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Article ; Online: The "Janus" Role of C/EBPs Family Members in Cancer Progression.

Tolomeo, Manlio / Grimaudo, Stefania

International journal of molecular sciences

2020 Volume 21, Issue 12

Abstract: CCAAT/enhancer-binding proteins (C/EBPs) constitute a family of transcription factors composed of six members that are critical for normal cellular differentiation in a variety of tissues. They promote the expression of genes through interaction with ... ...

Abstract	CCAAT/enhancer-binding proteins (C/EBPs) constitute a family of transcription factors composed of six members that are critical for normal cellular differentiation in a variety of tissues. They promote the expression of genes through interaction with their promoters. Moreover, they have a key role in regulating cellular proliferation through interaction with cell cycle proteins. C/EBPs are considered to be tumor suppressor factors due to their ability to arrest cell growth (contributing to the terminal differentiation of several cell types) and for their role in cellular response to DNA damage, nutrient deprivation, hypoxia, and genotoxic agents. However, C/EBPs can elicit completely opposite effects on cell proliferation and cancer development and they have been described as both tumor promoters and tumor suppressors. This "Janus" role of C/EBPs depends on different factors, such as the type of tumor, the isoform/s expressed in cells, the type of dimerization (homo- or heterodimerization), the presence of inhibitory elements, and the ability to inhibit the expression of other tumor suppressors. In this review, we discuss the implication of the C/EBPs family in cancer, focusing on the molecular aspects that make these transcription factors tumor promoters or tumor suppressors.
MeSH term(s)	Animals ; CCAAT-Enhancer-Binding Proteins/chemistry ; CCAAT-Enhancer-Binding Proteins/genetics ; CCAAT-Enhancer-Binding Proteins/metabolism ; Disease Progression ; Disease Susceptibility ; Gene Expression Regulation, Neoplastic ; Humans ; Multigene Family ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Protein Binding ; Protein Isoforms ; Signal Transduction ; Structure-Activity Relationship
Chemical Substances	CCAAT-Enhancer-Binding Proteins ; Protein Isoforms
Language	English
Publishing date	2020-06-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21124308
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Article ; Online: The PD-1/PD-L1 Axis in the Biology of MASLD.

Pipitone, Rosaria Maria / Lupo, Giulia / Zito, Rossella / Javed, Ayesha / Petta, Salvatore / Pennisi, Grazia / Grimaudo, Stefania

International journal of molecular sciences

2024 Volume 25, Issue 7

Abstract: Metabolic Dysfunction-Associated Steatotic Liver (MASL), previously named nonalcoholic fatty liver (NAFL), is a multifactorial disease in which metabolic, genetic, and environmental risk factors play a predominant role. Obesity and type 2 diabetes act as ...

Abstract	Metabolic Dysfunction-Associated Steatotic Liver (MASL), previously named nonalcoholic fatty liver (NAFL), is a multifactorial disease in which metabolic, genetic, and environmental risk factors play a predominant role. Obesity and type 2 diabetes act as triggers of the inflammatory response, which contributes to the progression of MASL to Metabolic Dysfunction-Associated Steatohepatitis and the development of hepatocellular carcinoma. In the liver, several parenchymal, nonparenchymal, and immune cells maintain immunological homeostasis, and different regulatory pathways balance the activation of the innate and adaptative immune system. PD-1/PD-L1 signaling acts, in the maintenance of the balance between the immune responses and the tissue immune homeostasis, promoting self-tolerance through the modulation of activated T cells. Recently, PD-1 has received much attention for its roles in inducing an exhausted T cells phenotype, promoting the tumor escape from immune responses. Indeed, in MASLD, the excessive fat accumulation dysregulates the immune system, increasing cytotoxic lymphocytes and decreasing their cytolytic activity. In this context, T cells exacerbate liver damage and promote tumor progression. The aim of this review is to illustrate the main pathogenetic mechanisms by which the immune system promotes the progression of MASLD and the transition to HCC, as well as to discuss the possible therapeutic applications of PD-1/PD-L1 target therapy to activate T cells and reinvigorate immune surveillance against cancer.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular ; B7-H1 Antigen ; Diabetes Mellitus, Type 2 ; Liver Neoplasms ; Programmed Cell Death 1 Receptor ; Fatty Liver ; Biology
Chemical Substances	B7-H1 Antigen ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2024-03-25
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25073671
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Article: MAFLD: a multisystem disease.

Pipitone, Rosaria Maria / Ciccioli, Carlo / Infantino, Giuseppe / La Mantia, Claudia / Parisi, Stefanie / Tulone, Adele / Pennisi, Grazia / Grimaudo, Stefania / Petta, Salvatore

Therapeutic advances in endocrinology and metabolism

2023 Volume 14, Page(s) 20420188221145549

Abstract: Nonalcoholic fatty liver disease (NAFLD), affecting about 25% of general population and more than 50% of dysmetabolic patients, is an emerging cause of chronic liver disease and its complications. Recently, an international consensus of experts proposed ... ...

Abstract	Nonalcoholic fatty liver disease (NAFLD), affecting about 25% of general population and more than 50% of dysmetabolic patients, is an emerging cause of chronic liver disease and its complications. Recently, an international consensus of experts proposed to rename this disease as 'Metabolic dysfunction-Associated Fatty Liver Disease' (MAFLD) to focus on the bidirectional interplay between fatty liver and metabolic alterations and to stress the need of assessing fatty liver independently from alcohol consumption and other coexisting causes of liver disease. The peculiarity of NAFLD/MAFLD lies in the presence of a higher risk of not only - as expected - liver-related events but also of extrahepatic events, mostly cardiovascular and cancers. Available evidence suggests that these associations are not only the expression of sharing the same risk factors but shed light about the ability of NAFLD/MAFLD and particularly of its progressive form - nonalcoholic/metabolic dysfunction-associated steatohepatitis - to act as an independent risk factor
Language	English
Publishing date	2023-01-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2554822-0
ISSN	2042-0196 ; 2042-0188
ISSN (online)	2042-0196
ISSN	2042-0188
DOI	10.1177/20420188221145549
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Article ; Online: STAT5 and STAT5 Inhibitors in Hematological Malignancies.

Tolomeo, Manlio / Meli, Maria / Grimaudo, Stefania

Anti-cancer agents in medicinal chemistry

2019 Volume 19, Issue 17, Page(s) 2036–2046

Abstract: The JAK-STAT pathway is an important physiologic regulator of different cellular functions including proliferation, apoptosis, differentiation, and immunological responses. Out of six different STAT proteins, STAT5 plays its main role in hematopoiesis ... ...

Abstract	The JAK-STAT pathway is an important physiologic regulator of different cellular functions including proliferation, apoptosis, differentiation, and immunological responses. Out of six different STAT proteins, STAT5 plays its main role in hematopoiesis and constitutive STAT5 activation seems to be a key event in the pathogenesis of several hematological malignancies. This has led many researchers to develop compounds capable of inhibiting STAT5 activation or interfering with its functions. Several anti-STAT5 molecules have shown potent STAT5 inhibitory activity in vitro. However, compared to the large amount of clinical studies with JAK inhibitors that are currently widely used in the clinics to treat myeloproliferative disorders, the clinical trials with STAT5 inhibitors are very limited. At present, a few STAT5 inhibitors are in phase I or II clinical trials for the treatment of leukemias and graft vs host disease. These studies seem to indicate that such compounds could be well tolerated and useful in reducing the occurrence of resistance to tyrosine kinase inhibitors in chronic myeloid leukemia. Of interest, STAT5 seems to play an important role in the regulation of hematopoietic stem cell self-renewal suggesting that combination therapies including STAT5 inhibitors can erode the cancer stem cell pool and possibly open the way for the complete cancer eradication. In this review, we discuss the implication of STAT5 in hematological malignancies and the results obtained with the novel STAT5 inhibitors.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Hematologic Neoplasms/drug therapy ; Hematologic Neoplasms/metabolism ; Humans ; STAT5 Transcription Factor/antagonists & inhibitors ; STAT5 Transcription Factor/metabolism
Chemical Substances	Antineoplastic Agents ; STAT5 Transcription Factor
Language	English
Publishing date	2019-09-06
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2217610-X
ISSN	1875-5992 ; 1871-5206
ISSN (online)	1875-5992
ISSN	1871-5206
DOI	10.2174/1871520619666190906160848
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Article ; Online: Curcumin and Andrographolide Co-Administration Safely Prevent Steatosis Induction and ROS Production in HepG2 Cell Line.

Pipitone, Rosaria Maria / Zito, Rossella / Lupo, Giulia / Javed, Ayesha / La Mantia, Claudia / Di Maria, Gabriele / Pratelli, Giovanni / Di Salvo, Francesca / Fontana, Simona / Pucci, Marzia / Carlisi, Daniela / Grimaudo, Stefania

Molecules (Basel, Switzerland)

2023 Volume 28, Issue 3

Abstract: Non-alcoholic fatty liver disease (NAFLD) is an emerging chronic liver disease worldwide. Curcumin and andrographolide are famous for improving hepatic functions, being able to reverse oxidative stress and release pro-inflammatory cytokines, and they are ...

Abstract	Non-alcoholic fatty liver disease (NAFLD) is an emerging chronic liver disease worldwide. Curcumin and andrographolide are famous for improving hepatic functions, being able to reverse oxidative stress and release pro-inflammatory cytokines, and they are implicated in hepatic stellate cell activation and in liver fibrosis development. Thus, we tested curcumin and andrographolide separately and in combination to determine their effect on triglyceride accumulation and ROS production, identifying the differential expression of genes involved in fatty liver and oxidative stress development. In vitro steatosis was induced in HepG2 cells and the protective effect of curcumin, andrographolide, and their combination was observed evaluating cell viability, lipid and triglyceride content, ROS levels, and microarray differential gene expression. Curcumin, andrographolide, and their association were effective in reducing steatosis, triglyceride content, and ROS stress, downregulating the genes involved in lipid accumulation. Moreover, the treatments were able to protect the cytotoxic effect of steatosis, promoting the expression of survival and anti-inflammatory genes. The present study showed that the association of curcumin and andrographolide could be used as a therapeutic approach to counter high lipid content and ROS levels in steatosis liver, avoiding the possible hepatotoxic effect of curcumin. Furthermore, this study improved our understanding of the antisteatosis and hepatoprotective properties of a curcumin and andrographolide combination.
MeSH term(s)	Humans ; Hep G2 Cells ; Curcumin/therapeutic use ; Reactive Oxygen Species/metabolism ; Non-alcoholic Fatty Liver Disease/drug therapy ; Non-alcoholic Fatty Liver Disease/prevention & control ; Non-alcoholic Fatty Liver Disease/genetics ; Triglycerides/metabolism ; Liver
Chemical Substances	Curcumin (IT942ZTH98) ; Reactive Oxygen Species ; andrographolide (410105JHGR) ; Triglycerides
Language	English
Publishing date	2023-01-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules28031261
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Article: Red and golden tomato administration improves fat diet-induced hepatic steatosis in rats by modulating HNF4α, Lepr, and GK expression.

Pipitone, Rosaria Maria / Zito, Rossella / Gambino, Giuditta / Di Maria, Gabriele / Javed, Ayesha / Lupo, Giulia / Giglia, Giuseppe / Sardo, Pierangelo / Ferraro, Giuseppe / Rappa, Francesca / Carlisi, Daniela / Di Majo, Danila / Grimaudo, Stefania

Frontiers in nutrition

2023 Volume 10, Page(s) 1221013

Abstract: Introduction: Nonalcoholic fatty liver disease (NAFLD), characterized by lipid accumulation within hepatocytes exceeding 5% of liver weight, is strongly related to metabolic disorders, obesity, and diabetes and represents a health emergency worldwide. ... ...

Abstract	Introduction: Nonalcoholic fatty liver disease (NAFLD), characterized by lipid accumulation within hepatocytes exceeding 5% of liver weight, is strongly related to metabolic disorders, obesity, and diabetes and represents a health emergency worldwide. There is no standard therapy available for NAFLD. Lifestyle intervention, including phytonutrient intake, is key in preventing NAFLD development and progression. Methods: We used a rat model of NAFLD to evaluate the effect of dietary supplementation with red tomato (RT) and golden tomato (GT)-a patented mix of fruit with varying degrees of ripeness and particularly rich in naringenin and chlorogenic acid-after steatosis development. We assessed the effects on body weight, metabolic profile, and hepatic steatosis. Results and discussion: We found a correlation between the amelioration of all the parameters and the liver gene expression. Our results showed that, together with the reversion of steatosis, the consumption of RT and GT can cause a significant reduction in triglycerides, low-density lipoprotein-cholesterol, fasting glucose, and homeostasis model assessment index. Meanwhile, we observed an increase in high-density lipoprotein-cholesterol according to the amelioration of the general lipidic profile. Regarding hepatic gene expression, we found the upregulation of Gk and
Language	English
Publishing date	2023-09-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2776676-7
ISSN	2296-861X
ISSN	2296-861X
DOI	10.3389/fnut.2023.1221013
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Article ; Online: IL32 downregulation lowers triglycerides and type I collagen in di-lineage human primary liver organoids.

Sasidharan, Kavitha / Caddeo, Andrea / Jamialahmadi, Oveis / Noto, Francesca Rita / Tomasi, Melissa / Malvestiti, Francesco / Ciociola, Ester / Tavaglione, Federica / Mancina, Rosellina M / Cherubini, Alessandro / Bianco, Cristiana / Mirarchi, Angela / Männistö, Ville / Pihlajamäki, Jussi / Kärjä, Vesa / Grimaudo, Stefania / Luukkonen, Panu K / Qadri, Sami / Yki-Järvinen, Hannele /

Petta, Salvatore / Manfrini, Silvia / Vespasiani-Gentilucci, Umberto / Bruni, Vincenzo / Valenti, Luca / Romeo, Stefano

Cell reports. Medicine

2024 Volume 5, Issue 1, Page(s) 101352

Abstract: Steatotic liver disease (SLD) prevails as the most common chronic liver disease yet lack approved treatments due to incomplete understanding of pathogenesis. Recently, elevated hepatic and circulating interleukin 32 (IL-32) levels were found in ... ...

Abstract	Steatotic liver disease (SLD) prevails as the most common chronic liver disease yet lack approved treatments due to incomplete understanding of pathogenesis. Recently, elevated hepatic and circulating interleukin 32 (IL-32) levels were found in individuals with severe SLD. However, the mechanistic link between IL-32 and intracellular triglyceride metabolism remains to be elucidated. We demonstrate in vitro that incubation with IL-32β protein leads to an increase in intracellular triglyceride synthesis, while downregulation of IL32 by small interfering RNA leads to lower triglyceride synthesis and secretion in organoids from human primary hepatocytes. This reduction requires the upregulation of Phospholipase A2 group IIA (PLA2G2A). Furthermore, downregulation of IL32 results in lower intracellular type I collagen levels in di-lineage human primary hepatic organoids. Finally, we identify a genetic variant of IL32 (rs76580947) associated with lower circulating IL-32 and protection against SLD measured by non-invasive tests. These data suggest that IL32 downregulation may be beneficial against SLD.
MeSH term(s)	Humans ; Collagen Type I/genetics ; Collagen Type I/metabolism ; Triglycerides/metabolism ; Down-Regulation/genetics ; Interleukins/genetics ; Fatty Liver ; Liver Diseases ; Organoids
Chemical Substances	Collagen Type I ; Triglycerides ; Interleukins ; IL32 protein, human
Language	English
Publishing date	2024-01-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2023.101352
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Article ; Online: Metabolic memory in diabetic foot syndrome (DFS): MICRO-RNAS, single nucleotide polymorphisms (SNPs) frequency and their relationship with indices of endothelial function and adipo-inflammatory dysfunction.

Del Cuore, Alessandro / Pipitone, Rosaria Maria / Casuccio, Alessandra / Mazzola, Marco Maria / Puleo, Maria Grazia / Pacinella, Gaetano / Riolo, Renata / Maida, Carlo / Di Chiara, Tiziana / Di Raimondo, Domenico / Zito, Rossella / Lupo, Giulia / Agnello, Luisa / Di Maria, Gabriele / Ciaccio, Marcello / Grimaudo, Stefania / Tuttolomondo, Antonino

Cardiovascular diabetology

2023 Volume 22, Issue 1, Page(s) 148

Abstract: Background: Diabetic foot is a significant cause of morbidity in diabetic patients, with a rate that is approximately twice that of patients without foot ulcers. "Metabolic memory" represents the epigenetic changes induced by chronic hyperglycaemia, ... ...

Abstract	Background: Diabetic foot is a significant cause of morbidity in diabetic patients, with a rate that is approximately twice that of patients without foot ulcers. "Metabolic memory" represents the epigenetic changes induced by chronic hyperglycaemia, despite the correction of the glucose levels themselves. These epigenetic modifications appear to perpetuate the damage caused by persistently elevated glucose levels even in their absence, acting at various levels, mostly affecting the molecular processes of diabetic ulcer healing. Methods: The aim of our cross-sectional study was to analyse a cohort of patients with diabetes with and without lower limb ulcers. We examined the effects of epigenetic changes on miRNA 126, 305, and 217 expression and the frequency of the SNPs of genes encoding inflammatory molecules (e.g., IL-6 and TNF-alpha) and their correlations with serum levels of proangiogenic molecules (e.g., ENOS, VEGF and HIF-1alpha) and several adipokines as well as with endothelial dysfunction, assessed noninvasively by reactive hyperaemia peripheral artery tonometry. Between March 2021 and June 2022, 110 patients were enrolled into the study: 50 diabetic patients with diabetic foot injuries, 40 diabetic patients without ulcerative complications and 20 nondiabetic patients as the control group. Results: Diabetic subjects with lower limb ulcerative lesions exhibited higher levels of inflammatory cytokines, such as VEGF (191.40 ± 200 pg/mL vs. 98.27 ± 56.92 pg/mL vs. 71.01 ± 52.96 pg/mL; p = 0.22), HIF-1alpha (40.18 ± 10.80 ng/mL vs. 33.50 ± 6.16 ng/mL vs. 33.85 ± 6.84 ng/mL; p = 0.10), and Gremlin-1 (1.72 ± 0.512 ng/mL vs. 1.31 ± 0.21 ng/mL vs. 1.11 ± 0.19 ng/mL; p < 0.0005), than those without lower limb ulcers and healthy controls. Furthermore, we observed that miR-217-5p and miR-503-5p were 2.19-fold (p < 0.05) and 6.21-fold (p = 0.001) more highly expressed in diabetic foot patients than in healthy controls, respectively. Additionally, diabetic patients without lower limb ulcerative complications showed 2.41-fold (p = 0) and 2.24-fold (p = 0.029) higher expression of miR-217-5p and miR-503-5p, respectively, than healthy controls. Finally, diabetic patients with and without ulcerative complications of the lower limbs showed higher expression of the VEGFC2578A CC polymorphism (p = 0.001) and lower expression of the VEGFC2578A AC polymorphism (p < 0.005) than the healthy control population. We observed a significant increase in Gremlin-1 levels in patients with diabetic foot, suggesting that this inflammatory adipokine may serve as a predictive marker for the diagnosis of diabetic foot. Conclusions: Our results highlighted that patients with diabetic foot showed predominant expression of the VEGF C2578A CC polymorphism and reduced expression of the AC allele. Additionally, we found an overexpression of miR-217-5p and miR-503-5p in diabetic patients with and without diabetic foot syndrome compared with healthy controls. These results align with those reported in the literature, in which the overexpression of miR-217-5p and miR-503-5p in the context of diabetic foot is reported. The identification of these epigenetic modifications could therefore be helpful in the early diagnosis of diabetic foot and the treatment of risk factors. However, further studies are necessary to confirm this hypothesis.
MeSH term(s)	Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Diabetic Foot/diagnosis ; Diabetic Foot/genetics ; Polymorphism, Single Nucleotide ; Ulcer ; Vascular Endothelial Growth Factor A/genetics ; Cross-Sectional Studies ; Glucose ; Diabetes Mellitus
Chemical Substances	MicroRNAs ; Vascular Endothelial Growth Factor A ; Glucose (IY9XDZ35W2) ; MIRN126 microRNA, human ; MIRN217 microRNA, human
Language	English
Publishing date	2023-06-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2093769-6
ISSN	1475-2840 ; 1475-2840
ISSN (online)	1475-2840
ISSN	1475-2840
DOI	10.1186/s12933-023-01880-x
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Article ; Online: Mer Tyrosine Kinase (MERTK) modulates liver fibrosis progression and hepatocellular carcinoma development.

Pipitone, Rosaria Maria / Calvaruso, Vincenza / Di Marco, Lorenza / Di Salvo, Francesca / Gaggianesi, Miriam / Lupo, Giulia / Zito, Rossella / La Mantia, Claudia / Ramazzotti, Matteo / Petta, Salvatore / Di Marco, Vito / Craxì, Antonio / Grimaudo, Stefania

Frontiers in immunology

2022 Volume 13, Page(s) 926236

Abstract: MerTK is a tyrosine kinase receptor that belongs to the TAM (Tyro3/Axl/Mer) receptor family. It is involved in different processes including cellular proliferation/survival, cellular adhesion/migration, and release of the inflammatory/anti-inflammatory ... ...

Abstract	MerTK is a tyrosine kinase receptor that belongs to the TAM (Tyro3/Axl/Mer) receptor family. It is involved in different processes including cellular proliferation/survival, cellular adhesion/migration, and release of the inflammatory/anti-inflammatory cytokines. Although it is reported that MERTK polymorphisms affect the severity of viral and metabolic liver diseases, being able to influence fibrosis progression and hepatocellular carcinoma development, the mechanisms remain unknown. Methods: using a microarray approach, we evaluated the liver expression of genes involved in fibrogenesis and hepatocarcinogenesis in patient with chronic hepatitis C (CHC), stratified for MERTK genotype and MERTK expression. Results: we found that the rs 4374383 AA homozygosity is associated with lower MERTK expression in CHC patients and that, depending on MERTK genotype, Matrix Metallopeptidase 9 (MMP9), Matrix Metallopeptidase 7 (MMP7), Secreted Frizzled Related Protein 1 (SFRP1) and WNT gene family 11(WNT11) show differential expression in patients with CHC with or without neoplastic progression. Conclusions: our results confirm that MERTK represents a genetic biomarker for progression of liver disease and are suggestive of translational relevance for the study of downstream pathways involved in fibrogenesis and hepatocarcinogenesis.
MeSH term(s)	Carcinoma, Hepatocellular/etiology ; Carcinoma, Hepatocellular/genetics ; Fibrosis ; Humans ; Liver Cirrhosis/genetics ; Liver Neoplasms/genetics ; Metalloproteases ; Protein-Tyrosine Kinases ; Proto-Oncogene Proteins/metabolism ; c-Mer Tyrosine Kinase/genetics ; c-Mer Tyrosine Kinase/metabolism
Chemical Substances	Proto-Oncogene Proteins ; MERTK protein, human (EC 2.7.10.1) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; c-Mer Tyrosine Kinase (EC 2.7.10.1) ; Metalloproteases (EC 3.4.-)
Language	English
Publishing date	2022-08-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.926236
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Article: Role of Myeloid-Epithelial-Reproductive Tyrosine Kinase and Macrophage Polarization in the Progression of Atherosclerotic Lesions Associated With Nonalcoholic Fatty Liver Disease.

Pastore, Mirella / Grimaudo, Stefania / Pipitone, Rosaria Maria / Lori, Giulia / Raggi, Chiara / Petta, Salvatore / Marra, Fabio

Frontiers in pharmacology

2019 Volume 10, Page(s) 604

Abstract: Recent lines of evidence highlight the involvement of myeloid-epithelial-reproductive tyrosine kinase (MerTK) in metabolic disease associated with liver damage. MerTK is mainly expressed in anti-inflammatory M2 macrophages where it mediates ... ...

Abstract	Recent lines of evidence highlight the involvement of myeloid-epithelial-reproductive tyrosine kinase (MerTK) in metabolic disease associated with liver damage. MerTK is mainly expressed in anti-inflammatory M2 macrophages where it mediates transcriptional changes including suppression of proinflammatory cytokines and enhancement of inflammatory repressors. MerTK is regulated by metabolic pathways through nuclear sensors including LXRs, PPARs, and RXRs, in response to apoptotic bodies or to other sources of cholesterol. Nonalcoholic fatty liver disease (NAFLD) is one of the most serious public health problems worldwide. It is a clinicopathological syndrome closely related to obesity, insulin resistance, and oxidative stress. It includes a spectrum of conditions ranging from simple steatosis, characterized by hepatic fat accumulation with or without inflammation, to nonalcoholic steatohepatitis (NASH), defined by hepatic fat deposition with hepatocellular damage, inflammation, and accumulating fibrosis. Several studies support an association between NAFLD and the incidence of cardiovascular diseases including atherosclerosis, a major cause of death worldwide. This pathological condition consists in a chronic and progressive inflammatory process in the intimal layer of large- and medium-sized arteries. The complications of advanced atherosclerosis include chronic or acute ischemic damage in the tissue perfused by the affected artery, leading to cellular death. By identifying specific targets influencing lipid metabolism and cardiovascular-related diseases, the present review highlights the role of MerTK in NAFLD-associated atherosclerotic lesions as a potential innovative therapeutic target. Therapeutic advantages might derive from the use of compounds selective for nuclear receptors targeting PPARs rather than LXRs regulating macrophage lipid metabolism and macrophage mediated inflammation, by favoring the expression of MerTK, which mediates an immunoregulatory action with a reduction in inflammation and in atherosclerosis.
Language	English
Publishing date	2019-05-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2019.00604
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