid CD14+/RANK+ and B cell CD19+/RANK+ cells in contrast to ED which inhibited the accumulation of these osteogenic populations. Also, ED changed the percentage of CD105+/F4/80+ and CD11c+ cells in the synovium. FSH augmented and ED suppressed macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast (OC) formation, and this correlated with a respective increase and decrease of IL-8 secretion. FSH did not influence osteoblast (OB) formation while ED enhanced this process in association with changes of TNF-α, IL-8, and osteocalcin production. ED reduced osteoclast generation in bone. The key outcome of the current study is that both hormones influenced BM cell differentiation, with FSH favoring osteoclast formation and ED favoring osteoblast accumulation.

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