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  1. Article ; Online: PPAR-δ: A key nuclear receptor in vascular function and remodeling.

    Xiao, Lei / Wang, Nanping

    Journal of molecular and cellular cardiology

    2022  Volume 169, Page(s) 1–9

    Abstract: Vascular function is critical for the maintenance of body's homeostasis and is tightly regulated by complex interactions among the vessel wall, hemodynamics, neuro-endocrine factors and metabolic alteration. A variety of cardiovascular risks instigate ... ...

    Abstract Vascular function is critical for the maintenance of body's homeostasis and is tightly regulated by complex interactions among the vessel wall, hemodynamics, neuro-endocrine factors and metabolic alteration. A variety of cardiovascular risks instigate pro-inflammatory and oxidative responses to impair vascular function, leading to pathological vascular remodeling. Peroxisome proliferator-activated receptor-δ (PPAR-δ) is a ligand-activated nuclear receptor and transcription factor that regulates cell growth and differentiation, metabolism and wound healing. Being expressed in vascular endothelial cells, smooth muscle cells and monocytes, PPAR-δ has pleotropic effects in vascular biology and pathology. In this review, we discussed recent advances regarding the functional roles of PPAR-δ as a critical regulator of vascular homeostasis and as a potential target for the intervention of cardiovascular diseases.
    MeSH term(s) Endothelial Cells/metabolism ; Gene Expression Regulation ; Myocytes, Smooth Muscle/metabolism ; PPAR delta/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism
    Chemical Substances PPAR delta ; Receptors, Cytoplasmic and Nuclear
    Language English
    Publishing date 2022-04-28
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2022.04.019
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  2. Article ; Online: IgG4-related autoimmune pancreatitis and sclerosing cholangitis: A case report and literature review.

    Wang, Nanping / Zhu, Peng / Xiang, Yue / Tao, Liping / Huang, Tao / Feng, Zhisong

    Medicine

    2024  Volume 103, Issue 17, Page(s) e37922

    Abstract: Rationale: Immunoglobulin G4-related disease (IgG4-RD) can involve various organs throughout the body, primarily manifesting as endocrine dysfunction, visual impairment, jaundice, and limited sexual function. IgG4-related autoimmune pancreatitis is ... ...

    Abstract Rationale: Immunoglobulin G4-related disease (IgG4-RD) can involve various organs throughout the body, primarily manifesting as endocrine dysfunction, visual impairment, jaundice, and limited sexual function. IgG4-related autoimmune pancreatitis is triggered by autoimmune reactions and characterized by structural changes in the pancreas and pancreatic ducts. The disease mainly affects middle-aged and elderly males, typically presenting as progressive painless jaundice and misdiagnosed as cholangiocarcinoma or pancreatic cancer.
    Patient concerns: This study reports a 54-year-old male who consulted with different institutions multiple times due to diabetes, pancreatitis, elevated liver enzymes, and jaundice.
    Diagnoses: Magnetic resonance imaging revealed swollen head of the pancreas and atrophic tail. Liver and pancreatic tissue pathology showed IgG4 plasma cell infiltration, while liver biopsy indicated interface hepatitis, liver fibrosis, and pseudolobule formation, with no evidence of bile duct damage.
    Interventions: Following hormone therapy, the patient's serum IgG4 levels and liver enzyme levels returned to normal.
    Outcomes: The disease relapsed 2 years after maintaining hormone therapy, and the patient underwent additional hormone-induced remission therapy combined with azathioprine.
    Lessons: The purpose of this research report is to enhance the awareness and understanding of IgG4-RD, emphasizing the necessity for personalized treatment strategies that take into account its recurrence, associations, and imaging features. This report provides valuable insights and guidance for clinicians in managing and diagnosing patients with IgG4-RD.
    MeSH term(s) Humans ; Male ; Middle Aged ; Cholangitis, Sclerosing/diagnosis ; Cholangitis, Sclerosing/immunology ; Autoimmune Pancreatitis/diagnosis ; Autoimmune Pancreatitis/immunology ; Autoimmune Pancreatitis/drug therapy ; Immunoglobulin G4-Related Disease/diagnosis ; Immunoglobulin G4-Related Disease/complications ; Immunoglobulin G/blood ; Immunoglobulin G/immunology ; Pancreas/pathology ; Pancreas/diagnostic imaging
    Chemical Substances Immunoglobulin G
    Language English
    Publishing date 2024-05-02
    Publishing country United States
    Document type Journal Article ; Case Reports ; Review
    ZDB-ID 80184-7
    ISSN 1536-5964 ; 0025-7974
    ISSN (online) 1536-5964
    ISSN 0025-7974
    DOI 10.1097/MD.0000000000037922
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  3. Article ; Online: Sodium-Glucose Cotransporter-2 Inhibitors in Vascular Biology: Cellular and Molecular Mechanisms.

    Xiao, Lei / Nie, Xin / Cheng, Yanyan / Wang, Nanping

    Cardiovascular drugs and therapy

    2021  Volume 35, Issue 6, Page(s) 1253–1267

    Abstract: Sodium-glucose cotransporter-2 (SGLT2) inhibitors are new antidiabetic drugs that reduce hyperglycemia by inhibiting the glucose reabsorption in renal proximal tubules. Clinical studies have shown that SGLT2 inhibitors not only improve glycemic control ... ...

    Abstract Sodium-glucose cotransporter-2 (SGLT2) inhibitors are new antidiabetic drugs that reduce hyperglycemia by inhibiting the glucose reabsorption in renal proximal tubules. Clinical studies have shown that SGLT2 inhibitors not only improve glycemic control but also reduce major adverse cardiovascular events (MACE, cardiovascular and total mortality, fatal or nonfatal myocardial infarction or stroke) and hospitalization for heart failure (HF), and improve outcome in chronic kidney disease. These cardiovascular and renal benefits have now been confirmed in both diabetes and non-diabetes patients. The precise mechanism(s) responsible for the protective effects are under intensive investigation. This review examines current evidence on the cardiovascular benefits of SGLT2 inhibitors, with a special emphasis on the vascular actions and their potential mechanisms.
    MeSH term(s) Animals ; Antioxidants/metabolism ; Atherosclerosis/pathology ; Cardiovascular Diseases/prevention & control ; Carotid Intima-Media Thickness ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Endothelial Cells/drug effects ; Hemodynamics/drug effects ; Humans ; Hypoglycemic Agents/pharmacology ; Hypoglycemic Agents/therapeutic use ; Inflammation Mediators/metabolism ; Randomized Controlled Trials as Topic ; Renal Insufficiency, Chronic/prevention & control ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use ; Vascular Stiffness/drug effects
    Chemical Substances Antioxidants ; Hypoglycemic Agents ; Inflammation Mediators ; Sodium-Glucose Transporter 2 Inhibitors
    Language English
    Publishing date 2021-07-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 639068-7
    ISSN 1573-7241 ; 0920-3206
    ISSN (online) 1573-7241
    ISSN 0920-3206
    DOI 10.1007/s10557-021-07216-9
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  4. Article ; Online: Activation of the endocannabinoid system mediates cardiac hypertrophy induced by rosiglitazone.

    Liu, Ya-Han / Liu, Yan / Zhang, Xu / Fang, Li / Zhao, Bei-Lei / Wang, Nan-Ping

    Acta pharmacologica Sinica

    2022  Volume 43, Issue 9, Page(s) 2302–2312

    Abstract: Rosiglitazone (RSG) is a synthetic agonist of peroxisome proliferator-activated receptor-γ (PPARγ), which plays a central role in the regulation of metabolism. Meta-analyses have suggested that RSG is associated with increased cardiovascular risk. ... ...

    Abstract Rosiglitazone (RSG) is a synthetic agonist of peroxisome proliferator-activated receptor-γ (PPARγ), which plays a central role in the regulation of metabolism. Meta-analyses have suggested that RSG is associated with increased cardiovascular risk. However, the mechanisms underlying such adverse cardiac effects are still poorly understood. Here, we found that activation of PPARγ by RSG stimulated the endocannabinoid system (ECS), a membrane lipid signaling system, which induced cardiac hypertrophy. In neonatal rat cardiomyocytes, RSG increased the level of anandamide (AEA); upregulated the expression of N-acyl phosphatidylethanolamine phospholipase D (NapePLD), a key enzyme for AEA synthesis; and downregulated the expression of fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of AEA. Importantly, PPARγ activation increased the expression of cannabinoid receptor type 1 (CB1) through an identified binding site for PPARγ in the CB1 promoter region. Moreover, both the in vitro and in vivo results showed that inhibition of the ECS by rimonabant, an antagonist of CB1, attenuated RSG-induced cardiac hypertrophy, as indicated by decreased expression of cardiac hypertrophy markers (ANP and BNP), deactivation of the mTOR pathway, and decreased cardiomyocyte size. Thus, these results demonstrated that the ECS functions as a novel target of PPARγ and that the AEA/CB1/mTOR axis mediates RSG-induced cardiac remodeling.
    MeSH term(s) Animals ; Cardiomegaly/chemically induced ; Endocannabinoids ; Myocytes, Cardiac/metabolism ; PPAR gamma/metabolism ; Rats ; Receptor, Cannabinoid, CB1 ; Rosiglitazone/pharmacology ; TOR Serine-Threonine Kinases
    Chemical Substances Endocannabinoids ; PPAR gamma ; Receptor, Cannabinoid, CB1 ; Rosiglitazone (05V02F2KDG) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2022-02-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1360774-1
    ISSN 1745-7254 ; 0253-9756 ; 1671-4083
    ISSN (online) 1745-7254
    ISSN 0253-9756 ; 1671-4083
    DOI 10.1038/s41401-022-00858-x
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  5. Article ; Online: GRK2-YAP signaling is implicated in pulmonary arterial hypertension development.

    Ye, Peng / Deng, Yunfei / Gu, Yue / Liu, Pengfei / Luo, Jie / Pu, Jiangqin / Chen, Jingyu / Huang, Yu / Wang, Nanping / Ji, Yong / Chen, Shaoliang

    Chinese medical journal

    2024  Volume 137, Issue 7, Page(s) 846–858

    Abstract: Background: Pulmonary arterial hypertension (PAH) is characterized by excessive proliferation of small pulmonary arterial vascular smooth muscle cells (PASMCs), endothelial dysfunction, and extracellular matrix remodeling. G protein-coupled receptor ... ...

    Abstract Background: Pulmonary arterial hypertension (PAH) is characterized by excessive proliferation of small pulmonary arterial vascular smooth muscle cells (PASMCs), endothelial dysfunction, and extracellular matrix remodeling. G protein-coupled receptor kinase 2 (GRK2) plays an important role in the maintenance of vascular tone and blood flow. However, the role of GRK2 in the pathogenesis of PAH is unknown.
    Methods: GRK2 levels were detected in lung tissues from healthy people and PAH patients. C57BL/6 mice, vascular smooth muscle cell-specific Grk2 -knockout mice ( Grk2ΔSM22 ), and littermate controls ( Grk2flox/flox ) were grouped into control and hypoxia mice ( n  = 8). Pulmonary hypertension (PH) was induced by exposure to chronic hypoxia (10%) combined with injection of the SU5416 (cHx/SU). The expression levels of GRK2 and Yes-associated protein (YAP) in pulmonary arteries and PASMCs were detected by Western blotting and immunofluorescence staining. The mRNA expression levels of Grk2 and Yes-associated protein ( YAP ) in PASMCs were quantified with real-time polymerase chain reaction (RT-PCR). Wound-healing assay, 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay, and 5-Ethynyl-2'-deoxyuridine (EdU) staining were performed to evaluate the proliferation and migration of PASMCs. Meanwhile, the interaction among proteins was detected by immunoprecipitation assays.
    Results: The expression levels of GRK2 were upregulated in the pulmonary arteries of patients with PAH and the lungs of PH mice. Moreover, cHx/SU-induced PH was attenuated in Grk2ΔSM22 mice compared with littermate controls. The amelioration of PH in Grk2ΔSM22 mice was accompanied by reduced pulmonary vascular remodeling. In vitro study further confirmed that GRK2 knock-down significantly altered hypoxia-induced PASMCs proliferation and migration, whereas this effect was severely intensified by overexpression of GRK2 . We also identified that GRK2 promoted YAP expression and nuclear translocation in PASMCs, resulting in excessive PASMCs proliferation and migration. Furthermore, GRK2 is stabilized by inhibiting phosphorylating GRK2 on Tyr86 and subsequently activating ubiquitylation under hypoxic conditions.
    Conclusion: Our findings suggest that GRK2 plays a critical role in the pathogenesis of PAH, via regulating YAP expression and nuclear translocation. Therefore, GRK2 serves as a novel therapeutic target for PAH treatment.
    MeSH term(s) Animals ; Humans ; Mice ; Cell Proliferation/genetics ; Cells, Cultured ; Hypertension, Pulmonary/pathology ; Hypoxia/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Myocytes, Smooth Muscle/metabolism ; Pulmonary Arterial Hypertension ; Pulmonary Artery/pathology ; YAP-Signaling Proteins
    Chemical Substances YAP-Signaling Proteins ; Yap1 protein, mouse ; GRK2 protein, human (EC 2.7.11.15) ; GRK2 protein, mouse (EC 2.7.11.15)
    Language English
    Publishing date 2024-01-19
    Publishing country China
    Document type Journal Article
    ZDB-ID 127089-8
    ISSN 2542-5641 ; 0366-6999 ; 1002-0187
    ISSN (online) 2542-5641
    ISSN 0366-6999 ; 1002-0187
    DOI 10.1097/CM9.0000000000002946
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  6. Article: PPAR-delta in Vascular Pathophysiology.

    Wang, Nanping

    PPAR research

    2009  Volume 2008, Page(s) 164163

    Abstract: Peroxisome proliferator-activated receptors belong to the superfamily of ligand-dependent nuclear receptor transcription factors, which include three subtypes: PPAR-alpha, beta/delta, and gamma. PPAR-delta, play important roles in the regulation of cell ... ...

    Abstract Peroxisome proliferator-activated receptors belong to the superfamily of ligand-dependent nuclear receptor transcription factors, which include three subtypes: PPAR-alpha, beta/delta, and gamma. PPAR-delta, play important roles in the regulation of cell growth and differentiation as well as tissue wound and repair. Emerging evidence has also demonstrated that PPAR-delta is implicated in lipids and glucose metabolism. Most recently, the direct effects of PPAR-delta on cardiovascular processes such as endothelial function and angiogenesis have also been investigated. Therefore, it is suggested that PPAR-delta may have critical roles in cardiovascular pathophysiology and is a potential target for therapeutic intervention of cardiovascular disorders such as atherosclerosis.
    Language English
    Publishing date 2009-01-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2237981-2
    ISSN 1687-4765 ; 1687-4757
    ISSN (online) 1687-4765
    ISSN 1687-4757
    DOI 10.1155/2008/164163
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  7. Article ; Online: S-nitrosylation attenuates pregnane X receptor hyperactivity and acetaminophen-induced liver injury.

    Cui, Qi / Jiang, Tingting / Xie, Xinya / Wang, Haodong / Qian, Lei / Cheng, Yanyan / Li, Qiang / Lu, Tingxu / Yao, Qinyu / Liu, Jia / Lai, Baochang / Chen, Chang / Xiao, Lei / Wang, Nanping

    JCI insight

    2024  Volume 9, Issue 2

    Abstract: Drug-induced liver injury (DILI), especially acetaminophen overdose, is the leading cause of acute liver failure. Pregnane X receptor (PXR) is a nuclear receptor and the master regulator of drug metabolism. Aberrant activation of PXR plays a pathogenic ... ...

    Abstract Drug-induced liver injury (DILI), especially acetaminophen overdose, is the leading cause of acute liver failure. Pregnane X receptor (PXR) is a nuclear receptor and the master regulator of drug metabolism. Aberrant activation of PXR plays a pathogenic role in the acetaminophen hepatotoxicity. Here, we aimed to examine the S-nitrosylation of PXR (SNO-PXR) in response to acetaminophen. We found that PXR was S-nitrosylated in hepatocytes and the mouse livers after exposure to acetaminophen or S-nitrosoglutathione (GSNO). Mass spectrometry and site-directed mutagenesis identified the cysteine 307 as the primary residue for S-nitrosylation (SNO) modification. In hepatocytes, SNO suppressed both agonist-induced (rifampicin and SR12813) and constitutively active PXR (VP-PXR, a human PXR fused to the minimal transactivator domain of the herpes virus transcription factor VP16) activations. Furthermore, in acetaminophen-overdosed mouse livers, PXR protein was decreased at the centrilobular regions overlapping with increased SNO. In PXR-/- mice, replenishing the livers with the SNO-deficient PXR significantly aggravated hepatic necrosis, increased HMGB1 release, and exacerbated liver injury and inflammation. Particularly, we demonstrated that S-nitrosoglutathione reductase (GSNOR) inhibitor N6022 promoted hepatoprotection by increasing the levels of SNO-PXR. In conclusion, PXR is posttranslationally modified by SNO in hepatocytes in response to acetaminophen. This modification mitigated the acetaminophen-induced PXR hyperactivity. It may serve as a target for therapeutical intervention.
    MeSH term(s) Animals ; Humans ; Mice ; Acetaminophen/toxicity ; Chemical and Drug Induced Liver Injury, Chronic/metabolism ; Hepatocytes/metabolism ; Pregnane X Receptor/metabolism
    Chemical Substances Acetaminophen (362O9ITL9D) ; Pregnane X Receptor ; Nr1i2 protein, mouse
    Language English
    Publishing date 2024-01-23
    Publishing country United States
    Document type Journal Article
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.172632
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  8. Article ; Online: Thermoregulatory pathway underlying the pyrogenic effects of prostaglandin E

    Xu, Jian-Hui / He, Tian-Hui / Wang, Nan-Ping / Gao, Wen-Min / Cheng, Yong-Jing / Ji, Qiao-Feng / Wu, Si-Hao / Wei, Yan-Lin / Tang, Yu / Yang, Wen Z / Zhang, Jie

    Acta pharmacologica Sinica

    2024  

    Abstract: It has been shown that prostaglandin (PG) ... ...

    Abstract It has been shown that prostaglandin (PG) E
    Language English
    Publishing date 2024-05-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1360774-1
    ISSN 1745-7254 ; 0253-9756 ; 1671-4083
    ISSN (online) 1745-7254
    ISSN 0253-9756 ; 1671-4083
    DOI 10.1038/s41401-024-01289-6
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  9. Article ; Online: Sonic hedgehog signaling instigates high-fat diet-induced insulin resistance by targeting PPARγ stability.

    Yao, Qinyu / Liu, Jia / Xiao, Lei / Wang, Nanping

    The Journal of biological chemistry

    2018  Volume 294, Issue 9, Page(s) 3284–3293

    Abstract: Obesity is a major risk for patients with chronic metabolic disorders including type 2 diabetes. Sonic hedgehog (Shh) is a morphogen that regulates the pancreas and adipose tissue formation during embryonic development. Peroxisome proliferator-activated ... ...

    Abstract Obesity is a major risk for patients with chronic metabolic disorders including type 2 diabetes. Sonic hedgehog (Shh) is a morphogen that regulates the pancreas and adipose tissue formation during embryonic development. Peroxisome proliferator-activated receptor γ (PPARγ) is a member of the nuclear receptor superfamily and one of the most important regulators of insulin action. Here, we evaluated the role and mechanism of Shh signaling in obesity-associated insulin resistance and characterized its effect on PPARγ. We showed that Shh expression was up-regulated in subcutaneous fat from obese mice. In differentiated 3T3-L1 and primary cultured adipocytes from rats, recombinant Shh protein and SAG (an agonist of Shh signaling) activated an extracellular signal-regulated kinase (ERK)-dependent noncanonical pathway and induced PPARγ phosphorylation at serine 112, which decreased PPARγ activity. Meanwhile, Shh signaling degraded PPARγ protein via binding of PPARγ to neural precursor cell-expressed developmentally down-regulated protein 4-1 (NEDD4-1). Furthermore, vismodegib, an inhibitor of Shh signaling, attenuated ERK phosphorylation induced by a high fat diet (HFD) and restored PPARγ protein level, thus ameliorating glucose intolerance and insulin resistance in obese mice. Our finding suggests that Shh in subcutaneous fat decreases PPARγ activity and stability via activation of an ERK-dependent noncanonical pathway, resulting in impaired insulin action. Inhibition of Shh may serve as a potential therapeutic approach to treat obesity-related diabetes.
    MeSH term(s) 3T3-L1 Cells ; Anilides/pharmacology ; Animals ; Diet, High-Fat/adverse effects ; Enzyme Activation/drug effects ; Extracellular Signal-Regulated MAP Kinases/metabolism ; HEK293 Cells ; Hedgehog Proteins/metabolism ; Humans ; Insulin Resistance ; Male ; Mice ; PPAR gamma/metabolism ; Protein Stability/drug effects ; Pyridines/pharmacology ; Rats ; Signal Transduction/drug effects ; Subcutaneous Fat/drug effects ; Subcutaneous Fat/metabolism ; Subcutaneous Fat/pathology ; Ubiquitin/metabolism
    Chemical Substances Anilides ; Hedgehog Proteins ; HhAntag691 ; PPAR gamma ; Pyridines ; Ubiquitin ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2018-12-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.RA118.004411
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  10. Article ; Online: Squid type II collagen as a novel biomaterial: Isolation, characterization, immunogenicity and relieving effect on degenerative osteoarthritis via inhibiting STAT1 signaling in pro-inflammatory macrophages.

    Dai, Meilu / Liu, Xin / Wang, Nanping / Sun, Jiao

    Materials science & engineering. C, Materials for biological applications

    2018  Volume 89, Page(s) 283–294

    Abstract: Collagen from marine organisms has a broad prospect in biomedical field, yet the knowledge on marine-derived type II collagen is rare. Herein, a novel type II collagen was successfully isolated from squid cartilage for the first time. After being ... ...

    Abstract Collagen from marine organisms has a broad prospect in biomedical field, yet the knowledge on marine-derived type II collagen is rare. Herein, a novel type II collagen was successfully isolated from squid cartilage for the first time. After being characterized, the immunogenicity of squid type II collagen (SCII) was evaluated and compared with that of bovine type II collagen (BCII). Then investigations were further conducted for the impacts of SCII on pro-inflammatory macrophages and macrophage chemotaxis. The degenerative osteoarthritis (OA) -relieving effects of SCII were explored using OA rat model in vivo. Our results demonstrated that the isolated SCII maintained triple-superhelical structure of native collagen with high purity. Different from BCII, SCII presented no immunogenicity since it neither induced abnormal proliferation of lymphocytes in vitro nor changed the basic levels of IgM, IgG, anti-type II collagen IgG and CD4
    MeSH term(s) Animals ; Antibodies/blood ; Biocompatible Materials/metabolism ; Biocompatible Materials/pharmacology ; Biocompatible Materials/therapeutic use ; CD4-Positive T-Lymphocytes/cytology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Cartilage/drug effects ; Cartilage/metabolism ; Cartilage/pathology ; Cell Survival/drug effects ; Collagen Type II/immunology ; Collagen Type II/metabolism ; Collagen Type II/pharmacology ; Decapodiformes/metabolism ; Disease Models, Animal ; Macrophages/cytology ; Macrophages/immunology ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Osteoarthritis/drug therapy ; Osteoarthritis/pathology ; Rats ; Rats, Sprague-Dawley ; STAT1 Transcription Factor/metabolism ; Signal Transduction/drug effects ; Synovial Membrane/drug effects ; Synovial Membrane/metabolism ; Synovial Membrane/pathology
    Chemical Substances Antibodies ; Biocompatible Materials ; Collagen Type II ; STAT1 Transcription Factor
    Language English
    Publishing date 2018-04-12
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2012160-X
    ISSN 1873-0191 ; 0928-4931
    ISSN (online) 1873-0191
    ISSN 0928-4931
    DOI 10.1016/j.msec.2018.04.021
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