M1/M2-macrophage Polarization-based Hepatotoxicity in <scp>d</scp>-galactosamine-induced Acute Liver Injury in Rats

Rahman, Nahid; Pervin, Munmun; Kuramochi, Mizuki; Karim, Mohammad Rabiul; Izawa, Takeshi; Kuwamura, Mitsuru; Yamate, Jyoji

doi:10.1177/0192623318801574

Cited by 35 publications

(42 citation statements)

References 37 publications

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“…Two-point-five microgram of total RNA was reverse-transcribed to cDNA by SuperScript VILO cDNA synthesis kit (Invitrogen, Carlsbad, CA, USA). Real-time PCR was performed with TaqMan gene expression assays (Life Technologies, Carlsbad, CA, USA) in a PikoReal Real-Time 96 PCR System (Thermo Scientific, Waltham, MA, USA) as previously described [ 17 ]. Details of probes are listed in Table 2 .…”

Section: Methodsmentioning

confidence: 99%

Dietary Iron Overload Differentially Modulates Chemically-Induced Liver Injury in Rats

et al. 2020

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Hepatic iron overload is well known as an important risk factor for progression of liver diseases; however, it is unknown whether it can alter the susceptibility to drug-induced hepatotoxicity. Here we investigate the pathological roles of iron overload in two single-dose models of chemically-induced liver injury. Rats were fed a high-iron (Fe) or standard diet (Cont) for four weeks and were then administered with allyl alcohol (AA) or carbon tetrachloride (CCl4). Twenty-four hours after administration mild mononuclear cell infiltration was seen in the periportal/portal area (Zone 1) in Cont-AA group, whereas extensive hepatocellular necrosis was seen in Fe-AA group. Centrilobular (Zone 3) hepatocellular necrosis was prominent in Cont-CCl4 group, which was attenuated in Fe-CCl4 group. Hepatic lipid peroxidation and hepatocellular DNA damage increased in Fe-AA group compared with Cont-AA group. Hepatic caspase-3 cleavage increased in Cont-CCl4 group, which was suppressed in Fe-CCl4 group. Our results showed that dietary iron overload exacerbates AA-induced Zone-1 liver injury via enhanced oxidative stress while it attenuates CCl4-induced Zone-3 liver injury, partly via the suppression of apoptosis pathway. This study suggested that susceptibility to drugs or chemical compounds can be differentially altered in iron-overloaded livers.

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Section: Methodsmentioning

confidence: 99%

Dietary Iron Overload Differentially Modulates Chemically-Induced Liver Injury in Rats

et al. 2020

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“…Наиболее высокая экспрессия и репертуар SR выявляются на клетках печени, а их дисфункция способствует инсулинорезистентности, гепатозу и фиброзу печени, а при дальнейшем прогрессировании процесса -неалкогольной жировой болезни печени, неинфекционному гепатиту, циррозу, развитию гепатоцеллюлярной карциномы [10,178]. При этом растворимые и мембранные формы многих SR могут использоваться как биомаркеры прогрессирующих заболеваний печени, включая цирроз и рак [10].…”

Section: Sr при развитии метаболического синдрома и диабета 2-го типаunclassified

“…При этом растворимые и мембранные формы многих SR могут использоваться как биомаркеры прогрессирующих заболеваний печени, включая цирроз и рак [10]. Особую патогенетическую роль в SR-зависимых процессах играют клетки Купфера, М1-М2 поляризация которых в этом случае носит нечеткий, эклектичный характер [178].…”

Section: Sr при развитии метаболического синдрома и диабета 2-го типаunclassified

Physiological and pathogenic role of scavenger receptors in humans

et al. 2020

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The scavenger receptors (SRs)) include > 30 different molecules structurally classified into 11 classes (A to L). They are expressed mostly on stromal macrophages, and their expression may be augmented in direct dependence with concentrations of their ligands. The SRs are heterogenous by their structure, however, being common in their functional potential. E.g., different SR classes may participate in absorption of modified low-density lipoproteins and glycated proteins, apoptotic and ageing cells, altered erythrocytes and platelets, like as a big variety of other endogenous ligands from metabolic and cellular “trash”. A common property of SRs is their participation in removal of small pathogen amounts from blood circulation, regulation of cell and tissue stress responses, ability to form complicated receptor complexes with other receptor types including integrins and toll-like receptors. Opposite to classic pattern-recognizing receptors, the SR involvement does not always elicit a pronounced cellular activation and development of pro-inflammatory cellular stress. The SR functional effects provide interactions between different physiological events and immune system, including the processes of neuroendocrine and metabolic regulation. These mechanisms provide both homeostatic stability and, likewise, act at the border of normal and pathological conditions, i.e., participating in pathogenesis of transitional processes, e.g., physiological ageing. Moreover, the SR-associated processes represent a key pathogenetic factor in different somatic diseases, e.g., those associated with low-intensity chronic inflammation, including obesity, type 2 diabetes, atherosclerosis, arterial hypertension, various neurodegenerative disorders. Similarly, the SRs are involved into the processes of cancer transformation and antitumor response, different processes of classical inflammation, from antigen presentation to the morphofunctional T cell and macrophage polarization in the inflammation foci and immunocompetent organs. SR are playing a controversial role in development of acute systemic inflammation, the main reason for lethal outcomes in the intensive care wards. Targeted effects upon the SRs represent a promising approach when treating a broad variety of diseases, whereas detection of membrane-bound and soluble SR forms could be performed by means of diagnostic and monitoring techniques in many human disorders.

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“…Such techniques include immunohistochemistry, single cell RNA sequencing, fluorescent magnetic nanoparticle labeling, and even non-invasive imaging including magnetic resonance imaging (MRI), given that T2* signal enhancement on MR images significantly correlated with TAM density in sarcoma patients (32,(46)(47)(48). Depending on their local microenvironments, TAMs can display phenotypic and functional heterogeneity, which is best understood through the concept of macrophage polarization (see next paragraph) (49). However, this dichotomous polarization paradigm is largely oversimplified, and there is a broad range of macrophage polarization phenotypes in vivo (50).…”

Section: Macrophages In Tumorigenesismentioning

confidence: 99%

Targeting Tumor-Associated Macrophages in the Pediatric Sarcoma Tumor Microenvironment

et al. 2020

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For many pediatric sarcoma patients, multi-modal therapy including chemotherapy, radiation, and surgery is sufficient to cure their disease. However, event-free and overall survival rates for patients with more advanced disease are grim, necessitating the development of novel therapeutic approaches. Within many pediatric sarcomas, the normal immune response, including recognition and destruction of cancer cells, is lost due to the highly immune suppressive tumor microenvironment (TME). In this setting, tumor cells evade immune detection and capitalize on the immune suppressed microenvironment, leading to unchecked proliferation and metastasis. Recent preclinical and clinical approaches are aimed at understanding this immune suppressive microenvironment and employing cancer immunotherapy in an attempt to overcome this, by renewing the ability of the immune system to recognize and destroy cancer cells. While there are several factors that drive the attenuation of immune responses in the sarcoma TME, one of the most remarkable are tumor associated macrophage (TAMs). TAMs suppress immune cytolytic function, promote tumor growth and metastases, and are generally associated with a poor prognosis in most pediatric sarcoma subtypes. In this review, we summarize the mechanisms underlying TAM-facilitated immune evasion and tumorigenesis and discuss the potential therapeutic application of TAM-focused drugs in the treatment of pediatric sarcomas.

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M1/M2-macrophage Polarization-based Hepatotoxicity in d-galactosamine-induced Acute Liver Injury in Rats

Cited by 35 publications

References 37 publications

Dietary Iron Overload Differentially Modulates Chemically-Induced Liver Injury in Rats

Dietary Iron Overload Differentially Modulates Chemically-Induced Liver Injury in Rats

Physiological and pathogenic role of scavenger receptors in humans

Targeting Tumor-Associated Macrophages in the Pediatric Sarcoma Tumor Microenvironment

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