Transforming growth factor-beta 1 inhibits scavenger receptor activity in THP-1 human macrophages.

Bottalico, L A; Wager, R E; Agellon, Luis B.; Assoian, R K; Tabas, Ira

doi:10.1016/s0021-9258(18)54434-3

Cited by 100 publications

(9 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A number of factors have been shown to regulate SR expression. In addition to modified or oxidized low-density lipoproteins, cytokines (Bottalico et al, 1991;Geng and Hansson, 1992;de Villiers et al, 1994;Hsu et al, 1996;Yesner et al, 1996;Khovidhunkit et al, 2001;Murphy et al, 2005;Hashizume and Mihara, 2012), including macrophage colony-stimulating factor (M-CSF), tumor necrosis factor (TNF)-α, IFN-γ, transforming growth factor (TGF)-β1, and IL-1, IL-4, and IL-6, hormones (testosterone and estrogen; Langer et al, 2002;Srivastava, 2003), cell differentiation transcription factors [peroxisome proliferator-activated receptors (PPAR) FIGURE 1 | Microglia/Macrophage polarization subtypes. Traditionally, the M1 or M2 phenotype is considered as the extreme activation state of macrophages/microglia in response to different microenvironmental stimuli.…”

Section: Microglia and Aβmentioning

confidence: 99%

“…A number of factors have been shown to regulate SR expression. In addition to modified or oxidized low-density lipoproteins, cytokines (Bottalico et al, 1991 ; Geng and Hansson, 1992 ; de Villiers et al, 1994 ; Hsu et al, 1996 ; Yesner et al, 1996 ; Khovidhunkit et al, 2001 ; Murphy et al, 2005 ; Hashizume and Mihara, 2012 ), including macrophage colony-stimulating factor (M-CSF), tumor necrosis factor (TNF)-α, IFN-γ, transforming growth factor (TGF)-β1, and IL-1, IL-4, and IL-6, hormones (testosterone and estrogen; Langer et al, 2002 ; Srivastava, 2003 ), cell differentiation transcription factors [peroxisome proliferator-activated receptors (PPAR) α and γ; Chinetti et al, 2000 ], antioxidants (N-acetylcysteine, kaempferol; Svensson et al, 2002 ; Li et al, 2013 ), endotoxin (LPS; Khovidhunkit et al, 2001 ; Baranova et al, 2002 ; Park et al, 2012 ), and bacteria or dead or apoptotic cells (Grolleau et al, 2003 ), also affect SRs expression.…”

Section: Microglia and Admentioning

confidence: 99%

See 1 more Smart Citation

Microglia in Alzheimer’s Disease: A Target for Therapeutic Intervention

Zhang

Wang

et al. 2021

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is one of the most common types of age-related dementia worldwide. In addition to extracellular amyloid plaques and intracellular neurofibrillary tangles, dysregulated microglia also play deleterious roles in the AD pathogenesis. Numerous studies have demonstrated that unbridled microglial activity induces a chronic neuroinflammatory environment, promotes β-amyloid accumulation and tau pathology, and impairs microglia-associated mitophagy. Thus, targeting microglia may pave the way for new therapeutic interventions. This review provides a thorough overview of the pathophysiological role of the microglia in AD and illustrates the potential avenues for microglia-targeted therapies, including microglial modification, immunoreceptors, and anti-inflammatory drugs.

show abstract

Section: Microglia and Aβmentioning

confidence: 99%

“…A number of factors have been shown to regulate SR expression. In addition to modified or oxidized low-density lipoproteins, cytokines (Bottalico et al, 1991 ; Geng and Hansson, 1992 ; de Villiers et al, 1994 ; Hsu et al, 1996 ; Yesner et al, 1996 ; Khovidhunkit et al, 2001 ; Murphy et al, 2005 ; Hashizume and Mihara, 2012 ), including macrophage colony-stimulating factor (M-CSF), tumor necrosis factor (TNF)-α, IFN-γ, transforming growth factor (TGF)-β1, and IL-1, IL-4, and IL-6, hormones (testosterone and estrogen; Langer et al, 2002 ; Srivastava, 2003 ), cell differentiation transcription factors [peroxisome proliferator-activated receptors (PPAR) α and γ; Chinetti et al, 2000 ], antioxidants (N-acetylcysteine, kaempferol; Svensson et al, 2002 ; Li et al, 2013 ), endotoxin (LPS; Khovidhunkit et al, 2001 ; Baranova et al, 2002 ; Park et al, 2012 ), and bacteria or dead or apoptotic cells (Grolleau et al, 2003 ), also affect SRs expression.…”

Section: Microglia and Admentioning

confidence: 99%

Microglia in Alzheimer’s Disease: A Target for Therapeutic Intervention

Zhang

Wang

et al. 2021

Front. Cell. Neurosci.

View full text Add to dashboard Cite

show abstract

“…TGF-β can control the excessive inflammatory responses by T-cells and stimulate IgA production. TGF-β1 inhibited the induction of scavenger receptor activity in macrophage-like cells derived from the monocytic cell line THP-1 [42]. The scavenger receptor can clear LPS during Gram-negative bacterial sepsis [42].…”

Section: Preterm Vs Term Milkmentioning

confidence: 99%

“…TGF-β1 inhibited the induction of scavenger receptor activity in macrophage-like cells derived from the monocytic cell line THP-1 [42]. The scavenger receptor can clear LPS during Gram-negative bacterial sepsis [42]. Therefore, higher level of TGF-β in PM may reduce macrophage phagocytosis activity, which could decrease the protective activity of innate immunity during neonatal infection.…”

Section: Preterm Vs Term Milkmentioning

confidence: 99%

Cytokine Expression by Human Macrophage-Like Cells Derived from the Monocytic Cell Line THP-1 Differs between Treatment with Milk from Preterm- and Term-Delivering Mothers and Pasteurized Donor Milk

2020

View full text Add to dashboard Cite

Immunomodulatory proteins from human milk may enhance the protection and development of the infant’s gut. This study compared the immunomodulatory effects of treatment with milk from preterm-(PM) and term-delivering (TM) mothers and pasteurized donor milk (DM) on cytokine gene expression in human macrophage-like cells derived from the monocytic cell line THP-1. The gene expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-12 (p40), IL-10 and GAPDH in macrophages treated with PM, TM and DM at steady and activated (inflammatory) states were measured using real-time reverse transcription-polymerase chain reaction. TNF-α and IL-6 in macrophages (both states) with DM were higher than PM or TM. IL-10 in steady state macrophages with DM was higher than PM whereas DM increased IL-10 in activated macrophages compared with TM. TM increased IL-6 and IL-12 (p40) in steady state macrophages compared with PM. IL-12 (p40) in activated macrophages with TM was higher than PM. IL-10 in steady state macrophages with TM was higher than PM. These results suggest that DM induces higher gene expression of pro-inflammatory and anti-inflammatory cytokines in macrophages compared with PM or TM. PM reduced gene expression of pro-inflammatory cytokines compared with TM, which may decrease the development of necrotizing enterocolitis and systematic inflammation.

show abstract

“…Furthermore, the ability of TGF-␤ to increase apoE synthesis could also, by reverse cholesterol transport, result in plaque regression (17). However, these effects are confounded by the ability of TGF-␤ to inhibit both type A and B SR expression including the downregulation of SR-BI and CD36 in macrophage-derived foam cells (12,18). In contrast, TGF-␤ has been suggested to contribute to the pathology associated with arterial rest-enosis.…”

mentioning

confidence: 99%

TGF-β increases cholesterol efflux and ABC-1 expression in macrophage-derived foam cells: opposing the effects of IFN-γ

Panousis

Evans

Zuckerman

2001

Journal of Lipid Research

View full text Add to dashboard Cite

The regulation of ATP-binding cassette transporter 1 (ABC-1) expression by cytokines present within the microenvironment of the atheroma may play an important role in determining the impact of reverse cholesterol transport on the atherosclerotic lesion. We recently reported that the macrophage-activating cytokine interferon (IFN)-␥ inhibited both cholesterol efflux and ABC-1 expression. In the present study, we investigated the effects of transforming growth factor (TGF)-␤ , a cytokine also apparent within the atheroma, on cholesterol efflux, ABC-1 expression, and its ability to antagonize the inhibitory effects of IFN-␥ . TGF-␤ significantly increased cholesterol efflux in macrophage-derived foam cells from apolipoprotein E (apoE) knockout mice, with maximal effects apparent at 300 pg/ml. The increases in efflux occurred without any effect on the passive diffusion component of efflux mediated by ␤ -cyclodextrin. Furthermore, the increase in cholesterol efflux occurred without any changes in free or esterified cholesterol pools and was consistent with an increase in both ABC-1 message and protein. Finally, TGF-␤ was also demonstrated to inhibit the IFN-␥ -mediated down-regulation of ABC-1. These results further demonstrate the importance of cytokine crosstalk to impact the process of reverse cholesterol transport through a multitude of processes including the regulation of ABC-1.-Panousis, C. G., G. Evans, and S. H. Zuckerman. TGF-␤ increases cholesterol efflux and ABC-1 expression in macrophage-derived foam cells: opposing the effects of IFN-␥ .

show abstract

Transforming growth factor-beta 1 inhibits scavenger receptor activity in THP-1 human macrophages.

Cited by 100 publications

References 29 publications

Microglia in Alzheimer’s Disease: A Target for Therapeutic Intervention

Microglia in Alzheimer’s Disease: A Target for Therapeutic Intervention

Cytokine Expression by Human Macrophage-Like Cells Derived from the Monocytic Cell Line THP-1 Differs between Treatment with Milk from Preterm- and Term-Delivering Mothers and Pasteurized Donor Milk

TGF-β increases cholesterol efflux and ABC-1 expression in macrophage-derived foam cells: opposing the effects of IFN-γ

Contact Info

Product

Resources

About