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Littérature scientifique sur le sujet « Tumor Necrosis Factor Alpha α-SMA »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 10 mars 2023

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Articles de revues sur le sujet "Tumor Necrosis Factor Alpha α-SMA"

Sullivan, K. E., A. B. M. Reddy, K. Dietzmann, et al. "Epigenetic Regulation of Tumor Necrosis Factor Alpha." Molecular and Cellular Biology 27, no. 14 (2007): 5147–60. http://dx.doi.org/10.1128/mcb.02429-06.

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ABSTRACT Tumor necrosis factor alpha (TNF-α) is a potent cytokine which regulates inflammation via the induction of adhesion molecules and chemokine expression. Its expression is known to be regulated in a complex manner with transcription, message turnover, message splicing, translation, and protein cleavage from the cell surface all being independently regulated. This study examined both cell lines and primary cells to understand the developmental regulation of epigenetic changes at the TNF-α locus. We demonstrate that epigenetic modifications of the TNF-α locus occur both developmentally and in response to acute stimulation and, importantly, that they actively regulate expression. DNA demethylates early in development, beginning with the hematopoietic stem cell. The TNF-α locus migrates from heterochromatin to euchromatin in a progressive fashion, reaching euchromatin slightly later in differentiation. Finally, histone modifications characteristic of a transcriptionally competent gene occur with myeloid differentiation and progress with differentiation. Additional histone modifications characteristic of active gene expression are acquired with stimulation. In each case, manipulation of these epigenetic variables altered the ability of the cell to express TNF-α. These studies demonstrate the importance of epigenetic regulation in the control of TNF-α expression. These findings may have relevance for inflammatory disorders in which TNF-α is overproduced.

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Topolyanskaya, S. V. "Tumor Necrosis Factor-Alpha and Age-Related Pathologies." Russian Archives of Internal Medicine 10, no. 6 (2020): 414–21. http://dx.doi.org/10.20514/2226-6704-2020-10-6-414-421.

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Modern concepts about the «inflammaging» and the role of subclinical inflammation in various age-associated pathology are described in the review. Particular attention is paid to the tumor necrosis factor-α, a key cytokine that plays an important role in the pathogenesis of chronic inflammatory diseases as well as in aging. The increased levels of tumor necrosis factor-α leads to the onset and progression of various diseases, to severity of frailty, to disability and mortality of elderly persons. Tumor necrosis factor-α affects different risk factors for cardiovascular diseases, contributes to the onset and progression of atherosclerosis and related pathology. This cytokine can also aggravate various metabolic disorders, mainly — insulin resistance and diabetes mellitus. Tumor necrosis factor-α is a key cytokine that stimulates bone resorption (up to osteoporosis) and sarcopenia (up to cachexia). Currently available data confirm the important role of tumor necrosis factor-α in various age-associated disorders.

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Miao, Kun, Ling Zhou, Hongping Ba, et al. "Transmembrane tumor necrosis factor alpha attenuates pressure-overload cardiac hypertrophy via tumor necrosis factor receptor 2." PLOS Biology 18, no. 12 (2020): e3000967. http://dx.doi.org/10.1371/journal.pbio.3000967.

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Tumor necrosis factor-alpha (TNF-α) plays an important pathogenic role in cardiac hypertrophy and heart failure (HF); however, anti-TNF is paradoxically negative in clinical trials and even worsens HF, indicating a possible protective role of TNF-α in HF. TNF-α exists in transmembrane (tmTNF-α) and soluble (sTNF-α) forms. Herein, we found that TNF receptor 1 (TNFR1) knockout (KO) or knockdown (KD) by short hairpin RNA or small interfering RNA (siRNA) significantly alleviated cardiac hypertrophy, heart dysfunction, fibrosis, and inflammation with increased tmTNF-α expression, whereas TNFR2 KO or KD exacerbated the pathological phenomena with increased sTNF-α secretion in transverse aortic constriction (TAC)- and isoproterenol (ISO)-induced cardiac hypertrophy in vivo and in vitro, respectively, indicating the beneficial effects of TNFR2 associated with tmTNF-α. Suppressing TNF-α converting enzyme by TNF-α Protease Inhibitor-1 (TAPI-1) to increase endogenous tmTNF-α expression significantly alleviated TAC-induced cardiac hypertrophy. Importantly, direct addition of exogenous tmTNF-α into cardiomyocytes in vitro significantly reduced ISO-induced cardiac hypertrophy and transcription of the pro-inflammatory cytokines and induced proliferation. The beneficial effects of tmTNF-α were completely blocked by TNFR2 KD in H9C2 cells and TNFR2 KO in primary myocardial cells. Furthermore, we demonstrated that tmTNF-α displayed antihypertrophic and anti-inflammatory effects by activating the AKT pathway and inhibiting the nuclear factor (NF)-κB pathway via TNFR2. Our data suggest that tmTNF-α exerts cardioprotective effects via TNFR2. Specific targeting of tmTNF-α processing, rather than anti-TNF therapy, may be more useful for the treatment of hypertrophy and HF.

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Cai, Weibo, Zachary J. Kerner, Hao Hong, and Jiangtao Sun. "Targeted Cancer Therapy with Tumor Necrosis Factor-Alpha." Biochemistry Insights 1 (January 2008): BCI.S901. http://dx.doi.org/10.4137/bci.s901.

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Tumor necrosis factor-alpha (TNF-α), a member of the TNF superfamily, was the first cytokine to be evaluated for cancer biotherapy. However, the clinical use of TNF-α is severely limited by its toxicity. Currently, TNF-α is administered only through locoregional drug delivery systems such as isolated limb perfusion and isolated hepatic perfusion. To reduce the systemic toxicity of TNF-α, various strategies have been explored over the last several decades. This review summarizes current state-of-the-art targeted cancer therapy using TNF-α. Passive targeting, cell-based therapy, gene therapy with inducible or tissue-specific promoters, targeted polymer-DNA complexes, tumor pre-targeting, antibody-TNF-α conjugate, scFv/TNF-α fusion proteins, and peptide/TNF-α fusion proteins have all been investigated to combat cancer. Many of these agents are already in advanced clinical trials. Molecular imaging, which can significantly speed up the drug development process, and nanomedicine, which can integrate both imaging and therapeutic components, has the potential to revolutionize future cancer patient management. Cooperative efforts from scientists within multiple disciplines, as well as close partnerships among many organizations/entities, are needed to quickly translate novel TNF-α-based therapeutics into clinical investigation.

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Suriano, April R., Amy N. Sanford, Nahmah Kim, et al. "GCF2/LRRFIP1 Represses Tumor Necrosis Factor Alpha Expression." Molecular and Cellular Biology 25, no. 20 (2005): 9073–81. http://dx.doi.org/10.1128/mcb.25.20.9073-9081.2005.

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ABSTRACT Tumor necrosis factor alpha (TNF-α) is an important mediator of inflammation, apoptosis, and the development of secondary lymphoid structures. Multiple polymorphic microsatellites have been identified in and around the gene, and there are also multiple single-base pair biallelic polymorphisms in the introns and promoter. The TNF-α −308 promoter polymorphism is a G-to-A transition which has been statistically associated with various autoimmune disorders. Some studies have found that it may directly mediate the increased transcription of TNF-α in some circumstances. This study characterizes proteins interacting at the polymorphic promoter site. Affinity purification of binding proteins and confirmatory chromatin immunoprecipitation assays were used to identify the proteins. Electrophoretic mobility shift analyses and surface plasmon resonance were used to define binding characteristics. Proteins interacting at this site include GCF2/LRRFIP1 and Ets-1. GCF2/LRRFIP1 appears to act as a repressor and occupies the −308 site in cells that do not make TNF-α. Cells competent to produce TNF-α have Ets-1 bound to the −308 promoter site. Active transcription is accompanied by NF-κB and c-Jun binding to the proximal promoter. Thus, dynamic changes on the TNF-α promoter, particularly at the −308 site, accompany the transition from repressed to active transcription. GCF2/LRRFIP1 is the first TNF-α repressor identified.

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Decourt, Boris, Debomoy K. Lahiri, and Marwan N. Sabbagh. "Targeting Tumor Necrosis Factor Alpha for Alzheimer’s Disease." Current Alzheimer Research 14, no. 4 (2017): 412–25. http://dx.doi.org/10.2174/1567205013666160930110551.

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Alzheimer’s disease (AD) affects an estimated 44 million individuals worldwide, yet no therapeutic intervention is available to stop the progression of the dementia. Neuropathological hallmarks of AD are extracellular deposits of amyloid beta (Aβ) peptides assembled in plaques, intraneuronal accumulation of hyperphosphorylated tau protein forming tangles, and chronic inflammation. A pivotal molecule in inflammation is the pro-inflammatory cytokine TNF-α. Several lines of evidence using genetic and pharmacological manipulations indicate that TNF-α signaling exacerbates both Aβ and tau pathologies in vivo. Interestingly, preventive and intervention anti-inflammatory strategies demonstrated a reduction in brain pathology and an amelioration of cognitive function in rodent models of AD. Phase I and IIa clinical trials suggest that TNF-α inhibitors might slow down cognitive decline and improve daily activities in AD patients. In the present review, we summarize the evidence pointing towards a beneficial role of anti-TNF-α therapies to prevent or slow the progression of AD. We also present possible physical and pharmacological interventions to modulate TNF-α signaling in AD subjects along with their limitations.

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Tseng, Wei-Cheng, Hou-Chuan Lai, Yi-Hsuan Huang, Shun-Ming Chan, and Zhi-Fu Wu. "Tumor Necrosis Factor Alpha: Implications of Anesthesia on Cancers." Cancers 15, no. 3 (2023): 739. http://dx.doi.org/10.3390/cancers15030739.

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Cancer remains a major public health issue and a leading cause of death worldwide. Despite advancements in chemotherapy, radiation therapy, and immunotherapy, surgery is the mainstay of cancer treatment for solid tumors. However, tumor cells are known to disseminate into the vascular and lymphatic systems during surgical manipulation. Additionally, surgery-induced stress responses can produce an immunosuppressive environment that is favorable for cancer relapse. Up to 90% of cancer-related deaths are the result of metastatic disease after surgical resection. Emerging evidence shows that the interactions between tumor cells and the tumor microenvironment (TME) not only play decisive roles in tumor initiation, progression, and metastasis but also have profound effects on therapeutic efficacy. Tumor necrosis factor alpha (TNF-α), a pleiotropic cytokine contributing to both physiological and pathological processes, is one of the main mediators of inflammation-associated carcinogenesis in the TME. Because TNF-α signaling may modulate the course of cancer, it can be therapeutically targeted to ameliorate clinical outcomes. As the incidence of cancer continues to grow, approximately 80% of cancer patients require anesthesia during cancer care for diagnostic, therapeutic, or palliative procedures, and over 60% of cancer patients receive anesthesia for primary surgical resection. Numerous studies have demonstrated that perioperative management, including surgical manipulation, anesthetics/analgesics, and other supportive care, may alter the TME and cancer progression by affecting inflammatory or immune responses during cancer surgery, but the literature about the impact of anesthesia on the TNF-α production and cancer progression is limited. Therefore, this review summarizes the current knowledge of the implications of anesthesia on cancers from the insights of TNF-α release and provides future anesthetic strategies for improving oncological survival.

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Gürsel, G., N. Gökçora, Ş. Elbeg, B. Samurkaşoğlu та N. Ekim. "Tumor necrosis factor-alpha (TNF-α) in pleural fluids". Tubercle and Lung Disease 76, № 4 (1995): 370–71. http://dx.doi.org/10.1016/s0962-8479(05)80039-5.

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Sutanto, Felix Candra, Max F. J. Mantik, and Vivekenanda Pateda. "Hubungan antara Tumor Necrosis Factor Alpha dengan Demam Berdarah Dengue." Sari Pediatri 15, no. 4 (2016): 244. http://dx.doi.org/10.14238/sp15.4.2013.244-8.

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Latar belakang. Sampai saat ini patogenesis demam berdarah dengue (DBD) belum dipahami secara sempurna. Pada kasus DBD didapatkan adanya peningkatan kadar TNF-α, sitokin yang poten dalam meningkatkan permeabilitas pembuluh darah. Penelitian sebelumnya mendapatkan adanya peningkatan kadar TNF-α yang bermakna pada DBD.Tujuan. Mengetahui hubungan antara kadar TNF-α dengan keparahan DBD.Metode. Penelitian analitik observasional dengan pendekatan potong lintang selama bulan Ju li hingga Desember 2011. Pasien didiagnosis DBD berdasarkan kriteria WHO. Data berupa hemoglobin, hematokrit, jumlah leukosit, jumlah trombosit, dan kadar TNF-α dikumpulkan selama penelitian. Analisis statistik menggunakan korelasi Spearman’s Rho dengan tingkat kemaknaan p<0,05.Hasil. Didapatkan tiga puluh delapan anak, 27 di antaranya didiagnosis DBD tanpa syok dan 11 DBD dengan syok. Rerata usia kelompok DBD tanpa syok adalah 7,56 (SB 3,06) tahun (95% IK 6,35-8,76 tahun) dan rerata usia kelompok DBD dengan syok adalah 6,82 (SB 3,25) tahun (95% IK 4,63-9,00 tahun). Rerata kadar TNF-α kelompok DBD tanpa syok adalah 13,13 (SB 7,57) pg/ml (95% IK 10,14-16,13 pg/ml) dan rerata kadar TNF-α kelompok DBD dengan syok adalah 260,52 (SB 239,08) pg/ml (95% IK 99,90-421,13 pg/ml). Didapatkan hubungan positif yang bermakna antara kadar TNFα plasma dengan tingkat keparahan/derajat DBD (rs 0,885; p<0,001).Kesimpulan. Semakin berat derajat DBD yang terjadi semakin tinggi kadar TNF-α

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Thèses sur le sujet "Tumor Necrosis Factor Alpha α-SMA"

Kumari, Vandana. "Mechanisms underlying the regulatory function of tumor necrosis factor-alpha in skin inflammation." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17389.

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Die Haut ist das größte Organ des Menschen und bildet die Barriere gegenüber Einwirkungen aus der Umwelt. Die Störung der Hautbarriere durch exogene und endogene Reize führt zu einer Entzündungsreaktion in der Haut. In der Folge können Hauterkrankungen wie die irritative oder Atopische Dermatitis entstehen. Der Tumor Nekrose Faktor-α (TNF-α) ist ein pleiotrop wirksames Zytokin, das eine zentrale Rolle bei entzündlichen Prozessen spielt. Ziel der vorgelegten Promotionsarbeit war zu untersuchen, ob und wie TNF-α zu Entzündungsgeschehen, ausgelöst durch exogene und endogene Faktoren, beiträgt. Die Bedeutung von TNF-α wurde in TNF-ko Mäusen in verschiedenen Hautmodellen untersucht. Für das Irritationsmodell wurden chemische und physikalische Reize verwendet. TSLP (Thymic stromal lymphopoietin) wurde durch die verschiedenen Stimuli signifikant induziert. Diese Induktion war unabhängig von der endogenen TNF-α Produktion, gezeigt durch den Einsatz von TNF- ko Mäusen . Da endogenes TNF-α für die Hautirritation keine notwendige Bedingung darstellte, wurde die Bedeutung von TNF-α bei der atopischen Dermatitis (AD) untersucht. TNF-α defiziente Mäuse zeigen verstärkt Ekzeme im Vergleich zu Wildtyp Mäusen. Die Behandlung von TNF-ko Mäusen mit einem TSLP Antikörper führte zu einer Verminderung des Ekzems. Mastzellen wurden vermehrt in läsionaler Haut gefunden und korrelierten mit dem Schweregrad des atopischen Ekzems sowie der TSLP-Expression.<br>The skin is the largest organ of an individuum and builds the barrier for a host against the environment. Skin barrier disruption by exogenous or endogenous stimuli can lead to skin inflammation. As a consequence, irritant or atopic eczema, frequent skin diseases, may evolve. Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine which plays a central role in inflammatory processes. The main aim of this thesis was to clarify whether and how endogenous TNF-α is contributing to skin inflammation driven by exogenous and endogenous triggers. The role of endogenous TNF-α was studied using TNF knockout (-/-) mice. In an irritation model, chemical and physical stimuli were applied on to mouse skin. Thymic stromal lymphopoietin (TSLP) was significantly induced by the used irritants. This TSLP induction was independent from endogenous TNF-α proven by using TNF-/- mice. Next the role of TNF-α in atopic dermatitis (AD) promoting an allergic skin inflammation was investigated. TNF-/- mice developed more severe AD compared to the wildtype mice and TSLP was significantly increased and correlated with the severity of the eczema. To prove the pathophysiological role of TSLP for AD progression, TNF-/- mice were pretreated with an TSLP antibody. Indeed, these mice developed less AD symptoms compared to the control mice. Mast cells (MCs) were also significantly increased in lesional skin in the AD model and moreover, correlated with AD severity, but also with TSLP expression.

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Osta, Bilal. "Effects of Interleukine-17A (Il-17A) and tumor necrosis factor alpha (TNF-α) on osteoblastic differentiation". Thesis, Lyon 1, 2014. http://www.theses.fr/2014LYO10278/document.

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L'interleukine-17A (IL-17A) et le facteur de nécrose tumorale alpha (TNF-α) sont des cytokines pro-inflammatoires impliquées dans la pathogénèse de plusieurs maladies articulaires. Au cours de la polyarthrite rhumatoïde (PR), une augmentation de la destruction osseuse ainsi qu'un defaut de réparation sont responsables des dommages articulaires. Cependant au cours de la spondylarthrite ankylosante (AS), une importante ossification ectopique est observée, conduisant à la formation de syndesmophytes, associé à une perte de la masse osseuse systémique. Récemment, l'étude de ces cytokines a conduit à la publication de résultats contradictoires. Notre objectif a donc été d'étudier l'effet de ces deux cytokines sur la différenciation ostéogénique de cellules souches mésenchymateuses humaines isolées (hMSCs) et de fibroblastes de la membrane synoviale (FLS). Tous les modèles de cellules utilisés, ont démontré que l'IL-17A et le TNF-α augmentent de manière synergique l'ostéogénèse. Ceci semble se rapprocher du modèle de l'AS où une formation d'os ectopique est observée dans laquelle l'IL-17A et le TNF-α jouent un rôle majeur. En parallèle, ces deux cytokines stimulent localement les ostéoclastes, entraînant une perte de masse osseuse observée à la fois dans la PR et dans l'ostéoporose. Cibler simultanément l'IL-17A et le TNF-α pourrait conduire à une diminution de l'infiltration de cellules et de la destruction articulaire observée dans la PR et pourrait ainsi réduire les effets des FLS PR sur l'activation de l'ostéoclastogénèse<br>Interleukin-17A (IL-17A) and tumor necrosis factor alpha (TNF-α) are pro-inflammatory cytokines involved in the pathogenesis of several arthritic diseases. In rheumatoid arthritis (RA), joint damage is a result of an increase in bone destruction and a decrease in bone repair. In contrast, in ankylosing spondylitis (AS), a bone mass loss accompanied by a significant ectopic ossification is observed leading to the formation of syndesmophytes. Recent studies led to contradictory findings regarding the role of IL-17A and TNF-α in arthritic disease. Therefore, our objective was to study the effect of these two cytokines on the osteogenic differentiation of isolated human mesenchymal stem cells (hMSCs) and fibroblasts of the synovial membrane (FLS). In all the cell models used, we demonstrated that Il-17A and TNF α synergistically increase osteogenesis. This seems to approach the model of AS where ectopic bone formation is observed and in which IL-17A and TNF-α both are involved. These cytokines stimulate osteoclasts locally resulting in loss of bone mass observed in both RA and osteoporosis. Thus, targeting IL-17A and TNF-α could lead to a decrease in cell infiltration and joint destruction which is observed in RA and may reduce the effects of RA FLS on the activation of osteoclastogenesis

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Tran, An Xuong. "Measuring the Changes in Tumor Necrosis Factor-Alpha (TNF-α) from Secretory Populations of U937 Monocytic Cells during Differentiation". Digital Commons @ East Tennessee State University, 2002. https://dc.etsu.edu/etd/685.

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Tumor necrosis factor-alpha (TNF-α) is a cytokine produced primarily by macrophages during acute inflammation. In this study we examined the differential effect of retinoic acid (RA) and phorbol 12-myristate 13-acetate (PMA) on the induction of TNF-α secretion from U937 monocytic cell populations by using the reverse hemolytic plaque assay (RHPA). The RHPA will allow us to investigate both changes in TNF-α secreting populations as well as monitor the relative amount of TNF-α released from individual cells. Our results indicate that treatment of U937 cells with RA (10-6M) moderately increases the secreting cell populations, and dramatically enhances the amount of TNF-α secreted from cells already committed to secretion. In contrast, treatment with PMA (250ng/ml) drastically increased the secreting population, but only slightly increasing the amount of TNF-α released. These results suggest that induction of TNF-α secretion from U937 cells occurs by different pathways.

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Tam, Ho-man Alex, та 譚浩文. "Mechanisms underlying the hyper-induction of tumour necrosis factor alpha (TNF-α) by avian influenza virus in human macrophages". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41508300.

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Rütten, Simon, Gerald F. Schusser, Getu Abraham та Wieland Schrödl. "Release kinetics of tumor necrosis factor-α and interleukin-1 receptor antagonist in the equine whole blood". Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-205268.

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Background: Horses are much predisposed and susceptible to excessive and acute inflammatory responses that cause the recruitment and stimulation of polymorphnuclear granulocytes (PMN) together with peripheral blood mononuclear cells (PBMC) and the release of cytokines. The aim of the study is to develop easy, quick, cheap and reproducible methods for measuring tumor necrosis factor alpha (TNF-α) and interleukin-1 receptor antagonist (IL-1Ra) in the equine whole blood cultures ex-vivo time- and concentration dependently. Results: Horse whole blood diluted to 10, 20 and 50 % was stimulated with lipopolysaccharide (LPS), PCPwL (a combination of phytohemagglutinin E, concanavalin A and pokeweed mitogen) or equine recombinant TNF-α (erTNF-α). TNF-α and IL-1Ra were analyzed in culture supernatants, which were collected at different time points using specific enzyme-linked immunosorbent assays (ELISA). Both cytokines could be detected optimal in stimulated 20 % whole blood cultures. TNF-α and IL-1Ra releases were time-dependent but the kinetic was different between them. PCPwL-induced TNF-α and IL-1Ra release was enhanced continuously over 24–48 h, respectively. Similarly, LPS-stimulated TNF-α was at maximum at time points between 8–12 h and started to decrease thereafter, whereas IL-1Ra peaked later between 12–24 h and rather continued to accumulate over 48 h. The equine recombinant TNF-α could induce also the IL-1Ra release. Conclusions: Our results demonstrate that similar to PCPwL, LPS stimulated TNF-α and IL-1Ra production time-dependently in whole blood cultures, suggesting the suitability of whole blood cultures to assess the release of a variety of cytokines in health and diseases of horse.

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Hantak, Alison Marie. "Ginsenosides enhance the cytotoxicity of tumor necrosis factor-α in human MDA-MB 231 and MCF-7 breast cancer cells in a caspase-dependent manner". OpenSIUC, 2009. https://opensiuc.lib.siu.edu/theses/123.

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Ginsenosides (GF) are a major bioactive constituent of ginseng and have been shown to elicit a multitude of actions ranging from the improvement of synaptic plasticity to the improved uptake of glucose into a cell. Furthermore, ginsenosides and their metabolites have been shown to be potent anti-cancer agents in multiple experimental cancer models. The aim of this study was to investigate the potential influence of GF derived from American ginseng root (Panax quinquefolius), and a ginsenoside metabolite Rh2, on tumor necrosis factor-α (TNF-α) cytotoxicity in MDA-MB 231 and MCF-7 human breast cancer cells. In combination, these agents significantly increased cell death in both cell lines. Together, ginsenosides and TNF-α induced a robust increase of the pre-G0/G1 and accompanying decrease in S phase cell populations in breast cancer cells. This cell death was the result of the induction of apoptosis, as determined by annexin-V/7-AAD and Hoechst staining. Furthermore, the mechanism of ginsenoside and TNF-α induced apoptosis is caspase-dependent, as determined by the pan-caspase inhibitor Z-VAD-FMK, with caspase-8, but not caspase-9, serving as initiator caspase in both cell lines. Additionally, ginsenoside treatment significantly XIAP expression in both MDA-MB 231 and MCF-7 cells, in the absence of TNF-α. In addition to enhancing apoptosis, it was also hypothesized that ginsenosides would abrogate pro-survival pathways induced by TNF-α. However, ginsenosides failed to block TNF-α effects on NFκB expression in either cell line. JNK which, when activated by TNF-α in MDA-MB 231 cells has a pro-survival function, was reduced by ginsenosides. However, JNK inhibition had no effect on cell death, suggesting that it does not play an integral role in the mechanism of action. In MCF-7 cells, JNK has been shown to have a pro-apoptotic function. Treatment with ginsenosides had no effect on TNF-α activation of JNK, but inhibition of JNK significantly reduced cell death in combined ginsenoside and TNF-α treated cells. To conclude, combined treatment with ginsenosides and TNF-α can enhance cell death in the sensitive MCF-7 cell line, and induce cell death in the insensitive MDA-MB 231 cell line in a caspase-dependent manner that is aided by the reduction of XIAP by ginsenosides.

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Lautrette, Alexandre. "Interaction entre la voie de l'épidermal growth factor et la voie de l'angiotensine : rôle dans la progression des lésions rénales." Paris 6, 2006. http://www.theses.fr/2006PA066376.

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Deux facteurs de croissance jouent un rôle prépondérant dans le processus lésionnel rénal : l’EGF et l’angiotensine II (AngII). Le but de mon travail de thèse a été d’évaluer si la transactivation du récepteur de l’EGF (R-EGF) était responsable de l’effet délétère de l’AngII lors du développement des lésions rénales, et, si c’était le cas, d’identifier les mécanismes moléculaires à l’origine de ce phénomène. Nous avons montré par des modèles expérimentaux de néphropathie chronique, des lignées de souris génétiquement modifiées et des inhibiteurs pharmacologiques, que les lésions rénales induites par l’AngII passent par l’activation du R-EGF, via la surexpression d’un de ces ligands, le TGF-, elle-même provoquée par l’activation de sa métalloprotéase de clivage, TACE. Puis nous avons débuté l’étude du rôle du TGF- et de sa modulation par la voie de l’AngII dans la pathologie rénale humaine et plus particulièrement dans la polykystose. Nous avons observé une surexpression de TGF- et de TACE dans l’épithélium kystique. L’excrétion urinaire de TGF- est associée à la sévérité de l’insuffisance rénale dans la polykystose et dans différentes néphropathies. Cette excrétion semble dépendre de la prise d’inhibiteur de la voie de l’AngII et être corrélée à une détérioration plus rapide de la fonction rénale. Ceci suggère que le TGF- est impliqué dans le processus lésionnel de diverses néphropathies chroniques humaines et que sa production pourrait être régulée par l’AngII. Ce travail ouvre de nouvelles perspectives dans la recherche de molécules susceptibles de modifier l’évolution des maladies rénales et de traitements capables de ralentir la progression des lésions rénales.

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Mauviel, Alain. "Modulation de l'expression des gènes du collagène par l' Interleukine 1 et le Tumor Necrosis Factor α : étude chez les fibroblastes dermiques et les cellules synoviales en culture". Paris 11, 1989. http://www.theses.fr/1989PA112085.

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L'effet de l'Interleukine 1 (IL-1) et du Tumor Necrosis Factor α (TNF-α) sur la production de collagène a été étudiée in vitro chez les fibroblastes dermiques et les cellules synoviales. L'IL-1 exerce un effet inhibiteur sur la synthèse collagénique, effet accompagné par une forte accumulation de prostaglandine E2 (PGE2) dans les milieux de culture. Le blocage de la voie de la cyclooxygénase du métabolisme de l'acide arachidonique empêche l'action de l'IL-1 chez les synoviocytes, ce qui suggère l'implication de la PGE2 dans l'effet exercé par cette cytokine, mais pas chez les fibroplastes. Les taux d'ARNm des procollagènes I et III sont augmentés par l'IL-1 chez les deux types cellulaires. Des mécanismes post-transcriptionnels interviennent donc pour s'opposer à l'augmentation de l'expression des gènes des procollagènes. Le TNF-α réduit la production de collagène des fibroplastes dermiques. Le blocage de la production de PGE2 par l'indométacine n'empêche pas l'action du TNF-α. Celui-ci induit une forte diminution des taux d'ARNm des procollagènes I et III. La réduction de la synthèse collagénique par le TNF-α s'exerce essentiellement au niveau transcriptionnel. La mesure des taux d'ARNm codant pour l'IL-1ß chez les fibroblastes dermiques indique une forte stimulation sous l'effet de l'IL-1 ainsi que du TNF-α. Ceci laisse présager une régulation locale de la synthèse de matrice conjonctive par les fibroblastes eux-mêmes.

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Al-Shudiefat, Abd Al-Rahman. "Protective role of olive oil and its major component oleic acid in TNF-α induced remodeling subsequent to myocardial infarction in rats". Springer, 2013. http://hdl.handle.net/1993/20074.

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Oxidative stress and inflammation are important factors involved in the progression of heart failure. An important cytokine produced during myocardial infarction (MI) is tumor necrosis factor alpha (TNF-α). TNF-α may induce oxidative stress, cell damage, apoptosis and cardiac dysfunction. Considering the anti-inflammatory and anti-oxidant properties of extra-virgin olive oil and its major component (80%) oleic acid (OA), and their benefits to the cardiovascular system, we hypothesized that the negative effects of TNF-α in the pathogenesis of heart failure will be mitigated by olive oil consumption. This hypothesis was tested by examining the effects of a special diet supplemented with 10% olive oil, in coronary artery ligated animal model of MI. Corn oil (10%) supplementation was used as a control for matching caloric intake. Animals in the sham and ligated groups fed regular chow, olive oil, and corn oil were studied at 4 and 16 weeks post myocardial infarction (PMI). Mortality, diet consumption, weight gain and conduction system abnormalities were comparable among all ligated groups. Echocardiography showed that MI deteriorated cardiac function, and olive oil restored the function. At 16 weeks PMI, only corn oil fed groups showed significant increase in both total cholesterol and HDL. Corn oil was not able to offer protection to the heart, suggesting that the beneficial effects of olive oil are not due to increased caloric intake or increased HDL. MI increased myocardial TNF-α, oxidative stress, lipid peroxidation, pro-apoptotic protein expression (Bax, cleaved Caspase 3, cleaved PARP, TGFβ, Bnip3), cytochrome C release, MAP kinase activation (p38, JNK) and decreased anti-apoptotic protein Bcl-xL expression at both 4 and 16 weeks PMI, and these changes were modulated by olive oil. In order to further test the central role of TNF-α PMI, we examined the possible miti-gation of TNF-α induced changes by OA in isolated adult rat cardiomyocytes. TNF-α in-creased oxidative stress, cell damage, cell death, and apoptosis, while OA treatment miti-gated these TNF-α induced effects. We concluded that TNF-α is implicated in the progression of heart failure subsequent to MI and that OA in olive oil may prevent this progression, through its anti-oxidant, anti-inflammatory, anti-hypertensive, and inotropic effects.

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Benderdour, Mohamed. "Bore et cicatrisation : mécanismes d'action pouvant expliquer le rôle du bore dans la cicatrisation." Nancy 1, 1998. http://www.theses.fr/1998NAN10330.

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Chapitres de livres sur le sujet "Tumor Necrosis Factor Alpha α-SMA"

El-Youssef, M., A. Hughes, K. J. Bloch, S. R. Martin, and P. R. Harmatz. "Identification of tumor necrosis factor alpha (TNF-α) and transforming growth factor beta (TGF-β) in murine milk." In Advances in Mucosal Immunology. Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_162.

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Meager, Anthony. "Cell-Based Assays for the Detection of Neutralizing Antibodies to Interferon Beta (IFN-β) and Tumor Necrosis Factor Alpha (TNF-α) Inhibitors." In Detection and Quantification of Antibodies to Biopharmaceuticals. John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118075685.ch8.

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Scott, Ian C., James B. Galloway, and David L. Scott. "Anti-Tumour Necrosis Factor-Alpha (TNF-α) Treatment." In Inflammatory Arthritis in Clinical Practice. Springer London, 2015. http://dx.doi.org/10.1007/978-1-4471-6648-1_8.

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"Tumor Necrosis Factor Alpha(α)." In Encyclopedia of Pain. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_202365.

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Levine, S. J. "TUMOR NECROSIS FACTOR ALPHA (TNF-α)." In Encyclopedia of Respiratory Medicine. Elsevier, 2006. http://dx.doi.org/10.1016/b0-12-370879-6/00404-x.

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Urbina, Francisco, and María Isabel Herane. "Lipoatrophia Semicircularis." In Rare Diseases - Recent Advances [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105920.

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Lipoatrophia semicircularis was first described in 1974. It is a rare, but benign and reversible subcutaneous tissue atrophy that mainly affects women. It consists of unilateral or bilateral transverse, semicircular, and depressed bands that appear on the anterior and lateral region of the thighs, with an approximate height of 72 cm from the ground. Its origin has not been clearly established, and several hypotheses have been raised, including circulatory abnormalities, microtraumas, wearing of tight trousers, electromagnetic fields generated in the work environment, or electrostatic charges generated from computers or printers at office works; this “electric factor” would provoque bioelectric changes in the skin, causing direct damage to adipocytes through activated macrophages that release cytokines, including tumor necrosis factor alpha (TNF-α). Isolated cases could be reasonably attributed to the wearing of constricting jeans (in fashion) or microtraumas produced by repetitive leaning against sharp desk furniture, among others. However, the description of multiple cases in the same company or office, a fact reported in several countries, points to an environmental origin. It has also been proposed a multifactorial origin, in which repeated trauma, environmental conditions, and individual electrosensitivity may contribute to the origin of the process.

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Malhotra, Hitesh, and Anjoo Kamboj. "Role of Biomarkers in Rheumatoid Arthritis." In Natural Products for the Management of Arthritic Disorders. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815050776122010005.

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Rheumatoid arthritis is a chronic inflammatory condition that mainly affects the joint due to hyperactive immune reactions. The disease involves each component of the joint tissue with varying degrees of inflammation and destruction. The basic pathogenesis includes two key points, i.e., hyperactive immune reaction and inflammation. The phenomenon is driven by biomolecules which form a complex pathophysiological network, resulting in disease development and progression. The biomolecules like cytokines, such as interleukins, tumor necrosis factor-alpha, and interferon, play a fundamental role in joint and cartilage destruction, production of destructive enzymes, inflammatory reaction, and comorbidities related to the disease. From various pre-clinical and clinical researches, various attributes of disease development and progression can be demonstrated by focusing on the biological contribution of mediators, like IL-1, TNF- α, IL-6, IL-15, IL-17, and IL-18. Numerous reports confer the successful treatment of RA that might be possible by blocking the activity of these biomarkers. In this chapter, we discuss the role of biomolecules in the pathology of arthritis.

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Pires Lopes, Marcia Quinhones, Raquel Lima de Figueiredo Teixeira, Antonio Basilio de Miranda, et al. "Influence of the Interferon–Gamma (IFN–γ) and Tumor Necrosis Factor Alpha (TNF–α) Gene Polymorphisms in TB Occurrence and Clinical Spectrum." In Tuberculosis - Current Issues in Diagnosis and Management. InTech, 2013. http://dx.doi.org/10.5772/55099.

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Komiya, Koichiro, Nobuki Terada, Yoshikazu Mizoguchi, and Harumoto Yam. "Expression of Tumor Necrosis Factor-Alpha (TNF-α TNF-α Converting Enzyme and Matrix Metalloproteinase-3 in SAPHO Syndrome Synovium - A Rare Case Accompanied by Acrodermatitis Continua of Hallopeau: A Case Report and Review of Anti-TNF-α Therapy." In Rheumatoid Arthritis - Treatment. InTech, 2012. http://dx.doi.org/10.5772/26324.

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Siow, J. K., A. Y. M. Rambe, E. M. Surbakti, D. Munir, L. I. Laksmi, and P. Eyanoer. "The effect of intranasal corticosteroids on nasal polyps as assessed by expression of Tumour Necrosis Factor Alpha (TNF-α)." In Stem Cell Oncology. CRC Press, 2018. http://dx.doi.org/10.1201/9781351190152-38.

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Actes de conférences sur le sujet "Tumor Necrosis Factor Alpha α-SMA"

Gorikov, Igor, and Irina Andrievskaya. "RELATIONSHIP OF IMMUNO-HISTOMETRIC INDICATORS OF THE PLACEENTA IN EXACERBATION OF CYTOMEGALOVIRAL INFECTION IN THE SECOND TRIMESTER OF PREGNANCY." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9c510d54.83584889.

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The relationship between the concentration of tumor necrosis factor-alpha (TNF-α) in the placenta homogenate and its histometric parameters in women during physiological pregnancy and during pregnancy complicated by an exacerbation of cytomegalovirus infection in the second trimester of gestation, leading to the development of chronic compensated placental insufficiency, was studied.

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Han, Bumsoo, Matthew D. Egberg, Pung-Pung Haung, David J. Swanlund, and John C. Bischof. "Cryoinjury Enhancement of Breast Cancer Cells by Use of a Molecular Adjuvant (TNF-alpha)." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61593.

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Cryoinjury of human breast cancer cells (MCF7) in engineered tissue equivalents and the enhancement of the cryoinjury by use of a molecular adjuvant (tumor necrosis factor alpha, TNF-α) was studied. Tissue equivalents (TEs) were constructed by seeding MCF7 cells in collagen solutions at the concentration of 100,000 cells/ml. After cultured in vitro for 2 days, the TEs were exposed with 100ng/ml TNF-α and cultured for 24 hours, and then underwent a single freeze-thaw cycle by a cryosurgery simulator. With the concentration and duration of TNF-α treatment studied, no apoptotic or necrotic cell death was observed by the administration of TNF-α only. After a freeze/thaw, MCF7 cells within the frozen region of the TEs were significantly injured immediately (i.e. ≤ 20% survival), but gradually repopulated and reached approximately 80% survival in Day3 without TNF-α pre-treatment. MCF7 with TNF-α pre-treatment showed the slight enhancement of immediate injury in the frozen region (i.e. ≤ 10% survival), and the repopulation was significantly inhibited so the viability remained below 40% even in Day 3. These results imply that TNF-α can be a potent adjuvant for cryosurgery.

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Wolfe, Valerie M., Seonghun Park, Marjana Tomic, Peter A. Torzilli, and C. T. Christopher Chen. "Load Down-Regulates TNF-Alpha Induced Cartilage Degradation in Part Through NF-KB and P38 Pathways." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176541.

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Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), can induce cartilage degradation after acute injury or in inflammatory diseases [1,2,3,7]. The degradative events are coordinated through the elevation and activation of two classes of enzymes, namely matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS-4 and −5) [1,6]. Prior studies suggested that pro-inflammatory responses induced by IL-1β can be inhibited by tensile load [2] and more recently by cyclic compression [8]. It is, however, not clear whether load affects other cytokines, such as TNF-α. TNF-α is known to bind its receptor (TNFR1) to cause a cascade that ends with degradation of an inhibitor, IκBα, and release of the transcription factor NF-κB [3]. The actions of TNF-α are also known to be affected by at least three NF-κB independent pathways including the p38, ERK, and JNK pathways [4]. The objective of this study was to determine whether cyclic compression could affect TNF-α induced cartilage degradation and to determine the roles of p38, ERK, and JNK pathways in TNF-induced cartilage degradation. We hypothesized that cyclic loading would inhibit the degradative effects caused by TNF-α.

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Yu, H., R. Tamfu, S. Mohan та M. Natarajan. "Low LET Radiation-Induced Abscopal Effect and Tumor Recurrence: Nuclear Factor Kappa B (NF-κB) and Tumor Necrosis Factor alpha (TNF-α) Mediated Positive Feedback Mechanism." У Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-2149.

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Effendy, Elmeida, та Mustafa Mahmud Amin. "The Relationship between Tumor Necrosis Factor-Alpha (Tnf- Α) Serum Level and Negative Scale of PANSS in Smoking Schizophrenic Batak Men". У International Conference of Science, Technology, Engineering, Environmental and Ramification Researches. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0010079605860589.

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Rahmawaty, Annis, Akrom, Endang Darmawan, Titis Indri Wahyuni, Dian Kumalasari та Adnan. "Tumor Necrosis Factor Alpha (Tnf-α) and Creatinine Levels in Patients at Risk of Metabolic Syndrome with Standard Therapy Combined with Black Cumin Seed Oil". У 1st Paris Van Java International Seminar on Health, Economics, Social Science and Humanities (PVJ-ISHESSH 2020). Atlantis Press, 2021. http://dx.doi.org/10.2991/assehr.k.210304.142.

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Simanjuntak, Leo, M. Fidel Ganis Siregar, Johannes C. Mose та Sarma N. Lumbanraja. "The Effects of Phaleria macrocarpa (Scheff.) Boerl Extract on Tumor Necrosis Factor-Alpha (TNF-α) Level in Preeclampsia-induced Human Umbilical Vein Endothelial Cell (HUVEC) Culture". У The 2nd Syiah Kuala International Conference on Medicine and Health Sciences. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0008789900100016.

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"Pro-inflammatory cytokines “Tumor necrosis factor alpha (TNF-α) and Interleukin beta (IL-1 β)” levels in albino rats after co-administration of diclofenac sodium and dexamethasone". У 2nd Hawler Pharmaceutical Sciences Conference. Hawler Medical University, 2020. http://dx.doi.org/10.15218/hpsc.02.13.

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Shimp, Samuel K., Christopher M. Reilly, and Marissa Nichole Rylander. "Empirical Modeling the Effect of Hsp90 Inhibition on Cytokines Associated With Impaired Biotransport of Apoptotic Debris." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19572.

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Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disorder that can affect nearly every organ in the body. A link has been established between abnormal biotransport of apoptotic cell debris and pathogenesis of SLE [1]. Lupus mice are hyper-responsive to immune stimulation and overproduce inflammatory mediators including IL-6, IL-12, and nitric oxide (NO) [2]. Extracellular expression and transport of inflammatory cytokines are thought to be involved with the inhibited clearance of cellular debris [1]. Hsp90 has a prominent role in folding and conformational regulation of several client proteins, including proteins involved with production of inflammatory mediators [3]. Hsp90 readily binds ATP at the amino (N-) terminal domain. This binding event causes a conformational change in Hsp90 making it “clamp down” on its client protein [3]. Geldanamycin (Geld) is a known inhibitor of Hsp90 that out competes ATP binding at the N-terminal. This prevents chaperone capability and ultimately leads to client protein deactivation, destabilization, and degradation [3]. Hsp90 inhibitors have been shown to suppress immune stimulated release of interleukin 6 (IL-6), IL-12, tumor necrosis factor alpha (TNF-α), and nitric oxide (NO) [4].

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Oliveira, Daniela, Ana Martins, Frederico Martins та ін. "The impact of antinuclear antibodies induced by anti-tumour necrosis factor alpha (anti-TNF-α) agents on the long-term treatment outcomes in rheumatoid arthritis patients". У SBR 2021 Congresso Brasileiro de Reumatologia. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2021.1746.

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Rapports d'organisations sur le sujet "Tumor Necrosis Factor Alpha α-SMA"

Tian, Cong, Jianlong Shu, Wenhui Shao, Zhengxin Zhou, Huayang Guo та Jingang Wang. The efficacy and safety of IL Inhibitors, TNF-α Inhibitors, and JAK Inhibitor on ankylosing spondylitis: A Bayesian network meta-analysis of a “randomized, double-blind, placebo-controlled” trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.9.0117.

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Review question / Objective: In this study, we conducted a Bayesian network meta-analysis to evaluate the efficacy and safety of interleukin (IL) inhibitors, tumor necrosis factor-alpha (TNF-α) inhibitors, and Janus kinase (JAK) inhibitors on ankylosing spondylitis (AS).The purpose of this study is to compare the effectiveness and safety of different interventions for treating AS to provide insights into the decision-making in clinicalpractice. Condition being studied: Ankylosing spondylitis. Based on the Bayesian hierarchical model, we conducted a network meta-analysis using the gemtc package in R software (version 4.1.3) and Stata software (version 15.1). Cong Tian and Jianlong Shu contributed to the conception and design of the study and supervised the tweet classification. All authors drafted the manuscript. Wenhui Shao, Zhengxin Zhou, Huayang Guo and Jingang Wang contributed to data management and tweet classification. Cong Tian, Jianlong Shu and Zhengxin Zhou performed the statistical analysis. Cong Tian, Jianlong Shu, Wenhui Shao and Zhengxin Zhou reviewed the manuscript.

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