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Search results for: Anti-ADAMTS-1(A disintegrin and metalloproteinase with thrombospondin motifs 1) Antibody

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#34049577   2021/05/28 To Up

Denosumab alleviates intervertebral disc degeneration adjacent to lumbar fusion by inhibiting endplate osteochondral remodeling and vertebral osteoporosis in ovariectomized rats.

Although adjacent segmental intervertebral disc degeneration (ASDD) is one of the most common complications after lumbar fusion, its exact mechanism remains unclear. As an antibody to RANKL, denosumab (Dmab) effectively reduces bone resorption and stimulates bone formation, which can increase bone mineral density (BMD) and improve osteoporosis. However, it has not been confirmed whether Dmab has a reversing or retarding effect on ASDD.
Qi Sun, Fa-Ming Tian, Fang Liu, Jia-Kang Fang, Yun-Peng Hu, Qiang-Qiang Lian, Zhuang Zhou, Liu Zhang

1837 related Products with: Denosumab alleviates intervertebral disc degeneration adjacent to lumbar fusion by inhibiting endplate osteochondral remodeling and vertebral osteoporosis in ovariectomized rats.

100 μg100 mg

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#33537811   2021/02/04 To Up

Inhibition of PDGF-BB reduces alkali-induced corneal neovascularization in mice.

The aim of the present study was to investigate the role of platelet‑derived growth factor (PDGF)‑BB/PDGF receptor (R)‑β signaling in an experimental murine corneal neovascularization (CrNV) model. Experimental CrNV was induced by alkali injury. The intra‑corneal expression of PDGF‑BB was examined using immunohistochemistry. The effect of PDGF‑BB on CrNV was evaluated using immunofluorescence staining. The expression levels of PDGFR‑β in human retinal endothelial cells (HRECs) under normal conditions or following cobalt chloride treatment, which induced hypoxic conditions, was assessed using reverse transcription‑quantitative PCR. The effect of exogenous treatment of PDGF‑BB on the proliferation, migration and tube formation of HRECs under normoxic or hypoxic conditions was evaluated using Cell Counting Kit‑8, wound healing and 3D Matrigel capillary tube formation assays, respectively. The results indicated that the intra‑corneal expression levels of the proteins of PDGF‑BB and PDGFR‑β were detectable on days 2 and 7 following alkali injury. The treatment with neutralizing anti‑PDGF‑BB antibody resulted in significant inhibition of CrNV. The intra‑corneal expression levels of vascular endothelial growth factor A, matrix metallopeptidase (MMP)‑2 and MMP‑9 proteins were downregulated, while the expression levels of thrombospondin (TSP)‑1, TSP‑2, a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)‑1 and ADAMTS‑2 were upregulated significantly in mice treated with anti‑PDGF‑BB antibody. The expression levels of PDGFR‑β were upregulated in HRECs under hypoxic conditions compared with those noted under normoxic conditions. Recombinant human PDGF‑BB promoted the proliferation, migration and tube formation of HRECs under hypoxic conditions. The data indicated that PDGF‑BB/PDGFR‑β signaling was involved in CrNV and that it promoted endothelial cell proliferation, migration and tube formation. The pro‑angiogenic effects of this pathway may be mediated via the induction of pro‑angiogenic cytokine secretion and the suppression of anti‑angiogenic cytokine secretion.
Lei Chen, Hongya Wu, Chi Ren, Gaoqin Liu, Wenpeng Zhang, Weiming Liu, Peirong Lu

1037 related Products with: Inhibition of PDGF-BB reduces alkali-induced corneal neovascularization in mice.

48 assays 1 mg96T100 ul2ug96 assays 1 mg50 ul48 assays96 assays

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#33221124   2020/11/07 To Up

Successful management of three patients with autoimmune thrombotic thrombocytopenic purpura with paradigm-changing therapy: Caplacizumab, steroids, plasma exchange, rituximab, and intravenous immunoglobulins (CASPERI).

Autoimmune thrombotic thrombocytopenic purpura (aTTP) is a severe disease caused by the production of autoantibodies against von Willebrand factor (vWF)-cleaving ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin-1 motifs; 13th member of the family). In 2018, caplacizumab was approved for the treatment of patients with acute aTTP in conjunction with plasma exchange (PE) and immunosuppressive therapy. Immunosuppressive standard of care includes mainly steroids whereas rituximab is usually reserved for refractory cases. We report three patients with a first acute episode of aTTP who were successfully treated with a paradigm-changing scheme including standard of care (caplacizumab, steroids and PE) plus upfront therapy with rituximab and intravenous immunoglobulins (CASPERI). Rituximab was added 1-4 days after diagnosis, when ADAMTS13 autoantibodies were detected and intravenous immunoglobulins were administered after performing PE using albumin as replacement solution. Successful outcome was observed in all three patients: platelet recovery (>150 × 10/L) was observed after 3, 4, and 5 days from diagnosis; ADAMTS13 activity >5% and ADAMTS13 autoantibodies were negative after 14, 15, and 21 days from diagnosis. In conclusion, caplacizumab, steroids, PE (using fresh frozen plasma or albumin as replacement solution and adding intravenous immunoglobulins) plus upfront rituximab therapy was a safe and efficient combination to induce remission in case of acute aTTP.
Joan Cid, Amanda Isabel Pérez-Valencia, Miguel Ángel Torrente, Alberto Ávarez-Larrán, Maribel Díaz-Ricart, Jordi Esteve, Miquel Lozano

1322 related Products with: Successful management of three patients with autoimmune thrombotic thrombocytopenic purpura with paradigm-changing therapy: Caplacizumab, steroids, plasma exchange, rituximab, and intravenous immunoglobulins (CASPERI).

96T100ml100 ml100ug

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#32055439   2020/02/01 To Up

Acute lung injury after plasma exchange in a patient with anti-MDA5 antibody-positive, rapidly progressive, interstitial lung disease:A case report.

The presence of anti-melanoma differentiation-associated gene 5 antibody (anti-MDA5 Ab) is closely associated with rapidly progressive interstitial lung disease (RP-ILD) in patients with clinically amyopathic dermatomyositis. Despite intensive immunosuppressive therapies, some of these patients still have a poor prognosis with few treatment options. Although removal of pathogenic autoantibodies and cytokines by plasma exchange (PE) could be a treatment option, its safety and efficacy have never been determined. We report a patient with anti-MDA5 Ab-positive RP-ILD who was refractory to intensive therapies including steroids, cyclosporine, and intravenous cyclophosphamide, and then treated by PE to prevent the progression of RP-ILD. Shortly after the initiation of PE therapy, however, his respiratory condition suddenly deteriorated due to acute pulmonary edema and the patient died on the following day. Transfusion-related acute lung injury (TRALI) would be the most likely cause of the acute pulmonary edema because there was no sign of circulatory overload. To the best of our knowledge, this is the first report showing a critical adverse event associated with PE therapy for these patients. This case supports the idea that the presence of ILD could increase a risk for TRALI and therefore we should carefully evaluate the eligibility for PE therapy of anti-MDA5 Ab-positive RP-ILD patients given the risk of acute lung injury. Further studies collecting more clinical data are necessary to assess the efficacy, safety, and risk factors of PE therapy for these patients.
Hiroyuki Kagawa, Kazuyuki Tsujino, Yuji Yamamoto, Ami Iwai, Reina Hara, Takanori Matsuki, Kiyoharu Fukushima, Yohei Oshitani, Kenji Yoshimura, Mari Miki, Keisuke Miki, Seigo Kitada, Masahide Mori, Hiroshi Kida

1293 related Products with: Acute lung injury after plasma exchange in a patient with anti-MDA5 antibody-positive, rapidly progressive, interstitial lung disease:A case report.



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#32004530   2020/01/29 To Up

The protective effects of dulaglutide against advanced glycation end products (AGEs)-induced degradation of type Ⅱ collagen and aggrecan in human SW1353 chondrocytes.

Osteoarthritis (OA) is one of the most prevalent degenerative joint diseases, and the risk of developing OA significantly increases with age as well as with concomitant diseases, such as diabetes. Advanced glycation end products (AGEs) accumulate in the body over time and are associated with increased expression of various molecules involved in the pathophysiology of OA. Prostaglandin E (PGE), along with its precursor cyclooxygenase (COX)-2, plays an integral role in the pathogenesis of OA and is highly upregulated in response to AGEs. The most significant event in OA is excessive degradation of the cartilage extracellular matrix, which is composed primarily of type II collagen and aggrecan. In the present study, we investigated the involvement of the receptor for glucagon-like peptide (GLP)-1 in the response of chondrocytes to insult from AGEs using the selective GLP-1 agonist dulaglutide. Firstly, our results indicate that AGEs reduced the expression of the receptor for GLP-1 (GLP-1R) in human SW1353 chondrocytes. Interestingly, we found that treatment with dulaglutide could ameliorate deterioration of the components of the articular extracellular matrix (ECM), such as type II collagen and aggrecan, induced by AGEs through downregulation of matrix metalloproteinase (MMP)-3 and MMP-13 and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4 and ADAMTS-5. We also found that dulaglutide exerted a potent inhibitory effect against the expression of several proinflammatory cytokines and chemokines closely associated with OA, as well as the production of reactive oxygen species (ROS). Finally, we showed that the effects of dulaglutide were mediated through the nuclear factor kappa-B (NF-κB) pathway. Our findings indicate that dulaglutide displayed a robust protective effect against AGEs-induced damage in chondrocytes, suggesting that it might be a possible therapeutic agent for the treatment of OA.
Hai Li, Jianhai Chen, Biao Li, Xiaoyan Fang

2122 related Products with: The protective effects of dulaglutide against advanced glycation end products (AGEs)-induced degradation of type Ⅱ collagen and aggrecan in human SW1353 chondrocytes.

50 UG 100 UG 10 UG96T

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#31708547   2019/11/08 To Up

Thrombotic Thrombocytopenic Purpura Treated with Rituximab Associated with Primary Sjögren's Syndrome and Primary Hypothyroidism.

A 47-year-old man was admitted to our hospital because of thrombocytopenia and consciousness disturbance. As his laboratory data showed undetectable activity of a disintegrin-like and metalloproteinase with thrombospondin type 1 motifs 13 (ADAMTS13) and the presence of ADAMTS13 inhibitor, he was diagnosed with acquired thrombotic thrombocytopenic purpura (TTP). Asymptomatic primary Sjögren's syndrome (SS) and primary hypothyroidism were incidentally diagnosed on screening. After initial plasma exchange therapy and pulse corticosteroid therapy, the patient received rituximab therapy for refractory TTP with "inhibitor boosting" and recovered. TTP secondary to primary SS is rare but can trigger refractory TTP. Treatment with rituximab, which is considered "inhibitor boosting," should be considered when re-exacerbation occurs.
Taiki Okumura, Koji Hashimoto, Daiki Aomura, Yukihumi Kurasawa, Yuuta Hara, Kazuaki Fujii, Tomoe Masuda, Kosuke Sonoda, Akinori Yamaguchi, Yohei Ogawa, Yuji Kamijo

1810 related Products with: Thrombotic Thrombocytopenic Purpura Treated with Rituximab Associated with Primary Sjögren's Syndrome and Primary Hypothyroidism.

100ug100ug100ug100ul100ug 100ul100ug100ug100ug100ug 100ul

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#31366218   2019/08/01 To Up

Mice Exhibit Altered Aggrecan Proteolytic Profiles That Correlate With Ascending Aortic Anomalies.

Investigate the requirement of Aggrecan (Acan) cleavage during aortic wall development in a murine model with ADAMTS (a disintegrin-like and metalloprotease domain with thrombospondin-type motifs) 5 deficiency and bicuspid aortic valves.
Loren E Dupuis, E Lockett Nelson, Brittany Hozik, Sarah C Porto, Alexandra Rogers-DeCotes, Amanda Fosang, Christine B Kern

1305 related Products with: Mice Exhibit Altered Aggrecan Proteolytic Profiles That Correlate With Ascending Aortic Anomalies.

1mg100μg100.00 ug100μg2 mL100μg1.00 flask100μg1.00 flask

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#31177384   2019/06/08 To Up

Atypical reduction of plasma ADAMTS13 activity by a non-IgG-type inhibitor in a patient with hemolytic uremic syndrome caused by Shiga toxin-producing Escherichia coli.

Thrombotic microangiopathies include hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP). Measurement of plasma levels of "a disintegrin-like and metalloproteinase with thrombospondin type 1 motifs 13" (ADAMTS13) activity can distinguish HUS from TTP. Reduced plasma ADAMTS13 activity (< 10% normal range) is atypical for HUS, but not for TTP. However, we detected reduced ADAMTS13 activity in a patient with Shiga toxin-producing Escherichia coli-associated HUS caused by non-IgG anti-ADMTS13 autoantibodies. Furthermore, the patient exhibited possible genetic abnormalities associated with atypical HUS. The patient fully recovered after administration of supportive therapy. To the best of our knowledge, very few cases of STEC-HUS with reduced ADAMTS13 activity have been reported; thus far, none have described the presence of non-IgG anti-ADMTS13 autoantibodies. Therefore, we suggest that anti-ADAMTS13 analyses should be performed in patients diagnosed with STEC-HUS, especially in those who present with prolonged healing or unexpected clinical symptoms.
Shinya Nakayama, Shuma Hirashio, Haruka Yorishima, Toshiki Doi, Yoko Yoshida, Masanori Matsumoto, Takao Masaki

2479 related Products with: Atypical reduction of plasma ADAMTS13 activity by a non-IgG-type inhibitor in a patient with hemolytic uremic syndrome caused by Shiga toxin-producing Escherichia coli.

100.00 ug96T400Tests96T100.00 ug20 96 assays 100 0.1ml (1mg/ml)200

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#30989556   2019/04/15 To Up

Pro-atherogenic proteoglycanase ADAMTS-1 is down-regulated by lauric acid through PI3K and JNK signaling pathways in THP-1 derived macrophages.

The prevalence of atherosclerosis has increased significantly in the recent years due to sedentary lifestyle and high-fat diet. However, the association between saturated fat intake and the increased risk for atherosclerotic cardiovascular diseases remains heavily debated. Lauric acid belongs to the saturated fatty acid group and its unique medium chain fatty acid properties are proven to be beneficial to humans in many ways. Thus, the aim of this project is to investigate the effect of lauric acid on the expression of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) genes-ADAMTS-1, ADAMTS-4, and ADAMTS-5-in macrophages. These genes encode for proteases that participate in the extracellular matrix remodeling and they play important roles in the vulnerability of atherosclerotic plaque. Here, we show that the treatment of 20 µM of lauric acid successfully reduced both transcriptional and translational expressions of these genes in THP-1 differentiated macrophages after 24-h incubation. Further cell signaling experiments using a panel of kinase inhibitors and phosphorylated antibodies proved that lauric acid down-regulated ADAMTS-1 by reducing the activation of PI3K and JNK at Tyr458 and Tyr185, respectively. Finally, JNK1 siRNA knockdown assay confirmed that ADAMTS-1 was regulated through JNK pathway, and lauric acid interfered with this pathway to down-regulate ADAMTS-1 expression. Although preliminary, this present study indicates that lauric acid has the potential to stabilize atherosclerotic plaque and may prevent thrombosis by interfering with the ADAMTS-1 expression through PI3K/JNK pathways.
Melissa-Hui-Ling Ong, Hong-Kin Wong, Tengku-Sifzizul Tengku-Muhammad, Quok-Cheong Choo, Choy-Hoong Chew

2622 related Products with: Pro-atherogenic proteoglycanase ADAMTS-1 is down-regulated by lauric acid through PI3K and JNK signaling pathways in THP-1 derived macrophages.

100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized

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