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Bin Yang, Ping Yan, Hui Gong, Lin Zuo, Ying Shi, Jian Guo, Rui Guo, Jun Xie, Bao Li
Myocyte apoptosis is a key determinant of cardiac recovery and prognosis of patients with acute myocardial infarction (AMI). Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK), a member of TNF superfamily, is a pro-inflammatory and pro-angiogenic cytokine implicated in physiological tissue regeneration and wound repair and is closely related to cardiac remodeling, dysfunction and fibrosis. However, the role of TWEAK and its receptor Fn14 in the cardiomyocyte apoptosis is still poorly understood...
2016: American Journal of Translational Research
Luca Di Martino, Maneesh Dave, Paola Menghini, Wei Xin, Kristen Arseneau, Theresa Pizarro, Fabio Cominelli
Inflammatory bowel disease causes chronic, relapsing intestinal inflammation that can lead to the development of colorectal cancer. Members of the TNF superfamily are key regulators of intestinal inflammation. In particular, TNF-like weak inducer of apoptosis (TWEAK) and its receptor, Fn14, are involved in normal and pathologic intestinal tissue remodeling. In this study, we show that the TWEAK/Fn14 signaling complex plays a protective role during the acute stage of intestinal inflammation and contributes to the prevention of colitis-associated cancer during chronic inflammation through its pro-apoptotic effects...
September 9, 2016: Cancer Research
Mehmet Asil, Ramazan Dertli
The mechanisms underlying hepatic inflammation and fibrogenesis in chronic hepatitis B (CHB) are complex and several cytokines are involved. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a member of the tumor necrosis factor superfamily which also acts as a cytokine. This study was conducted to evaluate serum soluble TWEAK (sTWEAK) levels in noncirrhotic CHB patients.Fifty-two treatment naive CHB patients and 30 healthy controls were included in the study and serum sTWEAK concentrations were measured using commercially available ELISA kits...
September 2016: Medicine (Baltimore)
Andrey Elchaninov, Timur Fatkhudinov, Natalia Usman, Evgeniya Kananykhina, Irina Arutyunyan, Andrey Makarov, Galina Bolshakova, Dmitry Goldshtein, Gennady Sukhikh
Proliferation of hepatocytes is known to be the main process in the hepatectomy-induced liver regrowth; however, in cases of extensive loss it may be insufficient for complete recovery unless supported by some additional sources e.g. mobilization of undifferentiated progenitors. The study was conducted on rat model of 80% subtotal hepatectomy; the objective was to evaluate contributions of hepatocytes and resident progenitor cells to the hepatic tissue recovery via monitoring specific mRNA and/or protein expression levels for a panel of genes implicated in growth, cell differentiation, angiogenesis, and inflammation...
2016: PloS One
Diego A González-Sánchez, Cristian M Álvarez, Gloria Vásquez, José A Gómez-Puerta
Knowledge of the signalling pathways involved in various diseases has enabled advances in the understanding of pathophysiological, diagnostic and therapeutic models of several inflammatory and autoimmune diseases. Systemic lupus erythematosus is a widely studied autoimmune disease that can affect multiple organs, with a major impact on morbidity and mortality when it involves the kidneys. Over the past 10 years, interest in the role of the TWEAK/Fn14 signalling pathway in lupus nephritis, as well as other clinical settings, has increased...
August 29, 2016: Nefrología: Publicación Oficial de la Sociedad Española Nefrologia
Cristian González-Guerrero, Pablo Cannata-Ortiz, Consuelo Guerri, Jesús Egido, Alberto Ortiz, Adrián M Ramos
Cyclosporine A (CsA) successfully prevents allograft rejection, but nephrotoxicity is still a dose-limiting adverse effect. TLR4 activation promotes kidney damage but whether this innate immunity receptor mediates CsA nephrotoxicity is unknown. The in vivo role of TLR4 during CsA nephrotoxicity was studied in mice co-treated with CsA and the TLR4 inhibitor TAK242 and also in TLR4(-/-) mice. CsA-induced renal TLR4 expression in wild-type mice. Pharmacological or genetic targeting of TLR4 reduced the activation of proinflammatory signaling, including JNK/c-jun, JAK2/STAT3, IRE1α and NF-κB and the expression of Fn14...
September 1, 2016: Archives of Toxicology
Clara Maria Pinheiro-Dardis, Thiago Luiz Russo
OBJECTIVE: The aim of this work was to investigate the effects of electrical stimulation (ES) of denervated muscles of rat in neuromuscular performance, muscle atrophy, and fibrosis formation. DESIGN: Wistar rats were divided into normal (N), 7- or 15-day denervation (D7d and D15d), D7d or D15d plus ES (DES7d and DES15d, respectively). Sciatic nerves were crushed causing muscle denervation. Two hundred muscle contractions were electrically induced daily by surface electrodes, considering muscle chronaxie...
August 31, 2016: American Journal of Physical Medicine & Rehabilitation
L Hénaut, A B Sanz, D Martin-Sanchez, S Carrasco, R Villa-Bellosta, G Aldamiz-Echevarria, Z A Massy, M D Sanchez-Nino, A Ortiz
Vascular calcification (VC) is associated with increased cardiovascular mortality in aging, chronic kidney disease (CKD), type 2 diabetes mellitus (T2DM) and atherosclerosis. TNF-like weak inducer of apoptosis (TWEAK) recently emerged as a new biomarker for the diagnosis and prognosis of cardiovascular diseases. TWEAK binding to its functional receptor Fn14 was reported to promote several steps of atherosclerotic plaque progression. However, no information is currently available on the role of TWEAK/Fn14 on the development of medial calcification, which is highly prevalent in aging, CKD and T2DM...
2016: Cell Death & Disease
Antonino Tuttolomondo, Irene Simonetta, Antonio Pinto
INTRODUCTION: Cardiac remodelling is a complex pathogenetic pathway involving genome expression, molecular, cellular, and interstitial changes that cause changes in size, shape and function of the heart after cardiac injury. AREAS COVERED: We will review recent advances in understanding the role of several receptor-mediated signaling pathways and micro-RNAs, in addition to their potential as candidate target pathways in the pathogenesis of heart failure. The myocyte is the main target cell involved in the remodelling process via ischemia, cell necrosis and apoptosis (by means of various receptor pathways), and other mechanisms mediated by micro-RNAs...
July 13, 2016: Expert Opinion on Therapeutic Targets
Lara Valiño-Rivas, Laura Gonzalez-Lafuente, Ana B Sanz, Marta Ruiz-Ortega, Alberto Ortiz, Maria D Sanchez-Niño
TNF-like weak inducer of apoptosis (TWEAK) receptor Fn14 is expressed by podocytes and Fn14 deficiency protects from experimental proteinuric kidney disease. However, the downstream effectors of TWEAK/Fn14 in podocytes are poorly characterized. We have explored TWEAK activation of non-canonical NFκB signaling in cultured podocytes. In cultured podocytes, TWEAK increased the expression of the chemokines CCL21, CCL19 and RANTES in a time-dependent manner. The inhibitor of canonical NFκB activation parthenolide inhibited the CCL19 and the early RANTES responses, but not the CCL21 or late RANTES responses...
2016: Scientific Reports
Ying Sun, Yong Han, Xiaoping Wang, Wuping Wang, Xuejiao Wang, Miaomiao Wen, Jinghua Xia, Hao Xing, Xiaofei Li, Zhipei Zhang
Previous research has shown that p-EGFR (particularly mutated EGFR) may activate fibroblast growth factor-inducible 14 (Fn14) expression in non-small cell lung cancer (NSCLC), and the JAK/STAT signaling pathway may participate in this process. Thus, in order to verify this hypothesis, correlations among the expression levels of EGFR Del 19, Fn14 and JAK/STAT were detected and analyzed. The expression and location of these molecules were assessed using IHC, immunohistofluorescence, RT-qPCR and western blotting...
August 2016: Oncology Reports
Ana B Sanz, Olga Ruiz-Andres, Maria Dolores Sanchez-Niño, Marta Ruiz-Ortega, Adrian M Ramos, Alberto Ortiz
Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a tumor necrosis factor superfamily cytokine that activates the fibroblast growth factor-inducible-14 (Fn14) receptor. Functional studies have established a role of TWEAK/Fn14 in experimental acute kidney injury (AKI) and the AKI to chronic kidney disease transition through actions on tubular cells and renal fibroblasts. The renal cell expression of TWEAK and Fn14 is increased in human and experimental AKI and targeting TWEAK or Fn14 by genetic means or neutralizing antibodies was protective in kidney injury induced by folic acid overdose, ischemia-reperfusion, or unilateral ureteral obstruction...
May 2016: Seminars in Nephrology
Jessica Doerner, Samantha A Chalmers, Adam Friedman, Chaim Putterman
The cytokine TWEAK and its receptor Fn14 are involved in cell survival and cytokine production. The TWEAK/Fn14 pathway plays a role in the pathogenesis of spontaneous cutaneous lesions in the MRL/lpr lupus strain; however, the role of TWEAK/Fn14 in disease induced by ultraviolet B (UVB) irradiation has not been explored. MRL/lpr Fn14 knockout (KO) were compared to MRL/lpr Fn14 wild-type (WT) mice following exposure to UVB. We found that irradiated MRL/lpr KO mice had significantly attenuated cutaneous disease when compared to their WT counterparts...
June 15, 2016: Experimental Dermatology
Amelia J Johnston, Nicholas J Hoogenraad
PURPOSE OF REVIEW: Although cancer cachexia is a very significant condition that is present in up to 80% of cancer cases, the cause of the condition has remained a puzzle. Cancer cachexia is a condition which is mainly characterised by muscle wasting, mobilization of fat reserves, and overall metabolic disturbance. This review aims to highlight some of the recent findings in cancer cachexia research. RECENT RESEARCH: It has been recently demonstrated that the expression of a single receptor, fibroblast growth factor-inducible 14, on a tumour can initiate cachexia and that this can be completely ablated by treatment with an antibody against this receptor...
July 2016: Current Opinion in Clinical Nutrition and Metabolic Care
M Nusrat Sharif, Gabriela Campanholle, Eva E Nagiec, Ju Wang, Jameel Syed, Shawn P O'Neil, Yutian Zhan, Karrie Brenneman, Bruce Homer, Hendrik Neubert, Riyez Karim, Nick Pullen, Steven M Evans, Margaret Fleming, Priya Chockalingam, Lih-Ling Lin
The cytokine TWEAK and its cognate receptor Fn14 are members of the TNF/TNFR superfamily and are upregulated in tissue injury to mediate local tissue responses including inflammation and tissue remodeling. We found that in various models of kidney disease, Fn14 expression (mRNA and protein) is upregulated in the kidney. These models include: lupus nephritis mouse models (Nephrotoxic serum Transfer Nephritis and MRL.Faslpr/lpr), acute kidney injury models (Ischemia reperfusion injury and Folic acid injury), and a ZSF-1 diabetic nephropathy rat model...
2016: PloS One
Nurdan Guldiken, Gokce Kobazi Ensari, Pooja Lahiri, Gabrielle Couchy, Christian Preisinger, Christian Liedtke, Henning W Zimmermann, Marianne Ziol, Peter Boor, Jessica Zucman-Rossi, Christian Trautwein, Pavel Strnad
BACKGROUND & AIMS: Keratins (K) constitute the epithelial intermediate filaments. Among them, K7/K19 are widely used markers of the regenerative liver response termed ductular reaction (DR) that consists of activated biliary epithelial cells (BECs) and hepatic progenitor cells (HPCs) and correlates with liver disease severity. In the present study we aimed to characterize K23 in the liver. METHODS: We analyzed the expression and localization of K23 in the digestive system under basal conditions as well as in various human and mouse liver diseases/stress models...
September 2016: Journal of Hepatology
J Lozano-Bartolomé, G Llauradó, M M Rodriguez, J M Fernandez-Real, J F Garcia-Fontgivell, J Puig, E Maymó-Masip, J Vendrell, M R Chacón
CONTEXT: Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome and is strongly associated with obesity, dyslipidaemia and altered glucose regulation. Previous data demonstrated that low circulating levels of tumour necrosis factor weak inducer of apoptosis (sTWEAK) were associated with obesity, diabetes and insulin resistance, all traits associated with an increased risk of NALFD. Circulating sTWEAK levels are expected to be reduced in the presence of NAFLD...
September 2016: International Journal of Obesity: Journal of the International Association for the Study of Obesity
Hong-Ki Min, Sung-Min Kim, Jin-Sil Park, Jae-Kyeong Byun, Jennifer Lee, Seung-Ki Kwok, Young-Woo Park, Mi-La Cho, Sung-Hwan Park
BACKGROUND: Systemic lupus erythematosus (SLE) is an autoimmune-mediated chronic inflammatory disease. Half of patients with SLE suffer from lupus nephritis, which is major cause of death in SLE. TNF-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible 14 (Fn14) interactions mediate inflammatory responses that are linked to the pathogenesis of lupus nephritis. Blocking of the TWEAK/Fn14 pathway by Fn14-Fc was performed in a SLE mouse model and the likely therapeutic mechanisms were investigated...
2016: Journal of Translational Medicine
D Y Chen, G F Su
Chronic inflammation develops in the retinal microvasculature under sustained hyperglycemia and is implicated in the pathogenesis of diabetic retinopathy. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor Fn14 have been reported to promote pro-inflammatory cytokines, which are involved in the pathogenesis of proliferative diabetic retinopathy (PDR). It is therefore possible that the TWEAK/Fn14 pathway can play a regulatory role in PDR. In the present study, we examined the expression of TWEAK and Fn14 in vitreous fluid from PDR patients...
2016: Genetics and Molecular Research: GMR
Xuefeng Qi, Mingzhu Lei, Lijuan Qin, Mengjie Xie, Dandan Zhao, Jingyu Wang
Uterine natural killer (uNK) cells are the most abundant lymphocyte population in the feto-maternal interface during early gestation, and uNK cells play a significant role in the establishment and maintenance of pregnancy-related vascularization, as well as in tolerance to the fetus. Tumour necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor-inducible molecule (Fn14), are involved in preventing local cytotoxicity and counterbalancing the cytotoxic function of uNK cells...
May 2016: Immunology
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